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ObjectiveExercise plays a crucial role in maintaining and improving human health. However, the precise molecular mechanisms that govern the body's response to exercise or/compared to periods of inactivity remain elusive. Current evidence appears to suggest that exercise exerts a seemingly dual influence on macrophage polarization states, inducing both pro-immune response M1 activation and cell-repair-focused M2 activation. To reconcile this apparent paradox, we leveraged a comprehensive meta-analysis of 75 diverse exercise and immobilization published datasets (7000+ samples), encompassing various exercise modalities, sampling techniques, and species.Methods75 exercise and immobilization expression datasets were identified and processed for analysis. The data was analyzed using boolean relationships which uses binary gene expression relationships in order to increase the signal to noise achieved from the data, allowing for the use of comparison across such a diverse set of datasets. We utilized a boolean relationship-aided macrophage gene model [1], to model the macrophage polarization state in pre and post exercise samples in both immediate exercise and long term training.ResultsOur modeling uncovered a key temporal dynamic: exercise triggers an immediate M1 surge, while long term training transitions to sustained M2 activation. These patterns were consistent across different species (human vs mouse), sampling methods (blood vs muscle biopsy), and exercise type (resistance vs endurance), and routinely showed statistically significant results. Immobilization was shown to have the opposite effect of exercise by triggering an immediate M2 activation. Individual characteristics like gender, exercise intensity and age were found to impact the degree of polarization without changing the overall patterns. To model macrophages within the specific context of muscle tissue, we identified a focused gene set signature of muscle resident macrophage polarization, allowing for the precise measurement of macrophage activity in response to exercise within the muscle.ConclusionsThese consistent patterns across all 75 examined studies suggest that the long term health benefits of exercise stem from its ability to orchestrate a balanced and temporally-regulated interplay between pro-immune response (M1) and reparative macrophage activity (M2). Similarly, it suggests that an imbalance between pro-immune and cell repair responses could facilitate disease development. Our findings shed light on the intricate molecular choreography behind exercise-induced health benefits with a particular insight on its effect on the macrophages within the muscle.

BackgroundPersistent inflammation affects people with HIV (PWH) despite antiretroviral therapy (ART). Selective serotonin and serotonin-norepinephrine reuptake inhibitors (SSRIs, SNRIs), HMG-CoA reductase-inhibitors (statins), and angiotensin-converting enzyme inhibitors (ACEIs) have immunomodulant properties. We evaluated the potential impact of these drugs on inflammation and neurodegeneration in PWH.MethodsCross-sectional single-center (United States) analysis in 184 PWH on ART with plasma HIV RNA < 200 copies/mL. All participants had 10 biomarkers measured in blood and cerebrospinal fluid (CSF). To reduce dimensionality, hierarchical clustering and principal components (PCs) analysis were employed. The analyses were adjusted for duration of the drugs and clinical conditions.ResultsParticipants were mostly middle-aged men, with median CD4+ T cells of 620/µL. In adjusted models, SSRI use was associated with 3 PCs: higher CSF and plasma Aβ42 and CSF CCL2 (aβ=.14, P = .040); lower CSF 8-oxo-dG, total tau, and sCD14 (aβ=-.12, P = .042); and higher plasma sCD14 with lower sCD40L (aβ=.15, P = .042). SNRI use was associated with higher values of CSF and plasma neopterin and CSF sTNFR-II (aβ=.22, P = .004). Statins and ACEIs showed no association.ConclusionsSSRIs and SNRIs had distinct biomarker signatures. SSRIs were associated with reduced neurodegeneration, immune activation, and oxidative stress in CSF, suggesting a role of SSRIs as adjunctive therapy in PWH.

