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Background: Evidence describing the types and annual costs of biological treatments for psoriasis in Latin America is scarce. This study aimed to estimate the frequency of use and costs of biologic therapy for psoriasis in Colombia in 2019. Methods: This secondary data analysis uses the International Classification of Diseases terms associated with psoriasis, excluding those related to psoriatic arthritis, based on data from the registry of the Colombian Ministry of Health. We estimated the prevalence of psoriasis per 100,000 inhabitants; then, we retrieved the frequency of use of biologic therapy in patients with psoriasis and estimated the cost per year of each and overall therapies in 2019 in US dollars (USD). Results: There were 100,823 patients with psoriasis in Colombia in 2019, which amounts to a prevalence of 0.2% in the general population. Of those patients, 4.9% received biologic therapy, most frequently males (60%). The most commonly used biological therapies for psoriasis in Colombia in 2019 were ustekinumab (35.2%), with an annual cost per patient of $12,880 USD; adalimumab (26%), with a yearly cost per patient of $7130 USD; and secukinumab (19.8%), with an annual cost per patient of $6825 USD. Conclusion: This is the first study to describe the use and cost of biological therapy for psoriasis in Colombia. It provides valuable cost‐awareness information for the Colombian health system. [ABSTRACT FROM AUTHOR]

The article discusses a case of cutaneous sarcoidosis in a 37-year-old African descent female patient who was refractory to various treatments but responded to intralesional adalimumab. The patient had red to violaceous nodules on the nose and under the eyelid, diagnosed as lupus pernio type of cutaneous sarcoidosis. Intralesional adalimumab injections resulted in the flattening of the lesions, suggesting it as a viable treatment option for cutaneous sarcoidosis not responsive to other therapies. The study highlights the importance of personalized treatment approaches for managing challenging cases of cutaneous sarcoidosis. [Extracted from the article]

Background: Older persons elicit heterogeneous antibody responses to vaccinations that generally are lower than those in younger, healthier individuals. As older age and certain comorbidities can influence these responses we aimed to identify health-related variables associated with antibody responses after repeated SARS-CoV-2 vaccinations and their persistence thereafter in SARS-CoV-2 infection-naïve and previously infected older persons. Method: In a large longitudinal study of older persons of the general population 50 years and over, a sub-cohort of the longitudinal Doetinchem cohort study (n = 1374), we measured IgG antibody concentrations in serum to SARS-CoV-2 Spike protein (S1) and Nucleoprotein (N). Samples were taken following primary vaccination with BNT162b2 or AZD1222, pre- and post-vaccination with a third and fourth BNT162b2 or mRNA-1273 (Wuhan), and up to a year after a fifth BNT162b2 bivalent (Wuhan/Omicron BA.1) vaccine. Associations between persistence of antibody concentrations over time and age, sex, health characteristics including cardiometabolic and inflammatory diseases as well as a frailty index were tested using univariable and multivariable models. Results: The booster doses substantially increased anti-SARS-CoV-2 Spike S1 (S1) antibody concentrations in older persons against both the Wuhan and Omicron strains. Older age was associated with decreased antibody persistence both after the primary vaccination series and up to 1 year after the fifth vaccine dose. In infection-naïve persons the presence of inflammatory diseases was associated with an increased antibody response to the third vaccine dose (Beta = 1.53) but was also associated with reduced persistence over the 12 months following the fifth (bivalent) vaccine dose (Beta = -1.7). The presence of cardiometabolic disease was associated with reduced antibody persistence following the primary vaccination series (Beta = -1.11), but this was no longer observed after bivalent vaccination. Conclusion: Although older persons with comorbidities such as inflammatory and cardiometabolic diseases responded well to SARS-CoV-2 booster vaccinations, they showed a reduced persistence of these responses. This might indicate that especially these more vulnerable older persons could benefit from repeated booster vaccinations. [ABSTRACT FROM AUTHOR]

Abstract\nPLAIN LANGUAGE SUMMARYBecause of numerous stress signals, intracellular protein complexes are called inflammasomes. They function as catalysts for the proteolytic transformation of pro-interleukin into the active form of interleukin. Inflammasomes can promote a type of cell death process known as pyroptosis. The NLRP3 inflammasome, comprised of the NLRP3 protein, procaspase-1, and ASC, tightly regulates inflammation. The NLRP3 inflammasome is activated by a variety of stimuli, and several molecular and cellular events, such as ion influx, mitochondrial dysfunction, reactive oxygen species production, and lysosomal damage have been shown to trigger its activation. Inflammation plays a major role in almost all types of human diseases. The NLRP3 inflammasome has been the most widely studied and plays an important pathogenic role in various inflammatory pathologies. This review briefly presents the basic features of NLRP3 inflammasome and their mechanisms of activation and regulation. In addition, recent studies report the role of NLRP3 inflammasome in several diseases have been summarized.Because of numerous stress signals, intracellular protein complexes are called inflammasomes. They function as catalysts for the proteolytic transformation of pro-interleukin into the active form of interleukin. Inflammasomes can promote a type of cell death process known as pyroptosis. The NLRP3 inflammasome, comprised of the NLRP3 protein, procaspase-1, and ASC, tightly regulates inflammation. The NLRP3 inflammasome is activated by a variety of stimuli, and several molecular and cellular events, such as ion influx, mitochondrial dysfunction, reactive oxygen species production, and lysosomal damage, have been shown to trigger its activation. Also, NLRP3 inflammasome plays a role in several different diseases. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Despite advancements in psoriasis treatment, a gap remains in aligning patient satisfaction with clinical outcomes. Our study aimed to evaluate which clinical and psychological factors may impact treatment satisfaction in psoriatic patients undergoing long‐term biological therapies.We performed an observational, cross‐sectional, single‐center study involving adult patients with moderate‐to‐severe psoriasis treated with biologics for at least 12 months. We collected sociodemographic characteristics and data on the course of the psoriasis. We also assessed the absolute (residual) Psoriasis Area and Severity Index (PASI), the site of the residual disease, and the severity of pruritus through the Visual Analogue Scale (VAS). Satisfaction was evaluated using the Treatment Satisfaction Questionnaire for Medication (TSQMv.II). The Type D Personality Scale (DS14 questionnaire and Patient Health Questionnaire‐9 assessed the psychological profile.Overall, 146 patients were included, and 82.1% were globally satisfied (global satisfaction TSQM score >75). Linear regression analysis showed a negative correlation between global satisfaction scoring and residual PASI. The multivariable analysis found a higher VAS‐pruritus score (OR = 1.20, 95% CI = 1.01–1.44; P = 0.043) and not reaching a residual PASI < 2 (OR = 0.30, 95% CI = 0.09–0.94, P = 0.039) as the strongest predictors of global unsatisfied patients (TSQM < 75%).Other factors unrelated to residual disease, such as gender, class of biologic agent, and type D personality, have also been found to impact patient satisfaction.Our study's findings underscore the complexity of patient satisfaction in psoriasis management and highlight the multifactorial nature of treatment success beyond traditional clinical measures. [ABSTRACT FROM AUTHOR]

Introduction: Atopic dermatitis (AD) is a chronic inflammatory dermatosis that affects all age groups. The impact of AD on patients' lives could differ across generations. Understanding the differences in objective and subjective severity of AD between generations may support more personalized care for the AD patients. Thus, this study aimed to compare the clinical severity and subjective impact of AD between generation Z (GZ) and the millennial generation (MG). Materials and methods: We carried out a cross‐sectional observational study in patients diagnosed with moderate to severe AD born between 1993–2001 (GZ) and 1978–1992 (MG) who attended an AD specialist care unit for the first time. We collected severity indices evaluated by the dermatologist, such as the Eczema Area and Severity Index (EASI) or the Investigator Global Assessment (IGA), and severity scales that included patient assessment, such as the SCORing Atopic Dermatitis (SCORAD) or the Patient‐Oriented Eczema Measure (POEM). Results: A total of 73 patients were included, of which 56.2% (41/73) were women. 52.86% (37/73) of the patients belonged to the MG, and 43.8% (33/73) belonged to GZ. Patients belonging to GZ presented lower severity of their AD compared to the MG (EASI: 9.75 ± 11.68 vs. 16.63 ± 14.66; P < 0.05). However, their perception of disease severity was similar to the MG (SCORAD: 43.54 ± 28.99 vs. 32.98 ± 21.91; P = 0.96; POEM: 13.21 ± 8.98 vs. 15.48 ± 6.69; P = 0.14). Conclusions: GZ presents a higher subjective perception of severity than millennials. Understanding these generational disparities contributes to creating more effective treatment strategies and provides a more targeted approach to care that addresses each generational group's unique needs and expectations. [ABSTRACT FROM AUTHOR]

