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Inflammatory responses in small vessels play an important role in the development of cardiovascular diseases, including hypertension, stroke, and small vessel disease. This involves various complex molecular processes including oxidative stress, inflammasome activation, immune-mediated responses, and protein misfolding, which together contribute to microvascular damage. In addition, epigenetic factors, including DNA methylation, histone modifications, and microRNAs influence vascular inflammation and injury. These phenomena may be acquired during the aging process or due to environmental factors. Activation of proinflammatory signaling pathways and molecular events induce low-grade and chronic inflammation with consequent cardiovascular damage. Identifying mechanism-specific targets might provide opportunities in the development of novel therapeutic approaches. Monoclonal antibodies targeting inflammatory cytokines and epigenetic drugs, show promise in reducing microvascular inflammation and associated cardiovascular diseases. In this article, we provide a comprehensive discussion of the complex mechanisms underlying microvascular inflammation and offer insights into innovative therapeutic strategies that may ameliorate vascular injury in cardiovascular disease., Competing Interests: Disclosures None.

Microcirculation is pervasive and orchestrates a profound regulatory cross-talk with the surrounding tissue and organs. Similarly, it is one of the earliest biological systems targeted by environmental stressors and consequently involved in the development and progression of ageing and age-related disease. Microvascular dysfunction, if not targeted, leads to a steady derangement of the phenotype, which cumulates comorbidities and eventually results in a nonrescuable, very high-cardiovascular risk. Along the broad spectrum of pathologies, both shared and distinct molecular pathways and pathophysiological alteration are involved in the disruption of microvascular homeostasis, all pointing to microvascular inflammation as the putative primary culprit. This position paper explores the presence and the detrimental contribution of microvascular inflammation across the whole spectrum of chronic age-related diseases, which characterise the 21st-century healthcare landscape. The manuscript aims to strongly affirm the centrality of microvascular inflammation by recapitulating the current evidence and providing a clear synoptic view of the whole cardiometabolic derangement. Indeed, there is an urgent need for further mechanistic exploration to identify clear, very early or disease-specific molecular targets to provide an effective therapeutic strategy against the otherwise unstoppable rising prevalence of age-related diseases., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.)

Exposure to early adverse experiences induces persistent changes in physiological, emotional and behavioural functions predisposing the individual to an enhanced vulnerability to develop different disorders during lifespan. The adverse outcomes depend upon the timing of the stressful experiences, and in this contest, adolescence represents a key sensitive period for brain development. Among the biological systems involved, gut microbiota has recently been proposed to act on the interplay between the stress response, brain functions and immune system, through the gut-brain axis communication. In the current study we aimed to evaluate, in a preclinical model, changes over time in the microbiota community structure in physiological condition and in response to stress during adolescence. We also aimed to correlate the microbiota composition to the inflammatory status in brain. We used the preclinical model of social deprivation in rats during adolescence, based on the lack of all social contacts, for four weeks after weaning, followed by re-socialization until adulthood. We collected fecal samples at different post-natal days to investigate the short- and long-lasting effects of social isolation on gut microbiota composition and we collected brain areas (dorsal and ventral hippocampus) samples at killing to measure a panel of inflammatory and microglia activation markers. 16 S metataxonomic sequencing analysis revealed that microbial changes were influenced by age in both isolated and controls rats, regardless of sex, whereas social isolation impacted the microbial composition in a sex-dependent manner. A multivariate analysis showed that social isolation induced short-term gut microbiota alterations in females but not in males. We also identified several stress-related genera associated with social isolation condition. In brain areas we found a specific inflammatory pattern, in dorsal and ventral hippocampus, that significantly correlated with gut microbiota composition. Overall, in this study we reported a novel sex-specific association between gut microbiota composition and inflammatory response related to social isolation paradigm during adolescence, suggesting that stressful experiences during this sensitive period could have a long-lasting impact on the development of different biological systems that could in turn influence the vulnerability to develop mental disorders later in life., (Copyright © 2021. Published by Elsevier Ltd.)