The tumor microenvironment (TME) plays a pivotal role in cancer development and progression, and comprises various cellular and non-cellular components that interact with tumor cells. Tenascin-C (TNC) is an extracellular matrix glycoprotein that is widely expressed in the cancer stroma and influences critical processes, such as cell adhesion, migration, and immune modulation. This review examines the multifaceted roles of TNC in different TMEs, including the mechanical, immune, and metabolic microenvironments, as well as the radiation microenvironment (RME). In the context of the mechanical microenvironment, TNC actively participates in extracellular matrix remodeling, thereby facilitating tumor invasion. Notably, TNC exhibits immunosuppressive effects on T cells and promotes the recruitment of immunosuppressive cells within the immune microenvironment. Furthermore, TNC is implicated in the tumor hypoxia response, glucose metabolism reprogramming, and regulation of pH balance, underscoring its role in the metabolic microenvironment. Intriguingly, TNC also influences radiosensitivity within RME. This review also explores the potential of TNC as a biomarker for cancer prognosis and as a target for therapeutic interventions. By integrating recent advances in single-cell sequencing and spatial omics, we propose innovative strategies for leveraging TNC in personalized cancer therapy. Future research directions are discussed, focusing on distinct isoforms of TNC, their interaction networks, and their roles in radiotherapy efficacy. This comprehensive analysis underscores the importance of TNC in understanding tumor dynamics and improving cancer treatment outcomes. [ABSTRACT FROM AUTHOR]

Spontaneous regression of a neoplasm is a rare oncologic phenomenon. Certain neoplasms, such as melanomas and neuroblastomas, display this phenomenon. To date, spontaneous regression of oral cavity squamous cell carcinomas has been documented in only a handful of case reports. We present a novel case of spontaneous regression of an oral tongue squamous cell carcinoma following biopsy. We discuss the tumor's unique genetic profile, immune response to cancer, and review the literature on possible mechanisms of spontaneous regression. Small-volume persistent cancer in our patient reinforces that tissue confirmation remains crucial to avoid missing remaining tumor. Further investigation is required to understand mechanisms of spontaneous regression and how these may be exploited to improve head and neck squamous cell carcinoma treatment. [ABSTRACT FROM AUTHOR]

Introduction: Ischemic stroke (IS) represents a significant global health challenge, characterized by elevated morbidity and mortality rates, largely driven by inflammatory responses. Double-negative T cells (DNTs), a distinct subset of T cells lacking both CD4 and CD8 markers, have been implicated in the pathogenesis of IS, exhibiting potentially dual roles. However, the precise functional contributions of DNTs in this context remain poorly understood. Methods: In this study, we investigated the role of DNTs during the acute phase of IS and assessed the influence of Huang-Lian-Jie-Du Decoction (HLJD), a traditional Chinese medicinal formula, on these cells. Using single-cell transcriptomics, we identified two distinct subtypes of DNTs: an activated, cytotoxic phenotype (Kill+) and a resting, immunosuppressive phenotype (Kill-). Results: Our findings indicate that HLJD treatment modulates the balance between these DNT subtypes, specifically reducing the proportion of cytotoxic DNTs while promoting an increase in immunosuppressive DNTs. This shift was associated with a reduction in immune cell infiltration and inflammation within the brain tissue, potentially mitigating neuronal damage. Discussion: These results suggest that HLJD exerts neuroprotective effects in IS by modulating the activity and distribution of DNT cells, offering valuable insights into the therapeutic potential of traditional Chinese medicine for the treatment of IS. Further studies are required to elucidate the mechanisms underlying DNT-mediated immune responses in IS and to explore the broader applications of HLJD in other neuroinflammatory conditions. [ABSTRACT FROM AUTHOR]