Several studies have described the proteomic profile of different immune cell types, but only a few have also analysed the content of their delivered small extracellular vesicles (sEVs). The aim of the present study was to compare the protein signature of sEVs delivered from granulocytes (i.e., neutrophils and eosinophils) and CD4+ T cells (i.e., TH1, TH2, and TH17) to identify potential biomarkers of the inflammatory profile in chronic inflammatory diseases. Qualitative (DDA) and quantitative (DIA-SWATH) analyses of in vitro-produced sEVs revealed proteome variations depending on the cell source. The main differences were found between granulocyte- and TH cell-derived sEVs, with a higher abundance of antimicrobial proteins (e.g., LCN2, LTF, MPO) in granulocyte-derived sEVs and an enrichment of ribosomal proteins (RPL and RPS proteins) in TH-derived sEVs. Additionally, we found differentially abundant proteins between neutrophil and eosinophil sEVs (e.g., ILF2, LTF, LCN2) and between sEVs from different TH subsets (e.g., ISG15, ITGA4, ITGB2, or NAMPT). A "proof-of-concept" assay was also performed, with TH2 biomarkers ITGA4 and ITGB2 displaying a differential abundance in sEVs from T2high and T2low asthma patients. Thus, our findings highlight the potential use of these sEVs as a source of biomarkers for diseases where the different immune cell subsets studied participate, particularly chronic inflammatory pathologies such as asthma or chronic obstructive pulmonary disease (COPD). [ABSTRACT FROM AUTHOR]

Chronic inflammatory diseases pose a substantial health challenge globally, significantly contributing to morbidity and mortality. Addressing this issue requires the use of effective anti-inflammatory strategies with fewer side effects than those provoked by currently used drugs. In this study, a range of phytochemicals (phenolic di-caffeoylquinic acid (Di-CQA), flavonoid cyanidin-3,5-diglucoside (Cy3,5DiG), aromatic isothiocyanate sinalbin (SNB) and aliphatic isothiocyanate sulforaphane (SFN)) sourced from vegetables and fruits underwent assessment for their potential anti-inflammatory activity. An in vitro model of human macrophage-like cells treated with a low dose of LPS to obtain a low degree of inflammation that emulates a chronic inflammation scenario revealed promising results. Cell viability and production of the key pro-inflammatory cytokines were assessed in the presence of various phytochemicals. The compounds Di-CQA and Cy-3,5-DiG, within low physiologically relevant doses, demonstrated notable anti-inflammatory effects by significantly reducing the production of key pro-inflammatory cytokines TNF-α and IL-6 without affecting cell viability. These findings underscore the potential of plant-derived bioactive compounds as valuable contributors to the prevention or treatment of chronic inflammatory diseases. These results suggest that these compounds, whether used individually or as part of natural mixtures, hold promise for their inclusion in nutritional interventions designed to mitigate inflammation in associated pathologies. [ABSTRACT FROM AUTHOR]

Objective: Inflammatory diseases are influenced by oxidative stress. Oxidatively damaged 8-oxoG in DNA is linked to inflammation. The enzyme OGG1 is responsible for repairing the damaged base in the DNA which is linked to pro-inflammatory signaling and severe inflammation. This study aims to explore the potential of targeting OGG1 as a therapeutic strategy in inflammatory disease conditions. Methods: A comprehensive search and review of literature were conducted using appropriate scientific databases such as Google Scholar, Scopus, PubMed, Web of Science, and other references to obtain relevant information that suited the title and content of this article. Results: Compelling pieces of evidence from many previous studies have shown the crucial role of the OGG1/8oxoG pathway in inflammatory disease conditions, leading to severe inflammatory response and death. Therefore, based on these pieces of evidence, targeting this enzyme (OGG1) using specific pharmacological inhibitors or interventions might lead to downregulation and amelioration of severe inflammation to reduce the morbimortality related to several disease conditions. Conclusion: This review highlighted the molecular mechanism of OGG1 activity via the 8-oxo/OGG1 pathway and its role in inflammation and inflammatory disease conditions. Due to the paucity of studies involving OGG1in inflammatory infectious diseases, further research projects are needed to explore the therapeutic potential of various OGG1 inhibitors to serve as novel therapeutic strategies in infectious inflammatory diseases of medical importance in developing countries such as malaria, meningitis, tuberculosis among others. [ABSTRACT FROM AUTHOR]

Inflammatory diseases, including psoriasis, atherosclerosis, rheumatoid arthritis, and ulcerative colitis, are characterized by persistent inflammation. Moreover, the existing treatments for inflammatory diseases only provide temporary relief by controlling symptoms, and treatments of unstable and expensive. Therefore, new therapeutic solutions are urgently needed to address the underlying causes or symptoms of inflammatory diseases. Inflammation frequently coincides with a high level of (reactive oxygen species) ROS activation, serving as a fundamental element in numerous physiological and pathological phenotypes that can result in serious harm to the organism. Given its pivotal role in inflammation, oxidative stress, and ferroptosis, ROS represents a focal node for investigating the (nuclear factor E2-related factor 2) Nrf2 pathway and ferroptosis, both of which are intricately linked to ROS. Ferroptosis is mainly triggered by oxidative stress and involves iron-dependent lipid peroxidation. The transcription factor Nrf2 targets several genes within the ferroptosis pathway. Recent studies have shown that Nrf2 plays a significant role in three key ferroptosis-related routes, including the synthesis and metabolism of glutathione/glutathione peroxidase 4, iron metabolism, and lipid processes. As a result, ferroptosis-related treatments for inflammatory diseases have attracted much attention. Moreover, drugs targeting Nrf2 can be used to manage inflammatory conditions. This review aimed to assess ferroptosis regulation mechanism and the role of Nrf2 in ferroptosis inhibition. Therefore, this review article may provide the basis for more research regarding the treatment of inflammatory diseases through Nrf2-inhibited ferroptosis. [ABSTRACT FROM AUTHOR]

Pediatric rheumatological diseases present with diverse manifestations affecting various tissues and organs. Though most childhood illnesses with immune dysregulation affect multiple organs or systems simultaneously or gradually, few inflammatory conditions affect certain organs as distinguished primary targets. Pediatric inflammatory diseases of the eye, bowel, and bone represent significant disorders with heterogeneous entities with varying pathophysiological basis like chronic inflammation, vasculitis, autoimmunity, and autoinflammation. Associations or complications of these diseases may remain obscure if their extensions are not explored specifically. Pediatric uveitis, non-uveitic inflammatory diseases, inflammatory bowel diseases, and autoinflammatory bone diseases are the important constituents of this cluster. The author concisely discusses these disorders in this review from pediatric rheumatological perspective. If untreated, these diseases may be organ-threatening. Outcomes are vastly different in undiagnosed patients and in timely diagnosed and treated patients. Lack of awareness and missed exploration of associated illnesses and complications may result in a missed diagnosis or inadequate symptomatic treatment. A multidisciplinary approach to diagnosis and treatment is desirable in these heterogeneous entities. Pediatricians must be aware of the immunological origin of organ-centered symptoms and signs. A proper understanding of molecular details of etiopathogenesis and significant advances in therapy have reduced the morbidity, disability, and mortality of such disorders. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) and prurigo nodularis (PN) are chronic dermatological conditions marked by severe itching and the presence of eczematous lesions such as papules and nodules. Both diseases can pose significant physical and psychological harm, leading to poor quality of life. Notably, AD and PN were clinically linked in the past, with suggestions by researchers that PN might be a distinct clinical phenotype of AD. However, the extent of their relationship had not been fully quantified until our recent investigations. Through a meticulous systematic review and meta‐analysis adhering to the PRISMA guidelines, we extensively searched databases, including PubMed, EMBASE, Scopus, and the Cochrane Library, up to February 18, 2024. Our random effects meta‐analysis presented a strikingly increased risk of AD in patients suffering from PN as opposed to control groups (pooled unadjusted odds ratio [OR], 16.85; 95% confidence interval [CI], 6.13–46.31; I2 = 100%). Correspondingly, an elevated prevalence of PN was identified in subjects with AD (2.00%; 95% CI, 1.62–2.37%). These findings underscore the close association between AD and PN, suggesting a multifaceted overlap and potential bi‐directionality in developing these skin conditions. However, further comprehensive studies are essential to validate these associations and understand their precise clinical implications, with the ultimate goal of refining patient management strategies. [ABSTRACT FROM AUTHOR]