Inflammation is a marker of arterial disease stemming from cholesterol-dependent to -independent molecular mechanisms. In recent years, the role of inflammation in atherogenesis has been underpinned by pharmacological approaches targeting systemic inflammation that have led to a significant reduction in cardiovascular disease (CVD) risk. Although the use of nutraceuticals to prevent CVD has largely focused on lipid-lowering (e.g, red-yeast rice and omega-3 fatty acids), there is growing interest and need, especially now in the time of coronavirus pandemic, in the use of nutraceuticals to reduce inflammatory markers, and potentially the inflammatory CVD burden, however, there is still not enough evidence to confirm this. Indeed, diet is an important lifestyle determinant of health and can influence both systemic and vascular inflammation, to varying extents, according to the individual nutraceutical constituents. Thus, the aim of this Position Paper is to provide the first attempt at recommendations on the use of nutraceuticals with effective anti-inflammatory properties., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Inflammation is an important driver of atherosclerosis, and the favourable outcomes of the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) trial revealed the large potential of anti-inflammatory drugs for the treatment of cardiovascular disease, especially in patients with a pro-inflammatory constitution. However, the complex immune reactions driving inflammation in the vascular wall in response to an atherosclerotic microenvironment are still being unravelled. Novel insights into the cellular processes driving immunity and inflammation revealed that alterations in intracellular metabolic pathways are strong drivers of survival, growth, and function of immune cells. Therefore, this position paper presents a brief overview of the recent developments in the immunometabolism field, focusing on its role in atherosclerosis. We will also highlight the potential impact of immunometabolic markers and targets in clinical cardiovascular medicine., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Dysregulated lipid metabolism induces an inflammatory and immune response leading to atherosclerosis. Conversely, inflammation may alter lipid metabolism. Recent treatment strategies in secondary prevention of atherosclerosis support beneficial effects of both anti-inflammatory and lipid-lowering therapies beyond current targets. There is a controversy about the possibility that anti-inflammatory effects of lipid-lowering therapy may be either independent or not of a decrease in low-density lipoprotein cholesterol. In this Position Paper, we critically interpret and integrate the results obtained in both experimental and clinical studies on anti-inflammatory actions of lipid-lowering therapy and the mechanisms involved. We highlight that: (i) besides decreasing cholesterol through different mechanisms, most lipid-lowering therapies share anti-inflammatory and immunomodulatory properties, and the anti-inflammatory response to lipid-lowering may be relevant to predict the effect of treatment, (ii) using surrogates for both lipid metabolism and inflammation as biomarkers or vascular inflammation imaging in future studies may contribute to a better understanding of the relative importance of different mechanisms of action, and (iii) comparative studies of further lipid lowering, anti-inflammation and a combination of both are crucial to identify effects that are specific or shared for each treatment strategy.

Persistent and unresolved inflammation is a common underlying factor observed in several and seemingly unrelated human diseases, including cardiovascular and neurodegenerative diseases. Particularly, in atopic conditions, acute inflammatory responses such as those triggered by insect venom, food or drug allergies possess also a life-threatening potential. However, respiratory allergies predominantly exhibit late immune responses associated with chronic inflammation, that can eventually progress into a severe phenotype displaying similar features as those observed in other chronic inflammatory diseases, as is the case of uncontrolled severe asthma. This review aims to explore the different facets and systems involved in chronic allergic inflammation, including processes such as tissue remodelling and immune cell dysregulation, as well as genetic, metabolic and microbiota alterations, which are common to other inflammatory conditions. Our goal here was to deepen on the understanding of an entangled disease as is chronic allergic inflammation and expose potential avenues for the development of better diagnostic and intervention strategies., (© 2024 The Author(s). Clinical & Experimental Allergy published by John Wiley & Sons Ltd.)

Tissue inflammation is a hallmark of tumour microenvironments. In the bone marrow, tumour-associated inflammation impacts normal niches for haematopoietic progenitor cells and mature immune cells and supports the outgrowth and survival of malignant cells residing in these niche compartments. This Review provides an overview of our current understanding of inflammatory changes in the bone marrow microenvironment of myeloid and lymphoid malignancies, using acute myeloid leukaemia and multiple myeloma as examples and highlights unique and shared features of inflammation in niches for progenitor cells and plasma cells. Importantly, inflammation exerts profoundly different effects on normal bone marrow niches in these malignancies, and we provide context for possible drivers of these divergent effects. We explore the role of tumour cells in inflammatory changes, as well as the role of cellular constituents of normal bone marrow niches, including myeloid cells and stromal cells. Integrating knowledge of disease-specific dynamics of malignancy-associated bone marrow inflammation will provide a necessary framework for future targeting of these processes to improve patient outcome., (© 2024. Springer Nature Limited.)