Periodontal disease is a chronic inflammatory condition that destroys the tooth-supporting structures due to the host's immune response to microbial biofilms. Traditional periodontal treatments, such as scaling and root planing, pharmacological interventions, and surgical procedures, have significant limitations, including difficulty accessing deep periodontal pockets, biofilm recolonization, and the development of antibiotic resistance. In light of these challenges, natural bioactive compounds derived from plants, herbs, and other natural sources offer a promising alternative due to their anti-inflammatory, antioxidant, antimicrobial, and tissue-regenerative properties. This review focuses on the molecular mechanisms through which bioactive compounds, such as curcumin, resveratrol, epigallocatechin gallate (EGCG), baicalin, carvacrol, berberine, essential oils, and Gum Arabic, exert therapeutic effects in periodontal disease. Bioactive compounds inhibit critical inflammatory pathways like NF-κB, JAK/STAT, and MAPK while activating protective pathways such as Nrf2/ARE, reducing cytokine production and oxidative stress. They also inhibit the activity of matrix metalloproteinases (MMPs), preventing tissue degradation and promoting healing. In addition, these compounds have demonstrated the potential to disrupt bacterial biofilms by interfering with quorum sensing, targeting bacterial cell membranes, and enhancing antibiotic efficacy.Bioactive compounds also modulate the immune system by shifting the balance from pro-inflammatory to anti-inflammatory responses and promoting efferocytosis, which helps resolve inflammation and supports tissue regeneration. However, despite the promising potential of these compounds, challenges related to their poor bioavailability, stability in the oral cavity, and the absence of large-scale clinical trials need to be addressed. Future strategies should prioritize the development of advanced delivery systems like nanoparticles and hydrogels to enhance bioavailability and sustain release, alongside long-term studies to assess the effects of these compounds in human populations. Furthermore, combining bioactive compounds with traditional treatments could provide synergistic benefits in managing periodontal disease. This review aims to explore the therapeutic potential of natural bioactive compounds in managing periodontal disease, emphasizing their molecular mechanisms of action and offering insights into their integration with conventional therapies for a more comprehensive approach to periodontal health. [ABSTRACT FROM AUTHOR]

In addition to its classical role in calcium and phosphate metabolism regulation, vitamin D also has an important impact on immunity modulation. Vitamin D regulates the immune response, shifting from a proinflammatory state to a more tolerogenic one by increasing the release of anti-inflammatory cytokines while downregulating proinflammatory cytokines. Thus, low levels of vitamin D have been associated with an increased risk of developing autoimmune diseases like multiple sclerosis and type 1 diabetes. Furthermore, this prohormone also enhances the release of well-known antimicrobial peptides, like cathelicidin LL-37 and β-defensins; therefore, it has been proposed that vitamin D serum levels might be related to the risk of well-known pathogen infections, including herpesviruses. These are a group of widely spread viral pathogens that can cause severe encephalitis or tumors like Kaposi's sarcoma and Burkitt lymphoma. However, there is no consensus on the minimum levels of vitamin D or the recommended daily dose, making it difficult to establish a possible association between these two factors. This narrative non-systematic review will analyze the mechanisms by which vitamin D regulates the immune system and recent studies about whether there is an association between vitamin D serum levels and herpesvirus infections. [ABSTRACT FROM AUTHOR]

Lecithin cholesterol acyltransferase (LCAT) is a crucial enzyme in high-density lipoprotein (HDL) metabolism that is often dysregulated in cancers, affecting tumor growth and therapy response. We extensively studied LCAT expression in various malignancies, linking it to clinical outcomes and genetic/epigenetic alterations. We analyzed LCAT expression in multiple cancers and used the Cox regression model to correlate it with patient survival metrics, including overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). We also examined the copy number variations (CNVs), single-nucleotide variations (SNVs), DNA methylation, and N6-methyladenosine (m6A) modifications of LCAT and their connections to tumor immune responses and drug sensitivity. LCAT expression varies among cancers and correlates with patient outcomes. Low expression is linked to poor prognosis in low-grade glioma (LGG) and liver hepatocellular carcinoma (LIHC), while high expression is associated with better outcomes in adrenocortical carcinoma (ACC) and colon adenocarcinoma (COAD). In kidney renal papillary cell carcinoma (KIRP) and uterine corpus endometrial carcinoma (UCEC), LCAT CNV and methylation levels are prognostic markers. LCAT interacts with m6A modifiers and immune molecules, suggesting a role in immune evasion and as a biomarker for immunotherapy response. LCAT expression correlates with chemotherapeutic drug IC50 values, indicating potential for predicting treatment response. In ACC and COAD, LCAT may promote tumor growth, while in LGG and LIHC, it may inhibit progression. LCAT expression and activity regulation could be a new cancer therapy target. As a key molecule linking lipid metabolism, immune modulation, and tumor progression, the potential of LCAT in cancer therapy is significant. Our findings provide new insights into the role of LCAT in cancer biology and support the development of personalized treatment strategies. [ABSTRACT FROM AUTHOR]