Introduction Methods Results Conclusions Severe recurrent aphthous stomatitis (RAS) represents a therapeutic challenge because of its impact on the patient's quality of life. Additionally, no approved systemic therapies are available. Roflumilast, a phosphodiesterase‐4 inhibitor, has shown promise in other inflammatory dermatological conditions. This study aimed to assess the characteristics, effectiveness, and safety of roflumilast in treating RAS in routine clinical practice.This is a single cohort ambispective observational study conducted in five Spanish centers. Twenty‐two patients with RAS treated with roflumilast participated. Data collection included demographic, clinical, and outcome variables. Statistical analysis compared the outcomes of 12 weeks of roflumilast treatment with a similar prior period without treatment.During treatment with roflumilast, a significant reduction in flare‐ups (88%) and oral ulcers (94%) was observed compared to the untreated period. A reduction in pain (66%) and ulcer duration (63%) was observed. Adverse effects (AEs) occurred in 13 patients, predominantly headache and gastrointestinal disturbances. Most of these were self‐limiting or manageable with dose adjustment. Treatment was withdrawn in three cases, mainly because of AEs.This study suggests that roflumilast may effectively treat RAS by reducing the number of flare‐ups and ulcers, their duration, and the symptomatology produced by the ulcers. In addition, roflumilast has a good safety profile, is well tolerated at low doses, and does not require close monitoring. These characteristics and its favorable economic profile make roflumilast a promising therapeutic option in this pathology. [ABSTRACT FROM AUTHOR]

Background Objective Method Results Limitations Conclusion Immune checkpoint inhibitors (ICIs) have transformed cancer treatment by targeting immune checkpoints such as PD‐1, PDL‐1, and CTLA‐4, but concerns about severe immune‐related adverse events persist. The scarcity of literature on dermatologic implications, especially severe reactions such as Stevens‐Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), highlights the urgent need for investigation.Our systematic review aims to address the gap in relevant literature by extensively examining the epidemiologic risk factors and management of SJS/TEN‐like illnesses in ICI‐treated patients to provide insights for risk assessment and clinical care.We identified 158 case reports that detailed the incidence of SJS/TEN in patients being treated with ICIs, examining demographic patterns, type of malignancy, clinical characteristics, and treatments linked to onset. We assessed mortality rates, risk elements, and the effectiveness of interventions to help guide clinical care.Analysis of 158 case reports revealed that SJS/TEN in ICI users is typically seen on average at the age of 63 and is more common in males. PD1 inhibitors such as nivolumab and pembrolizumab are often associated with various mucocutaneous patterns and significant risks with ICI use, especially TEN, which is linked to high morbidity and mortality rates.Our study notes limitations due to the inclusion of case reports or case series, such as potential publication and reporting biases, leading to skewed findings. Additionally, because of the heterogeneous reporting standards, the retrospective nature limits phenotypic precision, control for confounding variables, and data completeness.Our study provides valuable insights into the epidemiology, clinical features, management strategies, and outcomes of ICI‐induced SJS/TEN, underscoring the importance of vigilant monitoring and personalized risk assessment in oncology practice. Continued research efforts are essential to optimize patient outcomes and enhance the safety profile of ICIs in cancer therapy. [ABSTRACT FROM AUTHOR]

Inflammatory diseases compromise a clinically common and diverse group of conditions, causing detrimental effects on body functions. Gasdermins (GSDM) are pore-forming proteins, playing pivotal roles in modulating inflammation. Belonging to the GSDM family, gasdermin D (GSDMD) actively mediates the pathogenesis of inflammatory diseases by mechanistically regulating different forms of cell death, particularly pyroptosis, and cytokine release, in an inflammasome-dependent manner. Aberrant activation of GSDMD in different types of cells, such as immune cells, cardiovascular cells, pancreatic cells and hepatocytes, critically contributes to the persistent inflammation in different tissues and organs. The contributory role of GSDMD has been implicated in diabetes mellitus, liver diseases, cardiovascular diseases, neurodegenerative diseases, and inflammatory bowel disease (IBD). Clinically, alterations in GSDMD levels are potentially indicative to the occurrence and severity of diseases. GSDMD inhibition might represent an attractive therapeutic direction to counteract the progression of inflammatory diseases, whereas a number of GSDMD inhibitors have been shown to restrain GSDMD-mediated pyroptosis through different mechanisms. This review discusses the current understanding and future perspectives on the role of GSDMD in the development of inflammatory diseases, as well as the clinical insights of GSDMD alterations, and therapeutic potential of GSDMD inhibitors against inflammatory diseases. Further investigation on the comprehensive role of GSDM shall deepen our understanding towards inflammation, opening up more diagnostic and therapeutic opportunities against inflammatory diseases. [ABSTRACT FROM AUTHOR]

This article discusses a case report and literature review on the treatment of relapsing polychondritis with inverse psoriasis using tofacitinib and risankizumab. Relapsing polychondritis is an inflammatory condition that primarily affects cartilaginous tissues, while inverse psoriasis is a form of psoriasis that occurs in skin folds. The patient in the case study had a history of Hashimoto's thyroiditis and presented with symptoms such as chest pain, recurrent swelling of the nose and ears, joint pain, and psoriatic lesions. The patient was initially treated with methotrexate and systemic steroid therapy but did not respond well. Tofacitinib and risankizumab were then added to the treatment regimen, resulting in significant clinical improvement. The article also discusses the challenges of treating relapsing polychondritis and the effectiveness of different treatment options. [Extracted from the article]

Interleukin‐41 (IL‐41) is a newly discovered cytokine, named Cometin, Subfatin, meteorin‐like transcription (Metrnl), and so forth. It is widely expressed in animals and can exert its biological roles through autocrine and paracrine forms. It has functions such as anti‐inflammatory, improving body metabolism, regulating immunity, regulating fat metabolism and participates in the process of autoimmune disease or inflammatory injury. It plays an important role in psoriasis, diabetes, Crohn's disease (CD), osteoarthritis, Kawasaki disease (KD), Graves' disease, autoimmune hepatitis, infertility, obesity, sepsis, cardiovascular diseases and respiratory diseases. This paper reviews the biological functions of IL‐41, the relationship between IL‐41 and diseases, the effects of IL‐41 in the cytokine network and the possible signalling pathways. In order to explore the same target or the same drug for the treatment of different diseases from the perspective of homotherapy for heteropathy, cytokine strategies based on IL‐41 have been put forward for the precise treatment of immune diseases and inflammatory diseases. It is worth noting that IL‐41 related preparations for lung protection and smoking cessation are interesting research fields. [ABSTRACT FROM AUTHOR]

Eosinophilic dermatosis of hematologic malignancy (EDHM) is a cutaneous manifestation seen in patients with hematoproliferative and lymphoproliferative disorders, most commonly chronic lymphocytic leukemia. This systematic review aimed to summarize the therapeutic interventions of EDHM. A comprehensive search yielded 71 studies, predominantly case reports and series. The most frequently reported modalities were systemic and topical corticosteroids, as well as treatment of the underlying malignancy. Responses to these treatments varied. Targeted therapies, including dupilumab and omalizumab, showed promise, as did other modalities such as montelukast, dapsone, doxycycline, and phototherapy. Higher‐quality studies should be conducted to facilitate higher‐quality management recommendations for EDHM. [ABSTRACT FROM AUTHOR]