The European Forum for Research and Education in Allergy and Airways diseases (EUFOREA) organized its bi-annual forum EUFOREUM in Berlin in November 2023. The aim of EUFOREUM 2023 was to highlight pediatric action plans for prevention and optimizing care for type 2 inflammatory conditions starting in childhood, with a focus on early-stage diagnosis, ensuring neither under- nor overdiagnosis, optimal care, and suggestions for improvement of care. EUFOREA is an international not-for-profit organization forming an alliance of all stakeholders dedicated to reducing the prevalence and burden of chronic respiratory diseases through the implementation of optimal patient care via educational, research, and advocacy activities. The inclusive and multidisciplinary approach of EUFOREA was reflected in the keynote lectures and faculty of the virtual EUFOREUM 2023 (www.euforea.eu/euforeum) coming from the pediatric, allergology, pulmonology, ENT, dermatology, primary health care fields and patients around the central theme of type 2 inflammation. As most type 2 inflammatory conditions may start in childhood or adolescence, and most children have type 2 inflammation when suffering from a respiratory or skin disease, the moment has come to raise the bar of ambitions of care, including prevention, remission and disease modification at an early stage. The current report provides a comprehensive overview of key statements by the faculty of the EUFOREUM 2023 and the ambitions of EUFOREA allowing all stakeholders in the respiratory field to be updated and ready to join forces in Europe and beyond., (© 2024 The Author(s). Pediatric Allergy and Immunology published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.)

Muscle wasting is one of the main causes for exercise intolerance and ventilatory inefficiency in patients with heart failure and a strong predictor of frailty and reduced survival. The prevalence of sarcopenia is at least 20% in patients with heart failure. Patients with heart failure often have subclinical systemic inflammation, which may exert sustained effects on skeletal muscle. Besides exercise, nutrition should also be carefully evaluated as an appropriate diet with selected nutraceuticals may be able to stimulate muscle anabolism and inhibit muscle catabolism. This review summarizes the epidemiological and clinical trial evidence supporting the recommendations for the use of nutraceuticals with anti-inflammatory properties in heart failure and provides an overview of the state of the evidence for nutraceutical supplementation to prevent and/or mitigate heart failure muscle wasting.