Introduction: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a leading cause of mortality worldwide. A crucial factor in Mtb's virulence is the ESX-5 secretion system, which transports PE/PPE proteins such as PE18 and PPE26. These proteins modulate host-pathogen interactions, immune responses, and intracellular survival mechanisms. Despite their importance, the roles and molecular interactions of PE18 and PPE26 in Mtb pathogenesis require further investigation. Methods: We explored the roles of PE18 and PPE26 using recombinant Mycobacterium smegmatis (Msmeg) as a model organism. Protein-protein interactions were analyzed biochemically to identify partners within the ESX-5 secretion system, including EspG5 and other PE/PPE proteins. Subcellular localization of these proteins was assessed via cell fractionation studies. Functional assays, including in vitro cytokine production and antigen presentation studies, were performed using TLR2/Myd88 knockout and wild-type macrophages. In vivo experiments were conducted to assess effector T-cell activation and intracellular survival. Mechanistic insights into endosome-phagosome maturation and actin cytoskeleton dynamics were obtained through fluorescence microscopy. Results: Our biochemical analyses confirmed interactions between PE18/PPE26, PE18/PPE27, PE19/PPE25, and EspG5/PPE, highlighting their involvement in ESX-5-mediated secretion. Cell fractionation studies revealed that PE/PPE proteins predominantly localize to the cell wall, with PE18 also secreted extracellularly. In vitro and in vivo experiments demonstrated that PE18 and PPE26 activate cytokine production and antigen presentation via TLR2/Myd88-dependent signaling pathways, inducing robust effector memory T-cell responses. Recombinant Msmeg expressing PE18, PPE26, or their combination exhibited enhanced intracellular survival by disrupting endosome-phagosome maturation, likely through interference with actin cytoskeletal organization. Discussion: Our findings elucidate the pivotal roles of PE18 and PPE26 in Mtb pathogenesis, emphasizing their contributions to immune modulation and intracellular persistence. The observed disruption of actin dynamics and endosome-phagosome maturation underscores a novel mechanism by which Mtb evades host defenses. The ability of PE18 and PPE26 to induce effector T-cell responses highlights their potential as targets for host-directed therapies or vaccine development against TB. Further studies focusing on their structure-function relationships and interactions with host proteins could accelerate the development of innovative therapeutic strategies. [ABSTRACT FROM AUTHOR]

Over the past few years, the tumor microbiome is increasingly recognized for its multifaceted involvement in cancer initiation, progression, and metastasis. With the application of 16S ribosomal ribonucleic acid (16S rRNA) sequencing, the intratumoral microbiome, also referred to as tumor-intrinsic or tumor-resident microbiome, has also been found to play a significant role in the tumor microenvironment (TME). Understanding their complex functions is critical for identifying new therapeutic avenues and improving treatment outcomes. This review first summarizes the origins and composition of these microbial communities, emphasizing their adapted diversity across a diverse range of tumor types and stages. Moreover, we outline the general mechanisms by which specific microbes induce tumor initiation, including the activation of carcinogenic pathways, deoxyribonucleic acid (DNA) damage, epigenetic modifications, and chronic inflammation. We further propose the tumor microbiome may evade immunity and promote angiogenesis to support tumor progression, while uncovering specific microbial influences on each step of the metastatic cascade, such as invasion, circulation, and seeding in secondary sites. Additionally, tumor microbiome is closely associated with drug resistance and influences therapeutic efficacy by modulating immune responses, drug metabolism, and apoptotic pathways. Furthermore, we explore innovative microbe-based therapeutic strategies, such as engineered bacteria, oncolytic virotherapy, and other modalities aimed at enhancing immunotherapeutic efficacy, paving the way for microbiome-centered cancer treatment frameworks. [ABSTRACT FROM AUTHOR]