Background: Over the past few decades, advances in medical research and diagnostic tools have shed light on some aspects of pyoderma gangrenosum (PG). Nevertheless, the multifactorial etiology, pathogenesis, and optimal management strategies for PG need to be further investigated. To address these knowledge gaps and contribute to a better understanding of this complex dermatological disorder, we collected epidemiological, clinical, and therapeutic aspects of a case series of PG patients occurring in our department over the past 10 years. Methods: We performed a single‐centered, retrospective, observational study analyzing all cases with a diagnosis of PG observed at the Dermatology clinic of the Fondazione Policlinico A. Gemelli IRCCS Catholic University from January 1, 2013, to January 1, 2023. For each case, we retrieved demographic data, the presence of other skin and systemic conditions, and the histopathological and clinical characteristics of PG, such as clinical variant, number of lesions, disease localization, previous therapy, response to treatment, and occurrence of relapse. Results: We included 35 patients, 22 females and 13 males with a mean age of 40.0 years. Twenty patients (57.1%) had multiple localizations of disease, and the most commonly involved site was the lower limbs (85.7%). The lesions were mainly associated with inflammatory bowel diseases (51.4%) and hidradenitis suppurativa (37.1%). Clinical resolution with complete re‐epithelialization was achieved in 25 patients (71.4%) with an average time of 20.8 months. On average, patients who underwent therapy with biological drugs had better outcomes. Conclusions: PG is a severe, rare, and pleomorphic disease associated with a broad spectrum of conditions. Corticosteroids remain the primary first‐line approach for severe forms, but using biological immunosuppressants is promising. [ABSTRACT FROM AUTHOR]

Dysregulated inflammation after trauma or infection could result in the further disease and delayed tissue reconstruction. The conventional anti-inflammatory drug treatment suffers to the poor bioavailability and side effects. Herein, we developed an amphiphilic multifunctional poly (citrate-polyglycol-curcumin) (PCGC) nano oligomer with the robust anti-inflammatory activity for treating acute lung injury (ALI) and Methicillin-resistant staphylococcus aureus (MRSA) infected wound. PCGC demonstrated the sustained curcumin release, inherent photoluminescence, good cellular compatibility, hemocompatibility, robust antioxidant activity and enhanced cellular uptake. PCGC could efficiently scavenge nitrogen-based free radicals, oxygen-based free radicals, and intracellular oxygen species, enhance the endothelial cell migration and reduce the expression of pro-inflammatory factors through the NF-κB signal pathway. Combined the anti-inflammation and antioxidant properties, PCGC can shortened the inflammatory process. In animal model of ALI, PCGC was able to reduce the pulmonary edema, bronchial cell infiltration, and lung inflammation, while exhibiting rapid metabolic behavior in vivo. The MRSA-infection wound model showed that PCGC significantly reduced the expression of pro-inflammatory factors, promoted the angiogenesis and accelerated the wound healing. The transcriptome sequencing and molecular mechanism studies further demonstrated that PCGC could inhibit multiple inflammatory related pathways including TNFAIP3, IL-15RA, NF-κB. This work demonstrates that PCGC is efficient in resolving inflammation and promotes the prospect of application in inflammatory diseases as the drug-loaded therapeutic system.

Abstract Background Older persons elicit heterogeneous antibody responses to vaccinations that generally are lower than those in younger, healthier individuals. As older age and certain comorbidities can influence these responses we aimed to identify health-related variables associated with antibody responses after repeated SARS-CoV-2 vaccinations and their persistence thereafter in SARS-CoV-2 infection-naïve and previously infected older persons. Method In a large longitudinal study of older persons of the general population 50 years and over, a sub-cohort of the longitudinal Doetinchem cohort study (n = 1374), we measured IgG antibody concentrations in serum to SARS-CoV-2 Spike protein (S1) and Nucleoprotein (N). Samples were taken following primary vaccination with BNT162b2 or AZD1222, pre- and post-vaccination with a third and fourth BNT162b2 or mRNA-1273 (Wuhan), and up to a year after a fifth BNT162b2 bivalent (Wuhan/Omicron BA.1) vaccine. Associations between persistence of antibody concentrations over time and age, sex, health characteristics including cardiometabolic and inflammatory diseases as well as a frailty index were tested using univariable and multivariable models. Results The booster doses substantially increased anti-SARS-CoV-2 Spike S1 (S1) antibody concentrations in older persons against both the Wuhan and Omicron strains. Older age was associated with decreased antibody persistence both after the primary vaccination series and up to 1 year after the fifth vaccine dose. In infection-naïve persons the presence of inflammatory diseases was associated with an increased antibody response to the third vaccine dose (Beta = 1.53) but was also associated with reduced persistence over the 12 months following the fifth (bivalent) vaccine dose (Beta = -1.7). The presence of cardiometabolic disease was associated with reduced antibody persistence following the primary vaccination series (Beta = -1.11), but this was no longer observed after bivalent vaccination. Conclusion Although older persons with comorbidities such as inflammatory and cardiometabolic diseases responded well to SARS-CoV-2 booster vaccinations, they showed a reduced persistence of these responses. This might indicate that especially these more vulnerable older persons could benefit from repeated booster vaccinations.

Interleukin-6 (IL-6) plays a critical role in the pathogenesis of various chronic inflammatory diseases, tracked across numerous fields of research. Despite this, a crucial aspect often overlooked in studies is the differentiation between IL-6 classic-signaling and trans-signaling, leading to potential confounding of their findings; less than half of selected IL-6 studies included differentiation. This review delves into the distinction between IL-6 classic- and trans-signaling and their role in chronic inflammatory diseases and endometriosis. The unique pro-inflammatory nature of IL-6 trans-signaling, contrasted with the anti-inflammatory character of IL-6 classic-signaling, presents significant implications for research methodology, particularly in studies investigating anti-inflammatory interventions or interleukin inhibitors. Diagnostic failure to account for these distinct pathways may inadvertently misrepresent beneficial immune responses or the efficacy of interventions, posing significant challenges in predicting health outcomes. Interventions that do not differentiate these pathways could face reduced efficacy or safety. This review proposes adjustments to research methodologies and stresses the importance of careful interpretation of inflammatory markers in IL-6-related research. Examples of differentiation issues are discussed across the topics of endometriosis and multiple inflammatory diseases. By addressing this methodological issue, researchers could potentially improve patient outcomes, enhance the efficacy of interventions, and contribute to public health advancements.

Abstract The concept of Yin-Yang, originating in ancient Chinese philosophy, symbolizes two opposing but complementary forces or principles found in all aspects of life. This concept can be quite fitting in the context of extracellular vehicles (EVs) and inflammatory diseases. Over the past decades, numerous studies have revealed that EVs can exhibit dual sides, acting as both pro- and anti-inflammatory agents, akin to the concept of Yin-Yang theory (i.e., two sides of a coin). This has enabled EVs to serve as potential indicators of pathogenesis or be manipulated for therapeutic purposes by influencing immune and inflammatory pathways. This review delves into the recent advances in understanding the Yin-Yang sides of EVs and their regulation in specific inflammatory diseases. We shed light on the current prospects of engineering EVs for treating inflammatory conditions. The Yin-Yang principle of EVs bestows upon them great potential as, therapeutic, and preventive agents for inflammatory diseases. Graphical Abstract