There is considerable individual variability in vulnerability for developing posttraumatic stress disorder (PTSD); evidence suggests that this variability is related in part to genetic and environmental factors, including adverse early life experience. Interestingly, recent studies indicate that induction of chronic low-grade inflammation may be a common mechanism underlying gene and environment interactions that increase the risk for development of PTSD symptoms, and, therefore, may be a target for novel interventions for prevention or treatment of PTSD. Development of murine models with face, construct, and predictive validity would provide opportunities to investigate in detail complex genetic, environmental, endocrine, and immunologic factors that determine vulnerability to PTSD-like syndromes, and furthermore may provide mechanistic insight leading to development of novel interventions for both prevention and treatment of PTSD symptoms. Here we describe the potential use of the chronic subordinate colony housing (CSC) paradigm in mice as an adequate animal model for development of a PTSD-like syndrome and describe recent studies that suggest novel interventions for the prevention and treatment of PTSD., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Introduction Obesity has became a significant health concern over the past decade. According to a higher body mass index (BMI), obesity enhances the probability of malignancy, type 2 diabetes mellitus, cardiac disorders, and musculoskeletal diseases. Bariatric surgery, a typical and effective surgical intervention for patients with excess body weight with concurrent medical conditions, achieves significant weight loss over a long period. Numerous studies have been conducted on the effectiveness of various bariatric surgery techniques for improving glycemic homeostasis and helping patients lose weight. However, little is known about how bariatric surgery affects the lipid profile. The study aims to determine how patients' altered BMI affects lipid parameters following OAGB/MGB surgery. Methods To achieve this, the longitudinal observational study was conducted from January 2021 to January 2022 among 150 patients scheduled to undergo Anastomosis Gastric Bypass Surgery. The mean age of the patients was 41.7 years, with a standard deviation of 14.7 years (mean±SD: 41.7±14.7). Among the study participants, 56 individuals (37.3%) were male, while 94 (62.7%) were female. Objectives Regarding comorbidities, hypertension was identified as the most prevalent condition among the enrolled patients, affecting 49.3% of them. Results It was observed that the levels of S. Cholesterol and S. Triglyceride showed a significant decrease after one month (Visit-1) of the bypass surgery, with a reduction of 21.8 mg/dl (95% CI=-31.9, -11.6, p=<0.001) and 14 mg/dl (95% CI=-25.5, -2.51, p=0.017), respectively Conclusion OAGB outcome is associated with a healthier lipid profile and enhanced weight management. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) is both a gas and a ubiquitous inter- and intracellular messenger with numerous physiological functions. As its synthesis is markedly increased during inflammatory processes, NO can be used as a surrogate marker of acute and/or chronic inflammation. It is possible to quantify fractional concentration of NO in exhaled breath (FENO) to detect airway inflammation, and thus improve the diagnosis of asthma by better characterizing asthmatic patients with eosinophilic bronchial inflammation, and eventually improve the management of targeted asthmatic patients. FENO measurement can therefore be viewed as a new, reproducible and easy to perform pulmonary function test. Measuring FENO is the only non-invasive pulmonary function test allowing (1) detecting, (2) quantifying and (3) monitoring changes in inflammatory processes during the course of various respiratory disorders, including corticosensitive asthma., (Copyright © 2014 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Hypertension is a global health problem, with >1.3 billion individuals with high blood pressure worldwide. In this Review, we present an inflammatory paradigm for hypertension, emphasizing the crucial roles of immune cells, cytokines and chemokines in disease initiation and progression. T cells, monocytes, macrophages, dendritic cells, B cells and natural killer cells are all implicated in hypertension. Neoantigens, the NLRP3 inflammasome and increased sympathetic outflow, as well as cytokines (including IL-6, IL-7, IL-15, IL-18 and IL-21) and a high-salt environment, can contribute to immune activation in hypertension. The activated immune cells migrate to target organs such as arteries (especially the perivascular fat and adventitia), kidneys, the heart and the brain, where they release effector cytokines that elevate blood pressure and cause vascular remodelling, renal damage, cardiac hypertrophy, cognitive impairment and dementia. IL-17 secreted by CD4 + T helper 17 cells and γδ T cells, and interferon-γ and tumour necrosis factor secreted by immunosenescent CD8 + T cells, exert crucial effector roles in hypertension, whereas IL-10 and regulatory T cells are protective. Effector mediators impair nitric oxide bioavailability, leading to endothelial dysfunction and increased vascular contractility. Inflammatory effector mediators also alter renal sodium and water balance and promote renal fibrosis. These mechanisms link hypertension with obesity, autoimmunity, periodontitis and COVID-19. A comprehensive understanding of the immune and inflammatory mechanisms of hypertension is crucial for safely and effectively translating the findings to clinical practice., (© 2024. Springer Nature Limited.)

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The concept of cancer and inflammation has a long history. Virchow's irritation theory based on human cancer engendered the essential role of inflammation in carcinogenesis. Drs. Yamagiwa and Ichikawa first published a comprehensive paper entitled "Experimental study on the pathogenesis of epithelial tumors" (I report) in 1915 in German, and went on to publish five more reports (1915-1924) under the same title. They succeeded in demonstrating that inflammation is an important carcinogenic factor, and the mechanisms are now being investigated by numerous scientists all over the world. In order to introduce Yamagiwa's work to modern cancer researchers, the essentials of their six reports have been translated into English as a short review. Scientists' comments on Yamagiwa's contribution are attached by way of introduction., (© 2013 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.)

Objective: The aim of this study was to compare the effects of medium light roast (MLR) and medium roast (MR) paper-filtered coffee on cardiovascular risk factors in healthy volunteers., Methods: This randomized crossover trial compared the effects of consuming three or four cups (150 mL) of MLR or MR coffee per day for 4 wk in 20 healthy volunteers. Plasma lipids, lipoprotein(a) (Lp[a]), total homocysteine, and endothelial dysfunction-related inflammation biomarkers, serum glycemic biomarkers, and blood pressure were measured at baseline and after each intervention., Results: Both roasts increased plasma total cholesterol, low-density lipoprotein-cholesterol, and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations (10%, 12%, and 18% for MLR; 12%, 14%, and 14% for MR, respectively) (P < 0.05). MR also increased high-density lipoportein-cholesterol concentration by 7% (P = 0.003). Plasma fibrinogen concentration increased 8% after MR intake (P = 0.01), and soluble E-selectin increased 12% after MLR intake (P = 0.02). No changes were observed for Lp(a), total homocysteine, glycemic biomarkers, and blood pressure., Conclusion: Moderate paper-filtered coffee consumption may have an undesirable effect on plasma cholesterol and inflammation biomarkers in healthy individuals regardless of its antioxidant content., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Mitochondria retain bacterial traits due to their endosymbiotic origin, but host cells do not recognize them as foreign because the organelles are sequestered. However, the regulated release of mitochondrial factors into the cytosol can trigger cell death, innate immunity and inflammation. This selective breakdown in the 2-billion-year-old endosymbiotic relationship enables mitochondria to act as intracellular signalling hubs. Mitochondrial signals include proteins, nucleic acids, phospholipids, metabolites and reactive oxygen species, which have many modes of release from mitochondria, and of decoding in the cytosol and nucleus. Because these mitochondrial signals probably contribute to the homeostatic role of inflammation, dysregulation of these processes may lead to autoimmune and inflammatory diseases. A potential reason for the increased incidence of these diseases may be changes in mitochondrial function and signalling in response to such recent phenomena as obesity, dietary changes and other environmental factors. Focusing on the mixed heritage of mitochondria therefore leads to predictions for future insights, research paths and therapeutic opportunities. Thus, whereas mitochondria can be considered 'the enemy within' the cell, evolution has used this strained relationship in intriguing ways, with increasing evidence pointing to the recent failure of endosymbiosis being critical for the pathogenesis of inflammatory diseases., (© 2024. Springer Nature Limited.)