The gut microbiome has emerged as a pivotal area of research due to its significant influence on the immune system and cognitive functions. Cognitive disorders, including dementia and Parkinson's disease, represent substantial global health challenges. This review explores the relationship between gut microbiota, immune modulation, and cognitive decline, with a particular focus on the gut-brain axis. Research indicates that gut bacteria produce metabolites, including short-chain fatty acids (SCFAs), which affect mucosal immunity, antigen presentation, and immune responses, thereby influencing cognitive functions. A noteworthy correlation has been identified between imbalances in the gut microbiome and cognitive impairments, suggesting novel pathways for the treatment of cognitive disorders. Additionally, factors such as diet, environment, and pharmaceuticals play a role in shaping the composition of the gut microbiome, subsequently impacting both immune and cognitive health. This article aims to clarify the complex interactions among gut microbiota, immune regulation, and cognitive disorders, evaluating their potential as therapeutic targets. The goal is to promote microbiome-based treatments and lay the groundwork for future research in this field. [ABSTRACT FROM AUTHOR]

Neuropathic pain (NP) is a chronic pain condition resulting from damage to or dysfunction of the nervous system, characterized by spontaneous pain, hyperalgesia, and allodynia. Recently, the spleen-brain axis has attracted significant attention as a critical pathway in the regulation of pain perception and immune responses. As a pivotal lymphoid organ, the spleen communicates with the brain through both neural and immune signals, thereby modulating neuroinflammation and pain sensitivity. The mechanisms underlying the spleen-brain axis include the activation of immune cells within the spleen, neurotransmitter signaling, and neuronal interactions between the spleen and the brain. Extensive research into this axis has highlighted its central role in the initiation, persistence, and comorbidity of pain, particularly with respect to mood disorders. Building on current knowledge of the regulatory mechanisms of the spleen-brain axis, novel therapeutic targets and approaches are being actively explored, offering potential new avenues for the management of neuropathic pain. Future research should continue to probe the physiological and pathological mechanisms involved in the spleen-brain axis to further advance both pain management and neuroimmunology. [ABSTRACT FROM AUTHOR]

Simple Summary: Liver transplantation is the only therapeutic option for patients affected by end-stage liver disease (ESLD), but its feasibility is restricted by the shortage of donated organs. Stem cell therapy could represent a valid treatment option for these conditions. In particular, the mesenchymal stromal cells derived from the human umbilical cord matrix (WJ-MSCs), thanks to their specific features, can be considered good candidates for liver tissue repair and regeneration. We found that the WJ-MSCs differentiate in hepatocyte-like cells (HLCs) using a differentiation protocol that resembles the in vivo liver morphogenesis. We also showed that HLCs acquired mature hepatic functions and maintained their intrinsic hypoimmunogenicity, a key feature to avoid rejection in the host. Moreover, thanks to proteomic analysis, we highlighted several hepatic proteins in HLCs, demonstrating that these cells could be valid candidates for the treatment of ESLD. End-stage liver disease (ESLD), affecting millions worldwide, represents a challenging issue for clinical research and global public health. Liver transplantation is the gold standard therapeutic approach but shows some drawbacks. Hepatocyte transplantation could be a reliable alternative for patient treatment. Mesenchymal stromal cells derived from Wharton's jelly of the umbilical cord (WJ-MSCs) can differentiate into hepatocyte-like cells (HLCs) and show immunomodulatory functions. Due to the increasing demand for fully characterized cell therapy vehicles warranting both the safety and efficacy of treatments, in this work, we extensively characterized WJ-MSCs before and after the application of a hepatocyte-directed differentiation protocol. HLCs exhibited a morphology resembling that of hepatocytes, expressed early and late hepatic markers (α-fetoprotein, albumin, CK18, HNF4-α), and acquired hepatic functions (glycogen synthesis, xenobiotics detoxification), as also revealed by the shotgun proteomics approach. HLCs maintained the same pattern of immunomodulatory molecule expression and mesenchymal markers, other than displaying specific enzymes, suggesting these cells as promising candidates for cellular therapy of ESLD. Our work shed new light on the basic biology of HLCs, suggesting new therapeutic approaches to treat ESLD. [ABSTRACT FROM AUTHOR]