Yan Wang,1 Hui Ma,1 Xiaohua Zhang,1 Xia Xiao,1 Zecheng Yang2 1Department of Clinical Laboratory, The Second Hospital of Jilin University, Changchun, 130000, People’s Republic of China; 2Department of Gastrointestinal Surgery, The Second Hospital of Jilin University, Changchun, 130000, People’s Republic of ChinaCorrespondence: Hui Ma, Department of Clinical Laboratory, The Second Hospital of Jilin University, Changchun, 130000, People’s Republic of China, Tel +86-431-81136555, Email mahui4872@jlu.edu.cnAbstract: Inflammatory diseases provide substantial worldwide concerns, affecting millions of people and healthcare systems by causing ongoing discomfort, diminished quality of life, and increased expenses. In light of the progress made in treatments, the limited effectiveness and negative side effects of present pharmaceuticals need a more comprehensive comprehension of the underlying processes in order to develop more precise remedies. Exosomes, which are tiny vesicles that play a vital role in cell communication, have been identified as prospective vehicles for effective delivery of anti-inflammatory medicines, immunomodulators, and gene treatments. Vesicles, which are secreted by different cells, have a crucial function in communicating between cells. This makes them valuable in the fields of diagnostics and therapies, particularly for inflammatory conditions. Exosomes have a role in regulating the immune system, transporting cytokines, and influencing cell signaling pathways associated with inflammation. They consist of proteins, lipids, and genetic information that have an impact on immune responses and inflammation. Scientists are now investigating exosomes as biomarkers for inflammatory disease. This review article aims to develop non-invasive diagnostic techniques with improved sensitivity and specificity. Purpose of this review is a thorough examination of exosomes in pharmacology, specifically emphasizing their origin, contents, and functions, with the objective of enhancing diagnostic and therapeutic strategies for inflammatory conditions. Gaining a comprehensive understanding of the intricate mechanisms involved in exosome-mediated interactions and their impact on immune responses is of utmost importance in order to devise novel approaches for tackling inflammatory disease and enhancing patient care.Keywords: exosomes, inflammatory diseases, diagnostic biomarkers, biogenesis of exosomes, immune response

Honey is a natural substance produced by honeybees and is widely consumed as food worldwide. Honey has anti-inflammatory effects, which are related to its antibacterial and antioxidant functions. The anti-inflammatory properties of honey can be explored from two aspects: Basic research studies that reveal the molecular mechanisms underlying the biological functions of honey and identify its effective components, and clinical research studies that evaluate the healing effects of honey in inflammatory diseases. Basic research studies are indicated that honey has anti-inflammatory properties and further elucidated the relevant molecular mechanisms. The anti-inflammatory functions of honey are highly related to its components, specifically flavonoids, phenolic acids, glucose oxidase, hydrogen peroxide, and methylglyoxal. These effective constituents exhibit anti-inflammatory effects by regulating immune cell function, affecting inflammatory cytokines, inhibiting the growth of pathogenic bacteria, and acting as antioxidants. Honey can attenuate gastrointestinal inflammation, aid the recovery of intestinal microbiota, relieve symptoms of chronic sinusitis, and prevent radiation-induced oral mucositis. Based on honey-related basic and clinical research studies conducted over the past five years, this article reviews the anti-inflammatory mechanisms of honey, the functions of its effective constituents, and the applications of honey in inflammatory diseases.

Metabolism plays a crucial role in regulating the function of immune cells in both health and disease, with altered metabolism contributing to the pathogenesis of cancer and many inflammatory diseases. The local microenvironment has a profound impact on the metabolism of immune cells. Therefore, immunological and metabolic heterogeneity as well as the spatial organization of cells in tissues should be taken into account when studying immunometabolism. Here, we highlight challenges of investigating metabolic communication. Additionally, we review the capabilities and limitations of current technologies for studying metabolism in inflamed microenvironments, including single‐cell omics techniques, flow cytometry‐based methods (Met‐Flow, single‐cell energetic metabolism by profiling translation inhibition (SCENITH)), cytometry by time of flight (CyTOF), cellular indexing of transcriptomes and epitopes by sequencing (CITE‐Seq), and mass spectrometry imaging. Considering the importance of metabolism in regulating immune cells in diseased states, we also discuss the applications of metabolomics in clinical research, as well as some hurdles to overcome to implement these techniques in standard clinical practice. Finally, we provide a flowchart to assist scientists in designing effective strategies to unravel immunometabolism in disease‐relevant contexts.

The aryl hydrocarbon receptor (AhR) is a versatile environmental sensor and transcription factor found throughout the body, responding to a wide range of small molecules originating from the environment, our diets, host microbiomes, and internal metabolic processes. Increasing evidence highlights AhR's role as a critical regulator of numerous biological functions, such as cellular differentiation, immune response, metabolism, and even tumor formation. Typically located in the cytoplasm, AhR moves to the nucleus upon activation by an agonist where it partners with either the aryl hydrocarbon receptor nuclear translocator (ARNT) or hypoxia-inducible factor 1β (HIF-1β). This complex then interacts with xenobiotic response elements (XREs) to control the expression of key genes. AhR is notably present in various crucial immune cells, and recent research underscores its significant impact on both innate and adaptive immunity. This review delves into the latest insights on AhR's structure, activating ligands, and its multifaceted roles. We explore the sophisticated molecular pathways through which AhR influences immune and lymphoid cells, emphasizing its emerging importance in managing inflammatory diseases. Furthermore, we discuss the exciting potential of developing targeted therapies that modulate AhR activity, opening new avenues for medical intervention in immune-related conditions. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions identifier Pruritus is a common, bothersome symptom for patients with mild‐to‐moderate plaque psoriasis (PsO), yet no validated scale assesses it in this patient population. We aimed to validate the Peak Pruritus‐Numerical Rating Scale (PP‐NRS) using data from a Phase 2b study investigating the efficacy of brepocitinib in patients with mild‐to‐moderate chronic PsO.Patients completed the PP‐NRS daily from baseline for the first 2 weeks after the dose administration and subsequently only on visit days. Test–retest reliability (intraclass correlation coefficient [ICC]), construct validity (known group validity and convergent validity), ability to detect change, and meaningful within‐patient change (MWPC) were evaluated using correlation and regression analyses.The PP‐NRS demonstrated acceptable test–retest reliability (ICC: 0.86–0.89). Known‐group evidence demonstrated that PP‐NRS scores could discriminate between different degrees of disease severity. Convergent validity was supported by significant correlation coefficients between the PP‐NRS and Patient Global Assessment (PtGA), Dermatology Life Quality Index, and Psoriasis Symptom Inventory, which generally exceeded 0.50. The ability to detect change was evidenced by an approximately linear relationship between changes in PP‐NRS and Physician Global Assessment or PtGA of psoriasis scores. The value of 2.8 was determined as the MWPC for the PP‐NRS.PP‐NRS is a reliable, practical test for assessing pruritus in mild‐to‐moderate PsO clinical trials.NCT03850483. [ABSTRACT FROM AUTHOR]

Occupational dermatitis (OD) is an inflammatory skin disease stemming from exposure to specific substances within a work setting. As the second most prevalent occupational health concern in 2020, affecting 1.8 per 10,000 workers, OD poses a significant challenge to workforce well‐being and imposes a substantial economic burden through lost wages, decreased productivity, and increased healthcare spending. Dermatologists emerge as pivotal figures in recognizing risk factors and delivering essential care to individuals with OD. This review focuses on chemical hazards and toxic substances regulated by the Occupational Safety and Health Administration across general industry, maritime, and construction sectors. It explores the background of each hazard, pathophysiology to dermatitis, and human cases reported between 2017 and 2023 for formaldehyde, chromium, vinyl chloride, and cadmium. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions The association between psoriasis and pulmonary fibrosis has been reported in observational studies. However, the association is vulnerable to bias from using immunosuppressants such as methotrexate, which can cause fibrosis in multiple organs. The present study is to investigate whether psoriasis could independently increase the risk of idiopathic pulmonary fibrosis (IPF).We conducted a two‐sample Mendelian randomization (MR) study using summary statistics from genome‐wide association studies. The random‐effects inverse variance weighted analysis was used as the primary method. Some secondary analyses were further performed, including a sensitivity analysis using a genetic instrument that excluded extended single nucleotide polymorphisms (SNPs) in the major histocompatibility complex (MHC) gene region.Our study included 9267 cases and 364,071 controls for psoriasis, 2018 cases, and 373,064 controls for IPF of European ancestry, respectively. Genetically predicted psoriasis was associated with a higher risk of IPF (odds ratio (OR), 1.14; 95% confidence interval (CI), 1.08–1.22; P < 0.001). Sensitivity analyses did not uncover any statistically significant evidence of bias resulting from pleiotropy or the genetic instruments, including SNPs in the MHC gene region.These MR analyses support that genetically predicted psoriasis was associated with the risk of IPF, implying that pulmonary fibrosis in patients with psoriasis should not be neglected, even if they are not receiving immunosuppressant therapy. [ABSTRACT FROM AUTHOR]