Background: Several studies have shown that the intake of N. sativa has a beneficial effect on metabolic syndrome and related disorders. In this meta-analysis, our primary objective was to assess the impact of Nigella sativa consumption on inflammation and oxidative stress biomarkers among individuals diagnosed with metabolic syndrome and its associated conditions., Methods: Our search was conducted on prominent online databases such as Web of Science, Scopus, PubMed, and EMBASE, utilizing relevant keywords until August 2023., Results: This meta-analysis was performed on 16 RCTs comprising 1033 participants. Our results showed that intake of Nigella sativa significantly decreased CRP (SMD: -0.60; (95% CI: from -0.96 to -0.23); P = 0.00), TNF-α (SMD: -0.53; (95% CI: from -0.74 to -0.53); P = 0.00); IL-6 (SMD: -0.54 ; (95% CI: from -1.01 to -0.07); P = 0.02), and MDA: (SMD: -1.28; (95% CI: from -2.11 to -0.46); P = 0.00) levels. In addition, SOD: (SMD: 1.35; (95% CI, from 0.77 to 1.93); P = 0.00) and TAC (SMD: 2.82; (95% CI, from 0.55 to 5.084); P = 0.01) levels significantly increased in the intervention group compared to the placebo group., Conclusion: Our results showed that THE consumption of N. sativa could be associated with improved oxidative stress and inflammation in patients with metabolic syndrome and related disorders., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Unlabelled: Chronic immunosuppression is a known risk factor for tuberculosis. Our aim was to reach a consensus on screening and prevention of tuberculosis in patients with immune mediated inflammatory diseases candidates to biologic therapy., Methods: Critical appraisal of the literature and expert opinion on immunosuppressive therapies and risk of tuberculosis., Results and Conclusion: The currently recommended method for screening is the tuberculin skin test and the interferon gamma assay, after exclusion of active tuberculosis. Positively screened patients should be treated for latent tuberculosis infection. Patients may start biological therapy after 1 to 2 months, as long as they are strictly adhering to and tolerating their preventive regimen.

The currently available, standard soybean oil (SO)-based intravenous fat emulsions (IVFEs) meet the needs of most parenteral nutrition (PN) patients. There are alternative oil-based fat emulsions, such as medium-chain triglycerides (MCTs), olive oils (OOs), and fish oils (FOs), that, based on extensive usage in Europe, have an equivalent safety profile to SO. These alternative IVFEs are metabolized via different pathways, which may lead to less proinflammatory effects and less immune suppression. These alternative oil-based IVFEs are not currently available in the United States. Many patients who require IVFEs are already in a compromised state. Such patients could potentially have better clinical outcomes when receiving one of the alternative IVFEs to diminish the intake of the potentially proinflammatory ω-6 fatty acid-linoleic acid-which comprises more than 50% of the fatty acid profile in SO. Further research is needed on these alternative oil-based IVFEs to identify which IVFE oils or which combination of oils may be most clinically useful for specific patient populations.