Introduction: We sought to evaluate the effects of a 12-week pulmonary rehabilitation (PR) program on lung function, mechanics, as well as pulmonary and systemic inflammation in a cohort of 33 individuals with moderate to severe post-COVID-19. Material and Methods: The pulmonary rehabilitation (PR) program employed a combination of aerobic and resistance exercises. Thirty minutes of treadmill training at 75% of the maximum heart rate, combined with 30 min resistance training consisting of 75% of one maximum repetition, three times a week throughout 12 weeks. Results: PR improved the lung function, FVC (p < 0.02), FEV1 (p < 0.02), FEV1/FVC (p < 0.01), MEF25% (p < 0.006), MEF50% (p < 0.03), and MEF75% (p < 0.02). PR also positively influenced lung mechanics, reducing respiratory impedance (Z5Hz, p < 0.03), respiratory reactance (X5Hz, p < 0.01), resistance of the entire respiratory system (R5Hz, p < 0.03), central airway resistance (RCentral, p < 0.03), and peripheral airway resistance (RPeripheral, p < 0.02). Moreover, muscle strength gains were evident, with significant improvements observed in hand grip strength for both the right (p < 0.02) and left (p < 0.01) hands, as well as maximal inspiratory (p < 0.02) and expiratory (p < 0.03) pressures. Additionally, PR exhibited anti-inflammatory effects by reducing the pro-inflammatory cytokines IL-1β (p < 0.0001) and IL-6 (p < 0.0001) and increasing the anti-inflammatory IL-1RA (p < 0.0004) and IL-10 (p < 0.003) and anti-viral IFN-γ (p < 0.0002) and IFN-β (p < 0.008) cytokines in breath condensate and serum samples. Conclusions: Collectively, these findings highlight the effectiveness of PR in ameliorating COVID-19 sequel across respiratory system, skeletal muscle, and immune responses. This highlights its promising potential as a therapeutic intervention for individuals recovering from COVID-19. [ABSTRACT FROM AUTHOR]

Many kinds of diseases are accompanied by inflammatory response owing to abnormal immune system functions. It is necessary to take effective measures to dampen inflammatory and reshape microenvironment of local tissue. CD200-CD200R has been proved as an immune checkpoint signaling pathway to exert immunomodulatory effects on a variety of inflammatory diseases caused by multiple body parts, such as central nervous system, female reproductive system, gynecology, eyes, lungs, intestines and virus intrusion. There is also great potential in areas including clinical diagnostic markers, novel treatments and biomaterials. Therefore, it is of great significance to explore regulatory mechanism and proper uses of CD200-CD200R signaling pathway. [ABSTRACT FROM AUTHOR]

Mycoplasma pneumoniae is a prevalent respiratory microbe that causes acute inflammation in the respiratory system. Surfactant proteins (SP), particularly SP-A and SP-D, are essential for the immunological protection against M. pneumoniae infection. Variant SP-A2 may lead to immune reactions, which could account for the variability in clinical manifestations among individuals. Mechanistically, these surfactant proteins may act as candidate receptors, facilitating both the adhesion of M. pneumoniae and internalization of community-acquired respiratory distress syndrome toxin. They also exhibit a high affinity for lipid ligands on the surface of M. pneumoniae membranes via their carbohydrate recognition domains, which aid in the direct clearing of the bacteria. In addition, SP-A and SP-D demonstrated synergistic effects in augmenting the intake and elimination of M. pneumoniae by alveolar macrophages. Furthermore, these surfactant proteins negatively regulate pulmonary inflammation by influencing lymphocyte and dendritic cell activities, reducing airway eosinophilic infiltration, and managing asthma-related inflammatory responses. A thorough understanding of the immunomodulatory roles of surfactant proteins in M. pneumoniae infection will shed light on how homeostasis is preserved during mycoplasma pneumonia and may guide the development of novel therapeutic strategies against this organism. [ABSTRACT FROM AUTHOR]