Nowadays, GSK3 is accepted as an enzyme strongly involved in the regulation of inflammation by balancing the pro- and anti-inflammatory responses of cells and organisms, thus influencing the initiation, progression, and resolution of inflammatory processes at multiple levels. Disturbances within its broad functional scope, either intrinsically or extrinsically induced, harbor the risk of profound disruptions to the regular course of the immune response, including the formation of severe inflammation-related diseases. Therefore, this review aims at summarizing and contextualizing the current knowledge derived from animal models to further shape our understanding of GSK3α and β and their roles in the inflammatory process and the occurrence of tissue/organ damage. Following a short recapitulation of structure, function, and regulation of GSK3, we will focus on the lessons learned from GSK3α/β knock-out and knock-in/overexpression models, both conventional and conditional, as well as a variety of (predominantly rodent) disease models reflecting defined pathologic conditions with a significant proportion of inflammation and inflammation-related tissue injury. In summary, the literature suggests that GSK3 acts as a crucial switch driving pro-inflammatory and destructive processes and thus contributes significantly to the pathogenesis of inflammation-associated diseases. [ABSTRACT FROM AUTHOR]

Signaling proteins in eukaryotes usually comprise a catalytic domain coupled to one or several interaction domains, such as SH2 and SH3 domains. An additional class of proteins critically involved in cellular communication are adapter or scaffold proteins, which fulfill their purely non-enzymatic functions by organizing protein–protein interactions. Intriguingly, certain signaling enzymes, e.g., kinases and phosphatases, have been demonstrated to promote particular cellular functions by means of their interaction domains only. In this review, we will refer to such a function as "the adapter function of an enzyme". Though many stories can be told, we will concentrate on several proteins executing critical adapter functions in cells of the immune system, such as Bruton´s tyrosine kinase (BTK), phosphatidylinositol 3-kinase (PI3K), and SH2-containing inositol phosphatase 1 (SHIP1), as well as in cancer cells, such as proteins of the rat sarcoma/extracellular signal-regulated kinase (RAS/ERK) mitogen-activated protein kinase (MAPK) pathway. We will also discuss how these adaptor functions of enzymes determine or even undermine the efficacy of targeted therapy compounds, such as ATP-competitive kinase inhibitors. Thereby, we are highlighting the need to develop pharmacological approaches, such as proteolysis-targeting chimeras (PROTACs), that eliminate the entire protein, and thus both enzymatic and adapter functions of the signaling protein. We also review how genetic knock-out and knock-in approaches can be leveraged to identify adaptor functions of signaling proteins. [ABSTRACT FROM AUTHOR]

Interferon‐beta has been suggested as a trigger of psoriasis, yet a systematic investigation is lacking. This study aimed to assess the risk of developing psoriasis following interferon‐beta treatment, utilizing a pharmaco‐epidemiological approach to investigate the role of interferon‐beta in psoriasis pathogenesis. We included all treatment‐naïve patients with multiple sclerosis (MS) in Denmark who initiated interferon‐beta treatment for MS from January 1996 to June 2023. These patients were compared to a control cohort of patients with MS treated with other disease‐modifying drugs. We compared the incidence rates of psoriasis before and during the treatment. Data for this study were extracted from the Danish MS Registry and integrated with information from other national Danish health registries. Among 7174 patients treated with interferon‐beta, the incidence rate of psoriasis post‐treatment initiation was slightly higher (2.01 per 1000 person‐years) compared to the rate prior to treatment (1.67 per 1000 person‐years). This increase did not achieve statistical significance (P = 0.53), with an incidence rate ratio (IRR) of 1.20 (95% confidence interval [CI] 0.68–2.13). The control cohort showed an increase in psoriasis incidence post‐treatment initiation (3.12 per 1000 person‐years) compared to prior (1.11 per 1000 person‐years), with an IRR of 2.80 (95% CI 1.36–4.77, P = 0.0038). This registry‐based self‐controlled study does not support the theory that interferon‐beta acts as a trigger for psoriasis development. [ABSTRACT FROM AUTHOR]

Hydrogels, composed of three-dimensional polymer networks, are excellent delivery carriers and have been extensively employed in the biomedical field. Inflammation acts as a protective mechanism to prevent harmful substances from entering living organisms, but chronic, long-lasting inflammation can cause oxidative stress, which damages tissue and organs and adversely affects patients' quality of life. The aberrant expression of microRNAs (miRNAs) has been found to play a significant part in the etiology and progression of inflammatory diseases, as suggested by growing evidence. Numerous hydrogels that can act as gene carriers for the intracellular delivery of miRNA have been described during ongoing research into innovative hydrogel materials. MiRNA hydrogel delivery systems, which are loaded with exogenous miRNA inhibitors or mimics, enable targeted miRNA intervention in inflammatory diseases and effectively prevent environmental stressors from degrading or inactivating miRNA. In this review, we summarize the classification of miRNA hydrogel delivery systems, the basic strategies and mechanisms for loading miRNAs into hydrogels, highlight the biomedical applications of miRNA hydrogel delivery systems in inflammatory diseases, and share our viewpoints on potential opportunities and challenges in the promising region of miRNA delivery systems. These findings may provide a new theoretical basis for the prevention and treatment of inflammation-related diseases and lay the foundation for clinical translation. [ABSTRACT FROM AUTHOR]

AbstractEfferocytosis refers to the process by which phagocytes remove apoptotic cells and related apoptotic products. It is essential for the growth and development of the body, the repair of damaged or inflamed tissues, and the balance of the immune system. Damaged efferocytosis will cause a variety of chronic inflammation and immune system diseases. Many studies show that efferocytosis is a process mediated by mitochondria. Mitochondrial metabolism, mitochondrial dynamics, and communication between mitochondria and other organelles can all affect phagocytes’ clearance of apoptotic cells. Therefore, targeting mitochondria to modulate phagocyte efferocytosis is an anticipated strategy to prevent and treat chronic inflammatory diseases and autoimmune diseases. In this review, we introduced the mechanism of efferocytosis and the pivoted role of mitochondria in efferocytosis. In addition, we focused on the therapeutic implication of drugs targeting mitochondria in diseases related to efferocytosis dysfunction. [ABSTRACT FROM AUTHOR]