The use of murine models to investigate human diseases has been an invaluable tool. In the areas of inflammation and oncogenesis, such models have provided unique insights into pathogenesis and mechanisms to evaluate potential therapy. As such, one facet of these disease processes links inflammation and cancer. Inflammation is associated with at least 15% of the world's malignancies. One example of this relationship is documented in the association between colitis and colorectal cancer. To date, the precise molecular events linking inflammation and cancer remain unclear. A new paradigm that may bridge these processes includes the cancer stem cell hypothesis. In this review, murine models of colitis, colon cancer, and colitis-associated cancer are discussed in reference to the potential of this paradigm to clarify the relationship of these devastating diseases.

Inflammation is a risk factor for the development of many types of neoplasia, including skin, colon, gastric, and mammary cancers, among others. Chronic pulmonary diseases, such as chronic bronchitis and asthma, predispose to lung neoplasia. We will review the mouse literature examining the role of inflammation in lung neoplasia, focusing specifically on genetic susceptibility, pharmacologic modulation of inflammatory pathways, and both transgenic and knockout mouse models used to assess pro- and anti-inflammatory pathways involved in lung neoplasia. Identification of molecular mechanisms that govern the association between inflammation and pulmonary neoplasia could provide novel preventive, diagnostic, and therapeutic strategies for a disease in which few biomarkers currently exist.

Stings by Polistes wasps can cause life-threatening allergic reactions, pain and inflammation. We examined the changes in microvascular permeability and neutrophil influx caused by the venom of Polistes lanio a paper wasp found in southeastern Brazil. The intradermal injection of wasp venom caused long-lasting paw oedema and dose-dependently increased microvascular permeability in mouse dorsal skin. SR140333, an NK(1) receptor antagonist, markedly inhibited the response, but the NK(2) receptor antagonist SR48968 was ineffective. The oedema was reduced in capsaicin-treated rats, indicating a direct activation of sensory fibres. Dialysis of the venom partially reduced the oedema and the remaining response was further inhibited by SR140333. Mass spectrometric analysis of the venom revealed two peptides (QPPTPPEHRFPGLM and ASEPTALGLPRIFPGLM) with sequence similarities to the C-terminal region of tachykinin-like peptides found in Phoneutria nigriventer spider venom and vertebrates. Wasp venom failed to release histamine from mast cells in vitro and spectrofluorometric assay of the venom revealed a negligible content of histamine in the usual dose of P. l. lanio venom (1nmol of histamine/7mug of venom) that was removed by dialysis. The histamine H(1) receptor antagonist pyrilamine, but not bradykinin B(1) or B(2) receptor antagonists, inhibited venom-induced oedema. In conclusion, P. l. lanio venom induces potent oedema and increases vascular permeability in mice, primarily through activation of tachykinin NK(1) receptors by substance P released from sensory C fibres, which in turn releases histamine from dermal mast cells. This is the first description of a neurovascular mechanism for P. l. lanio venom-mediated inflammation. The extent to which the two tachykinin-like peptides identified here contribute to this neurogenic inflammatory response remains to be elucidated.

Alzheimer disease (AD) includes inflammatory processes in the senile plaques and surrounding glia, with increased expression of acute phase proteins such as C-reactive protein (CRP) and IL-6. Increased IL-6 expression during normal brain aging suggests a link of age-related inflammation to the onset of AD during aging. Blood levels of CRP and IL-6 are also associated with higher risk of Alzheimer disease and cognitive decline during aging. Some infections are known to induce inflammation and amyloid deposits. For example, HIV induces the deposition of the same beta-amyloid as in Alzheimer disease. The ApoE4 allele may increase HIV-associated dementia, in addition to its well-known effect on accelerating the onset age of AD. Many other adverse effects of apoE4 are recognized, which suggested the hypothesis that apoE4 persists in human populations because of balancing selection (Charlesworth-Martin hypothesis). The apoE4 allele was acquired during human evolution and may have conferred initial advantages in pathogen resistance. As evidence for this hypothesis, apoE4 carriers have less severe liver damage during hepatitis C infections. As human lifespan lengthened and cognitive and cardiovascular health became more important, the apoE3 allele spread, while the E4 allele was maintained in all populations by balancing selection.