There is growing interest in understanding the complex relationship between psychosocial stress and the human gastrointestinal microbiome (GIM). This review explores the potential physiological pathways connecting these two and how they contribute to a proinflammatory environment that can lead to the development and progression of the disease. Exposure to psychosocial stress triggers the activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary axis (HPA), leading to various physiological responses essential for survival and coping with the stressor. However, chronic stress in susceptible individuals could cause sustained activation of HPA and SNS, leading to immune dysregulation consisting of redistribution of natural killer (NK) cells in the bloodstream, decreased function of T and B cells, and elevation of proinflammatory cytokines such as interleukin-1, interleukin-6, tumor necrotic factor-α, interferon-gamma. It also leads to disruption of the GIM composition and increased intestinal barrier permeability, contributing to GIM dysbiosis. The GIM dysbiosis and elevated cytokines can lead to reciprocal effects and further stimulate the HPA and SNS, creating a positive feedback loop that results in a proinflammatory state underlying the pathogenesis and progression of stress-associated cardiovascular, gastrointestinal, autoimmune, and psychiatric disorders. Understanding these relationships is critical for developing new strategies for managing stress-related health disorders. [ABSTRACT FROM AUTHOR]

Simple Summary: This study explored the therapeutic potential of Artemisia argyi essential oil (AAEO) in managing feline herpesvirus type 1 (FeHV-1) infections. FeHV-1, the causative agent of feline viral rhinotracheitis (FVR), leads to severe respiratory and systemic complications in cats. In this study, cats treated with AAEO showed reduced clinical symptoms, improved tissue integrity, and better immune responses. AAEO-treated groups had higher survival rates, stabilized body temperatures, and less weight loss compared to untreated FeHV-1-infected cats. Tissue analysis revealed better integrity in nasal, tracheal, and bronchial tissues. AAEO was also shown to suppress inflammation and protect tissues by modulating immune pathways such as IL-17 signaling. These results suggest that AAEO enhances immune defenses and reduces FeHV-1-induced damage through immune modulation and tissue protection. This study aimed to explore the therapeutic potential and mechanisms of Artemisia argyi essential oil (AAEO) in managing feline herpesvirus type 1 (FeHV-1) infections. FeHV-1, the causative agent of feline viral rhinotracheitis (FVR), leads to severe respiratory and systemic complications in cats. In this study, 35 cats were divided into blank, FeHV-1 infection, and AAEO treatment groups (high, medium, and low doses). In vivo experiments demonstrated that AAEO alleviated clinical symptoms, reduced tissue damage, and modulated immune responses. The AAEO-treated groups showed higher survival rates, stabilized body temperatures, and less severe weight loss compared to the FeHV-1 group. Histopathological analysis revealed improved integrity in nasal, tracheal, and bronchial tissues. Transcriptomic and proteomic analyses identified critical pathways, such as IL-17 signaling, influenced by AAEO treatment, highlighting its role in suppressing inflammation and protecting tissue integrity. In vitro assays revealed that AAEO has concentration-dependent cytotoxicity in feline kidney cells (F81) and provides protective effects when used as a pre-treatment. These findings suggest that AAEO enhances host immune defenses and mitigates FeHV-1-induced damage through immune modulation and tissue protection. [ABSTRACT FROM AUTHOR]

Background: Recent advances in mRNA vaccine technology, accelerated by the global COVID-19 pandemic, have generated significant interest in their applications beyond infectious diseases. Dentistry has emerged as a promising field for exploring the potential of mRNA-based therapies in preventing and treating oral diseases. Objectives: This narrative review aims to evaluate the current status of mRNA vaccine development and its preclinical applications in oral health, focusing on periodontal disease, dental caries, regenerative medicine, implantology, and oral cancer. Methods: The review synthesizes findings from preclinical studies, including research conducted in animal models and in vitro, to assess the potential of mRNA-based therapies to modulate immune responses and promote tissue regeneration in the oral cavity. Clinical trials were only mentioned in the context of broader areas of mRNA vaccine implementation such as oncology and immunotherapy. Results: The preclinical studies highlight the capacity of mRNA vaccines to enhance the body's immune response and facilitate tissue repair processes. Despite these promising results, challenges persist in delivering mRNA vaccines effectively within the complex oral environment. These challenges include vaccine stability, delivery mechanisms, and the modulation of immune responses. Conclusions: While mRNA vaccines offer significant promise for revolutionizing oral health care, they face notable limitations concerning safety, efficacy, and clinical feasibility. Overcoming these obstacles through further research is essential to unlock their full translational potential and ensure their safe and effective integration into dental practice. [ABSTRACT FROM AUTHOR]