AbstractObjectiveData sourcesStudy selectionsResultsConclusionsThe purpose of this study is to systematically investigate the different phenotypes and functional analyses of macrophages in lung tissue.A search was performed using three databases (Web of Science, Science Direct, and MEDLINE) for all relevant studies published from January 1, 2019, to December 31, 2023.This systematic review complied with the PRlSMA document’s requirements, including studies related to the signaling pathway relationship between pulmonary macrophages and asthma phenotype. The search includedstudies published in English or French lanquage, and was based on title, abstract, and complete textDocuments not meeting inclusion requirements were excludedWe have identified studies published within the past five years that meet the criteria for inclusion in this review. We found that asthma is a heterogeneous chronic inflammatory lung disease, and lung tissue macrophages are important immune cells in the respiratory tract. Pulmonary macrophages are also heterogeneous, as they have different subgroups with varying effector functions depending on the environment. They have different phenotypes and biological functions in different disease environments. The phenotypic changes of pulmonary macrophages occur during asthma, and the study of the different phenotypes and functions of macrophages in lung tissue is of great significance for treatment.This review summarizes current literature and provides a detailed introduction to the role of macrophages as key inflammatory mediators in the pathogenesis of asthma, as well as existing knowledge gaps. In addition, we propose that regulatory macrophages may prevent the development of asthma by producing IL-10, and regulating the polarization of pulmonary macrophages may be a new direction for asthma treatment. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Recently, it has been questioned whether vaccination of patients with inflammatory (auto)immune diseases under anti‐tumor necrosis factor (TNF) treatment leads to impaired vaccine‐induced immune responses and protection against breakthrough infections. However, the effects of TNF blockade on short‐ and long‐term immune responses after repeated vaccination remain unclear. Vaccination studies have shown that initial short‐term IgG antibodies (Abs) carry highly galactosylated and sialylated Fc glycans, whilst long‐term IgG Abs have low levels of galactosylation and sialylation and are most likely generated by long‐lived plasma cells (PCs) derived primarily from the germinal center (GC) response. Thus, IgG Fc glycosylation patterns may be applicable to distinguish short‐ and long‐term vaccine responses after repeated vaccination under the influence of anti‐TNF treatment.We used COVID‐19 vaccination as a model to investigate vaccine‐induced IgG subclass levels and Fc glycosylation patterns, B cell subsets, and effector functions of short‐ and long‐term Ab responses after up to three vaccinations in patients on anti‐TNF or other immunosuppressive treatments and in healthy individuals. Using TriNetX, a global healthcare database, we determined the risk of SARS‐CoV‐2 breakthrough infections in vaccinated patients treated with anti‐TNF or other immunosuppressive drugs.Anti‐TNF treatment reduced the long‐term abundance of all anti‐S IgG subclasses with low levels of galactosylation and sialylation. Re‐activation of potential memory B cells initially generated highly galactosylated and sialylated IgG antibodies, which were progressively reduced after each booster dose in anti‐TNF‐treated patients, especially in the elderly. The reduced short‐ and long‐term IgG (1) levels in anti‐TNF‐treated patients correlated with diminished functional activity and an increased risk for the development of COVID‐19.The data suggest that anti‐TNF treatment reduces both GC‐dependent long‐lived PCs and GC‐dependent memory B cell‐derived short‐lived PCs, hence both the long‐ and short‐term IgG subclass responses, respectively, after repeated vaccination. We propose that anti‐TNF therapy, especially in the elderly, reduces the benefit of booster vaccination. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Psoriasis significantly burdens patients' lives, but there is limited data on this in Brazil.Between May 2022 and January 2023, we conducted a cross‐sectional online survey of 563 Brazilian residents aged ≥18 years who had been diagnosed with psoriasis. Spearman's correlation (r) was used to test the correlation between self‐assessed disease severity (Simplified Psoriasis Index [saSPI] extent score; range 0 [clear/minor] to 40 [widespread/severe]) and health‐related quality of life (QoL, score of 1 means perfect health) and capability (ICECAP‐A: score of 1 means full capability) measures. Multivariable linear regression was used to identify predictors of QoL and capability. A thematic analysis examined the free‐text responses and identified common themes.The mean age of participants was 42.1 ± 12.4 years, and over half had at least one other long‐term condition. The mean QoL score was 0.59 ± 0.25, and the mean capability score was 0.71 ± 0.21. At the time of survey completion, over 80% of respondents reported some level of pain and/or discomfort, and 86% reported feeling anxious and/or depressed. The mean self‐assessed saSPI was 7.8 ± 8.6, which negatively correlated with health‐related QoL (r = −0.49, P < 0.05) and capability (r = −0.44, P < 0.05). Significant predictors of poorer QoL and reduced capability included high saSPI, number of psoriasis flares and comorbidities, female gender, Black ethnicity, and employment status (unemployed, long‐term sick). Frequently reported areas that impacted patients were social stigma/prejudice, powerlessness, lack of education and public awareness, and difficulty obtaining appropriate care/treatment.We found that the clinical manifestations, severity, and associated comorbidities of psoriasis negatively impacted health‐related QoL and capability, along with feelings of stigmatization and barriers to specialist treatment. This highlights the need for better access to care and awareness of the disease to improve the lives of people living with psoriasis in Brazil. [ABSTRACT FROM AUTHOR]

The emergence of inflammatory diseases is a heavy burden on modern societies. Cannabis has been used for several millennia to treat inflammatory disorders such as rheumatism or gout. Since the characterization of cannabinoid receptors, CB1 and CB2, the potential of cannabinoid pharmacotherapy in inflammatory conditions has received great interest. Several studies have identified the importance of these receptors in immune cell migration and in the production of inflammatory mediators. As the presence of the CB2 receptor was documented to be more predominant in immune cells, several pharmacological agonists and antagonists have been designed to treat inflammation. To better define the potential of the CB2 receptor, three online databases, PubMed, Google Scholar and clinicaltrial.gov, were searched without language restriction. The full texts of articles presenting data on the endocannabinoid system, the CB2 receptor and its role in modulating inflammation in vitro, in animal models and in the context of clinical trials were reviewed. Finally, we discuss the clinical potential of the latest cannabinoid-based therapies in inflammatory diseases. [ABSTRACT FROM AUTHOR]

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Inflammation has been shown to trigger a wide range of chronic diseases, particularly inflammatory diseases. As a result, the focus of research has been on anti-inflammatory drugs and foods. In recent years, the field of medicinal and edible homology (MEH) has developed rapidly in both medical and food sciences, with 95% of MEH being associated with plants. Phenolic acids are a crucial group of natural bioactive substances found in medicinal and edible homologous plants (MEHPs). Their anti-inflammatory activity is significant as they play a vital role in treating several inflammatory diseases. These compounds possess enormous potential for developing anti-inflammatory drugs and functional foods. However, their development is far from satisfactory due to their diverse structure and intricate anti-inflammatory mechanisms. In this review, we summarize the various types, structures, and distribution of MEHP phenolic acids that have been identified as of 2023. We also analyze their anti-inflammatory activity and molecular mechanisms in inflammatory diseases through NF-kB, MAPK, NLRP3, Nrf2, TLRs, and IL-17 pathways. Additionally, we investigate their impact on regulating the composition of the gut microbiota and immune responses. This analysis lays the groundwork for further exploration of the anti-inflammatory structure-activity relationship of MEHP phenolic acids, aiming to inspire structural optimization and deepen our understanding of their mechanism, and provides valuable insights for future research and development in this field. [ABSTRACT FROM AUTHOR]

Macrophage Migration Inhibitory Factor (MIF) is a critical cytokine implicated in various human disorders, with significant roles in innate and acquired immunity and inflammatory diseases. Recent investigations have linked MIF to the pathophysiology of cancer. Extensive research has been dedicated to studying its structure and actions, leading to its classification as both an enzyme and a hormone. Its isomerase enzymatic activity is exciting, which has sparked enthusiasm for developing specific small-molecule inhibitors targeting this unique enzymatic function to treat inflammatory illnesses potentially. While there is growing awareness of MIF's importance in inflammation and cancer, the availability of adequate and extensively studied MIF inhibitors for relevant disease models remains limited. Advancing drug discovery necessitates the development of highly potent and selective small-molecule MIF inhibitors, along with rigorous validation in disease models. Our review article comprehensively summarizes recent progress recognizing MIF as a pharmaceutical target for inflammatory conditions and cancer. Furthermore, it highlights promising areas for future research in this domain and outlines recent advancements in identifying and designing small-molecule MIF inhibitors. These efforts aim to facilitate the development of novel therapies that target MIF and have the potential to address various disease conditions associated with its dysregulation. [ABSTRACT FROM AUTHOR]

Macrophages, which display remarkable specificity and plasticity, are the first-line immune cells for inflammation. After activation, they polarise into pro-inflammatory type M1 and anti-inflammatory type M2, with M1 producing pro-inflammatory factors such as TNF-α and IL-6 and M2 producing anti-inflammatory factors. In the inflammatory state, the ratio of pro-inflammatory factors to anti-inflammatory factors is imbalanced, and its long-term existence will lead to tissue damage and the development of inflammatory diseases, which seriously endanger human health. Currently, non-steroidal anti-inflammatory drugs and immunosuppressants are mostly used for the treatment of this type of disease, but patients are prone to drug resistance and other side effects. Therefore, there is an urgent need to find a new direction for treatment. Chlorogenic acid, as a typical natural phenolic compound with high content in many plants such as Eucommia, Flos Lonicerae, Coffea species, etc., has significant anti-inflammatory activities. This article comprehensively examines the distribution and metabolism of chlorogenic acid, elucidates its role in regulating the M1/M2 macrophage imbalance, and highlights its potential therapeutic value in inflammatory diseases such as enteritis, hepatitis, pneumonia, arthritis, and neuroinflammation. These findings contribute to a deeper understanding of its clinical significance and provide novel insights for the multi-targeted treatment of inflammatory disorders. [ABSTRACT FROM AUTHOR]