Purpose: Inflammation is thought to be a vital element in the etiology of cancer-related fatigue (CRF), and circulating blood cell parameters could be important markers of inflammatory response. However, the associations of several major blood cell counts and their derived inflammatory indices with CRF are not well described. The present study aimed to establish whether a relationship exists between the counts of three white blood cell (WBC) types, platelets, and CRF and investigate whether several systemic inflammatory indices were associated with CRF in patients with breast cancer (BC)., Methods: A cross-sectional survey was conducted with a sample of 824 patients with BC undergoing chemotherapy. The cancer fatigue scale was administered to assess CRF. Hematological indicators, including neutrophils, lymphocytes, monocytes, and platelets, were retrieved from routine blood test. Network analyses were used to examine the associations among them., Results: Among 824 participants, the mean score of CRF was (27 ± 10), ranging from 0 to 57. The results of network models indicated that physical fatigue was negatively linked to lymphocyte counts (weight =  - 0.161), and affective fatigue was positively associated with neutrophil counts (weight = 0.070). Additionally, physical fatigue was positively linked to the platelet-to-lymphocyte ratio (PLR) (weight = 0.049)., Conclusion: There were preliminary associations of counts of three WBC types, platelet counts, and systemic inflammatory indices, with distinct dimensions of CRF in patients with BC. Findings provide empirical support for the cellular basis of fatigue-associated inflammatory states., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The objective of this meta-epidemiological study was to explore the impact of attrition rates on treatment effect estimates in randomised trials of chronic inflammatory diseases (CID) treated with biological and targeted synthetic disease-modifying drugs. We sampled trials from Cochrane reviews. Attrition rates and primary endpoint results were retrieved from trial publications; Odds ratios (ORs) were calculated from the odds of withdrawing in the experimental intervention compared to the control comparison groups (i.e., differential attrition), as well as the odds of achieving a clinical response (i.e., the trial outcome). Trials were combined using random effects restricted maximum likelihood meta-regression models and associations between estimates of treatment effects and attrition rates were analysed. From 37 meta-analyses, 179 trials were included, and 163 were analysed (301 randomised comparisons; n = 62,220 patients). Overall, the odds of withdrawal were lower in the experimental compared to control groups (random effects summary OR = 0.45, 95% CI, 0.41-0.50). The corresponding overall treatment effects were large (random effects summary OR = 4.43, 95% CI 3.92-4.99) with considerable heterogeneity across interventions and clinical specialties (I 2  = 85.7%). The ORs estimating treatment effect showed larger treatment benefits when the differential attrition was more prominent with more attrition in the control group (OR = 0.73, 95% CI 0.55-0.96). Higher attrition rates from the control arm are associated with larger estimated benefits of treatments with biological or targeted synthetic disease-modifying drugs in CID trials; differential attrition may affect estimates of treatment benefit in randomised trials., (© 2024 The Authors. Research Synthesis Methods published by John Wiley & Sons Ltd.)

Abstract Skin microdialysis (SMD) is a versatile sampling technique that can be used to recover soluble endogenous and exogenous molecules from the extracellular compartment of human skin. Due to its minimally invasive character, SMD can be applied in both clinical and preclinical settings. Despite being available since the 1990s, the technique has still not reached its full potential use as a tool to explore pathophysiological mechanisms of allergic and inflammatory reactions in the skin. Therefore, an EAACI Task Force on SMD was formed to disseminate knowledge about the technique and its many applications. This position paper from the task force provides an overview of the current use of SMD in the investigation of the pathogenesis of chronic inflammatory skin diseases, such as atopic dermatitis, chronic urticaria, psoriasis, and in studies of cutaneous events during type 1 hypersensitivity reactions. Furthermore, this paper covers drug hypersensitivity, UVB-induced- and neurogenic inflammation, and drug penetration investigated by SMD. The aim of this paper is to encourage the use of SMD and to make the technique easily accessible by providing an overview of methodology and applications, supported by standardized operating procedures for SMD in vivo and ex vivo.

Muscle wasting is one of the main causes for exercise intolerance and ventilatory inefficiency in patients with heart failure and a strong predictor of frailty and reduced survival. The prevalence of sarcopenia is at least 20% in patients with heart failure. Patients with heart failure often have subclinical systemic inflammation, which may exert sustained effects on skeletal muscle. Besides exercise, nutrition should also be carefully evaluated as an appropriate diet with selected nutraceuticals may be able to stimulate muscle anabolism and inhibit muscle catabolism. This review summarizes the epidemiological and clinical trial evidence supporting the recommendations for the use of nutraceuticals with anti-inflammatory properties in heart failure and provides an overview of the state of the evidence for nutraceutical supplementation to prevent and/or mitigate heart failure muscle wasting. [ABSTRACT FROM AUTHOR]