Itaconate (ITA) research began as an industrial application as a precursor for polymer synthesis and has advanced significantly since the discovery of the Irg1 gene in 1995. A deep exploration of ITA as an immunomodulatory metabolite has provided a profound understanding of the functional significance and mechanistic basis of metabolic reprogramming in the context of inflammatory responses and cancer development. ITA rapidly accumulates to high levels in myeloid cells during both infectious and sterile inflammatory conditions. This metabolite acts as a signaling molecule to modulate immune response by binding, covalently and noncovalently, to multiple proteins and regulating the oxidative response, cell metabolism, epigenetic modification, and gene expression intrinsically, and activating G protein-coupled receptor (GPCR) signaling via paracrine signaling. Genetic and preclinical studies in animal models support the therapeutic potential for treating a wide range of inflammatory diseases and cancer. Developing novel therapies based on ITA and targeting aconitate decarboxylase (ACOD1) holds exciting potential for treating many diseases that currently lack effective therapy. Immune cells undergo rapid and extensive metabolic changes during inflammation. In addition to contributing to energetic and biosynthetic demands, metabolites can also function as signaling molecules. Itaconate (ITA) rapidly accumulates to high levels in myeloid cells under infectious and sterile inflammatory conditions. This metabolite binds to and regulates the function of diverse proteins intracellularly to influence metabolism, oxidative response, epigenetic modification, and gene expression and to signal extracellularly through binding the G protein-coupled receptor (GPCR). Administration of ITA protects against inflammatory diseases and blockade of ITA production enhances antitumor immunity in preclinical models. In this article, we review ITA metabolism and its regulation, discuss its target proteins and mechanisms, and conjecture a rationale for developing ITA-based therapeutics to treat inflammatory diseases and cancer. [ABSTRACT FROM AUTHOR]

Metabolism plays a crucial role in regulating the function of immune cells in both health and disease, with altered metabolism contributing to the pathogenesis of cancer and many inflammatory diseases. The local microenvironment has a profound impact on the metabolism of immune cells. Therefore, immunological and metabolic heterogeneity as well as the spatial organization of cells in tissues should be taken into account when studying immunometabolism. Here, we highlight challenges of investigating metabolic communication. Additionally, we review the capabilities and limitations of current technologies for studying metabolism in inflamed microenvironments, including single‐cell omics techniques, flow cytometry‐based methods (Met‐Flow, single‐cell energetic metabolism by profiling translation inhibition (SCENITH)), cytometry by time of flight (CyTOF), cellular indexing of transcriptomes and epitopes by sequencing (CITE‐Seq), and mass spectrometry imaging. Considering the importance of metabolism in regulating immune cells in diseased states, we also discuss the applications of metabolomics in clinical research, as well as some hurdles to overcome to implement these techniques in standard clinical practice. Finally, we provide a flowchart to assist scientists in designing effective strategies to unravel immunometabolism in disease‐relevant contexts. [ABSTRACT FROM AUTHOR]

Conventional immunization methods such as intramuscular injections lack effective mucosal protection against pathogens that enter through the mucosal surfaces. Moreover, conventional therapy often leads to adverse events and compromised immunity, followed by complicated outcomes, leading to the need to switch to other options. Thus, a need to develop safe and effective treatment with long-term beneficial outcomes to reduce the risk of relapse is mandatory. Mucosal vaccines administered across mucosal surfaces, such as the respiratory or intestinal mucosa, to prompt robust localized and systemic immune responses to prevent the public from acquiring pathogenic diseases. Mucosal immunity contains a unique immune cell milieu that selectively identify pathogens and limits the transmission and progression of mucosal diseases, such as allergic dermatitis and inflammatory bowel disease (IBD). It also offers protection from localized infection at the site of entry, enables the clearance of pathogens on mucosal surfaces, and leads to the induction of long-term immunity with the ability to shape regulatory responses. Regulatory T (Treg) cells have been a promising strategy to suppress mucosal diseases. To find advances in mucosal treatment, we investigated the therapeutic effects of intranasal pep27 mutant immunization. Nasal immunization protects mucosal surfaces, but nasal antigen presentation appears to entail the need for an adjuvant to stimulate immunogenicity. Here, a novel method is developed to induce Tregs via intranasal immunization without an adjuvant to potentially overcome allergic diseases and gut and lung inflammation using lung–gut axis communication in animal models. The implementation of the pep27 mutant for these therapies should be preceded by studies on Treg resilience through clinical translational studies on dietary changes. [ABSTRACT FROM AUTHOR]

Background: Uncaria tomentosa (Willd. ex Schult.) DC. (Rubiaceae) is traditionally used by Amazonian indigenous groups to treat inflammatory diseases. To date, there are no systematic reviews and meta-analyses on the use of U. tomentosa for inflammation control in animals supporting the traditional knowledge about this species. This study was conducted to evaluate the effect of U. tomentosa extracts in modulating inflammatory mediators and to determine which types of inflammatory diseases can be treated by this species. Methods: We conducted a systematic review and meta-analysis of preclinical studies published before 26 July 2023, identified in PubMed, Embase, and Scopus. Four independent reviewers extracted the data and assessed the risks of bias. The effects of U. tomentosa on inflammatory diseases and the inflammatory mediators involved were extracted from the studies. Standardized mean differences (SMD) and 95% confidence intervals (95%CI) of the outcomes were estimated. The meta-analyses were conducted using RevMan 5.4 (Cochrane Collaboration). This protocol was registered in PROSPERO (CRD42023450869). Results: Twenty-four of 523 studies were included. U. tomentosa extracts decreased the cytokines interleukin (IL)-6 (SMD: -0.72, 95%CI: -1.15, -0.29, p = 0.001) and transcription factor nuclear factor kappa-B (NF-κB) (SMD: -1.19, 95%CI: -1.89, -0.48, p = 0.001). However, the extracts did not significantly alter IL-1 (SMD: -0.16, 95%CI: -0.87, +0.56, p = 0.67), IL-10 (SMD: -0.05, 95%CI:-0.35, 0.45, p = 0.80), or tumor necrosis factor-alpha (TNF-α) levels (SMD: 0.18, 95%CI: -0.25, 0.62, p = 0.41). Conclusion: Many extracts of stem bark, roots, and leaves of U. tomentosa, mostly aqueous and hydroethanolic, exhibited anti-inflammatory and/or immunomodulatory activities and low toxicity. The extracts decreased NF-κB and IL-6. These findings suggest that this species has the potential to treat inflammatory diseases in which these markers are increased, according to the ethnopharmacological use. These activities are not related to a specific class of compounds. [ABSTRACT FROM AUTHOR]

Nanomaterials are becoming important tools for vaccine development owing to their tunable and adaptable nature. Unique properties of nanomaterials afford opportunities to modulate trafficking through various tissues, complement or augment adjuvant activities, and specify antigen valency and display. This versatility has enabled recent work designing nanomaterial vaccines for a broad range of diseases, including cancer, inflammatory diseases, and various infectious diseases. Recent successes of nanoparticle vaccines during the coronavirus disease 2019 (COVID-19) pandemic have fueled enthusiasm further. In this review, the most recent developments in nanovaccines for infectious disease, cancer, inflammatory diseases, allergic diseases, and nanoadjuvants are summarized. Additionally, challenges and opportunities for clinical translation of this unique class of materials are discussed. [ABSTRACT FROM AUTHOR]

Androgens can modulate immune cell function and may contribute to differences in the prevalence and severity of common inflammatory conditions. Although most immune cells are androgen targets, our understanding of how changes in androgen bioavailability can affect immune responses is incomplete. Androgens alter immune cell composition, phenotype, and activation by modulating the expression and secretion of inflammatory mediators or by altering the development and maturation of immune cell precursors. Androgens are generally associated with having suppressive effects on the immune system, but their impacts are cell and tissue context-dependent and can be highly nuanced even within immune cell subsets. In response to androgens, innate immune cells such as neutrophils, monocytes, and macrophages increase the production of the anti-inflammatory cytokine IL-10 and decrease nitric oxide production. Androgens promote the differentiation of T cell subsets and reduce the production of inflammatory mediators, such as IFNG, IL-4 and IL-5. Additionally, androgens/androgen receptor can promote the maturation of B cells. Thus, androgens can be considered as immunomodulatory agents, but further work is required to understand the precise molecular pathways that are regulated at the intersection between endocrine and inflammatory signals. This narrative review focusses on summarising our current understanding of how androgens can alter immune cell function and how this might affect inflammatory responses in health and disease. [ABSTRACT FROM AUTHOR]