Nanopore protein (α-hemolysin) was used to detect sub-nanosized plastic particles leached from a PE-coated paper cup. These sub-nanosized plastic particles can increase the inflammation response of macrophages. [Display omitted] • Nanopore sensing detects sub-nanosized plastics in PE-coated paper cups. • Sub-nanosized plastic particles in paper cups were 1.8 times more detected in boiled water than in room temperature water. • Sub-nanosized and microplastic particles alter cell membrane dynamics. • Sub-nanosized plastic particles can induce inflammatory cell responses. In recent years, there has been growing global concern about environmental pollution, and the increasing use of plastic products has made microplastics a serious environmental pollutant worldwide. Accordingly, the development of microplastic detection methods and research on the harmful effects of microplastics on human health are being actively pursued. In this study, we detected particle leaching from PE-coated paper cups using label-free nanopore sensing to identify and quantify the presence of sub-nanosized plastic particles. Plastic particles leached from the paper cups were classified as < 1 nm and > 1 nm, and their interactions with artificial cell membranes and inflammatory responses in the cells were evaluated. The results demonstrated that in a commonly used paper cup, particles < 1.4 nm were present at a concentration of approximately 1.13 mM in hot water and 0.62 mM in room-temperature water. It was demonstrated that plastic particles < 1 nm could condense the artificial cell membrane, whereas particles > 1 nm could thicken the artificial cell membrane. Furthermore, both size ranges of particles leached from the paper cups triggered an inflammatory response in the cells, with the inflammatory response increasing in proportion to the concentration and treatment time. The detection and analysis revealed the presence of sub-nanosized plastic particles in PE-coated paper cups, which are commonly used in daily life. These particles pose health threats and contribute to environmental pollution. [ABSTRACT FROM AUTHOR]

Objectives: The objectives of this study were to assess the effect of 8 weeks of moderate-intensity aerobic training on permeability inflammatory indicators of matrix metalloproteinases (MMPs) and specific tissue inhibitors of MMPs in female migraineurs., Methods: Female migraineurs (n = 28, age 32 ± 6) were randomised into two groups: migraine with exercise training (EXE + Mig, n = 13) and migraine without exercise training (NON-EXE + Mig, n = 15). Matched healthy women were also recruited as a healthy control group (CON, n = 15). The EXE-Mig group performed 8 weeks of aerobic training. Pre and post intervention, serum matrix metalloproteinases (MMP-2 and 9) and specific tissue inhibitors of MMPs (TIMP-1 and 2) were measured. In addition, body composition indices and VO 2max were determined., Results: Exercise training reduced serum MMP-9 in female migraineurs with between-group changes and a time x group interaction (p < 0.05). In addition, exercise training reduced the serum MMP-9/TIMP-1 ratio in female migraineurs with between-group changes and time x group interaction (p < 0.05). However, no training-induced effect was observed in serum TIMP-1, TIMP-2, MMP-2 contents (p > 0.05) and MMP-2/TIMP-2 ratio (p > 0.05). Finally, exercise training reduced body fat content, WHR and BMI, and improved VO 2max (p < 0.01)., Conclusions: Our results demonstrated beneficial effects of aerobic exercise training on some circulatory inflammation factors (MMP9, MMP-9/TIMP-1) and some health indicators in female migraineurs, suggesting that such training can be employed as a non-pharmacological therapeutic method., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The aim of this study was to investigate the associations between cardiorespiratory fitness (CRF), long-term air pollution exposure and biochemical markers of oxidative status and inflammation. This is a cross-sectional investigation focusing on biochemical markers of oxidative status and inflammation. Participants were Caucasian (N = 1188; age 18-65 years) who lived for at least 5 years in a high air-polluted (Moravian-Silesian; MS) or low air-polluted (South Bohemia; SB) region of the Czech Republic. Healthy runners and inactive individuals were recruited. A multiple regression analysis was used to explain the relationship between multiple independent variables (CRF, trunk fat mass, sex, socioeconomic status, and region (MS region vs. SB region) and dependent variables (oxidative status, inflammation). CRF, trunk fat mass, age and sex significantly predicted almost all selected markers of oxidative status and inflammation (except GSSG, GSH/GSSG and BDNF). Participants living in the MS region presented significantly higher GPx (by 3.1%) and lower BDNF values (by 4.5%). All other investigated biochemical markers were not significantly influenced by region. We did not find meaningful interactions between long-term air-pollution exposure versus markers of oxidative status and inflammation. However, we showed various significant interactions with sex, age, CRF and body composition. The significant association of living in the high air polluted MS region with the BDNF level warrants further attention., (© 2024. The Author(s).)