Chronic inflammation is central to the pathogenesis of many chronic inflammatory conditions. This review aims to analyze whether the practice of yoga, or yogic meditation and breathing, has any effect on the levels of inflammatory cytokines and other inflammatory markers in patients with various chronic inflammatory diseases such as rheumatoid arthritis, neoplastic disorders, and asthma, as well as in healthy subjects, compared to usual care or sham interventions. A comprehensive search of databases (PubMed, CENTRAL, Embase, and CINAHL) was performed. Randomized controlled trials (RCTs) that evaluated the effects of yoga as an intervention on inflammatory markers were analyzed. A total of 26 studies were included. Only two studies had a low risk of bias (RoB); 24 other studies had a high RoB. Most studies (n=24) reported a favorable outcome with yoga, irrespective of the type of yoga used, the condition studied, and the duration of the intervention. The commonly reported inflammatory markers included IL-6 (n=17), tumor necrosis factor-alpha (TNF-a) (n=13), and C-reactive protein (CRP) (n=10). Most studies showed a significant reduction in inflammatory markers in the yoga group (YG) compared to the control group (CG). Few studies also showed significant improvement in markers of cellular immunity (interferon gamma (IFN-g), IL-10, and transforming growth factor-beta (TGF-b); n=2 each) and improved mucosal defense (IgA, IL-6, and IL-2; n=2 each). A meta-analysis of IL-6, TNF-a, and CRP showed yoga had a favorable effect on the levels of these markers, but it was not statistically significant. Current evidence suggests that yoga can be a complementary intervention for various chronic inflammatory conditions. However, the quality of the evidence is poor, along with considerable heterogeneity. In the future, investigators should describe the intervention better, with a uniform assortment of outcome measures and treatment conditions, to generate high-quality evidence.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS), affecting approximately 1 billion adults globally, is characterized by recurrent airway obstruction during sleep, leading to oxygen desaturation, elevated carbon dioxide levels, and disrupted sleep architecture. OSAS significantly impacts quality of life and is associated with increased morbidity and mortality, particularly in the cardiovascular and cognitive domains. The cyclic pattern of intermittent hypoxia in OSAS triggers oxidative stress, contributing to cellular damage. This review explores the intricate relationship between OSAS and oxidative stress, shedding light on molecular mechanisms and potential therapeutic interventions.
METHODS: A comprehensive review spanning from 2000 to 2023 was conducted using the PubMed, Cochrane, and EMBASE databases. Inclusion criteria encompassed English articles focusing on adults or animals and reporting values for oxidative stress and inflammation biomarkers.
RESULTS: The review delineates the imbalance between pro-inflammatory and anti-inflammatory factors in OSAS, leading to heightened oxidative stress. Reactive oxygen species biomarkers, nitric oxide, inflammatory cytokines, endothelial dysfunction, and antioxidant defense mechanisms are explored in the context of OSAS. OSAS-related complications include cardiovascular disorders, neurological impairments, metabolic dysfunction, and a potential link to cancer. This review emphasizes the potential of antioxidant therapy as a complementary treatment strategy.
CONCLUSIONS: Understanding the molecular intricacies of oxidative stress in OSAS is crucial for developing targeted therapeutic interventions. The comprehensive analysis of biomarkers provides insights into the complex interplay between OSAS and systemic complications, offering avenues for future research and therapeutic advancements in this multifaceted sleep disorder.

Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis of the affected joints. Total glucosides of paeony (TGP) capsules have been widely used clinically for the treatment of RA with good efficacy and safety. However, its effect on inflammatory cytokines remains unclear. Objectives: This study aimed to summarize the effect of TGP on the expression level of serum inflammatory cytokines in RA animal models and its potential mechanisms. Methods: Six databases were searched up to 14 August 2023, relevant animal experiment studies were screened, data were extracted, and the SYRCLE animal experiment bias risk assessment tool was used for risk assessment. Results: A total of 24 studies were included, including 581 animals. Results showed that compared with the model control group, TGP decreased the levels of TNF-α, IL-1β, IL-6, and PGE2 and increased the levels of TGF-β1 after 1-2 weeks of intervention, decreased the levels of TNF-α, IL-1β, IL-6, IL-2, IL-17, IL-17α, IL-21, VEGF, IFN-γ and PGE2 and increased the levels of IL-10 and IL-4 after 3-4 weeks of intervention, decreased the levels of TNF-α, IL-6, IL-17α and increased the level of IL-10 after 8 weeks of intervention. There was no significant difference in the effects of TGP on the levels of IL-10, IL-17, and IFN-γ after 1-2 weeks of intervention and IL-1 and TGF-β1 after 3-4 weeks of intervention. Conclusion: In summary, based on the existing studies, this study found that compared with the control group of the RA animal model, TGP can reduce the levels of serum pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 and increase the levels of serum anti-inflammatory cytokines such as IL-10, exerting an anti-inflammatory effect by regulating and improving the levels of inflammatory cytokines, and thus alleviating the disease. Given the low quality of the included studies and the lack of sufficient evidence, more high-quality studies are still needed to validate the results of this study.

This narrative review examines the intricate landscape of gold-induced cytokine responses, delving into the anti-inflammatory and immune-modulating properties of gold compounds, with a primary focus on their application in treating rheumatoid arthritis and other autoimmune conditions. Utilizing a comprehensive search strategy across major scientific databases, we identified and analyzed a diverse range of studies published within the last two decades. The aim of this review is to provide a nuanced understanding of the current state of knowledge, addressing key questions regarding the mechanisms by which gold compounds modulate cytokine responses and their clinical implications. Our review encompasses an in-depth exploration of the anti-inflammatory effects of gold compounds, emphasizing their impact on pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6). Moreover, we investigate the lesser-explored terrain of immune modulation, shedding light on the ability of gold compounds to influence anti-inflammatory cytokines, notably interleukin 10 (IL-10). Through an extensive analysis of the literature, we unravel the multifaceted mechanisms underlying gold-induced cytokine responses, including the inhibition of nuclear factor kappa B (NF-κB) signaling and interference with janus kinase/signal transducers and activators of transcription (JAK/STAT) pathways. In exploring the clinical applications of gold-induced cytokine modulation, we synthesize findings from relevant studies, elucidating the potential of gold compounds as therapeutic agents. However, challenges such as variability in formulations and diverse cytokine assessment methods are discussed, emphasizing the need for standardization in both research and clinical settings. Looking ahead, our scoping review identifies key unanswered questions and proposes future directions for research in this domain. We discuss emerging therapeutic strategies, considering the integration of gold compounds with other modalities to optimize treatment outcomes. This comprehensive review serves as a foundational resource for researchers, clinicians, and policymakers seeking a nuanced understanding of gold-induced cytokine responses, paving the way for further advancements in this critical area of study.

Bipolar disorder (BD) is a severe mental disorder with various hypotheses regarding its pathogenesis. This article provides a summary of numerous studies on the variations in inflammatory cytokine levels in patients with BD and the effects of treatment with antipsychotics, mood stabilizers, and antidepressants on these levels. In addition, patients with autoimmune diseases who use anti-inflammatory monoclonal antibodies experience symptoms, such as depression, anxiety, and insomnia. These pieces of evidence suggest a potential association between immune inflammation and BD and offer new possibilities for therapy. Building upon this relationship, the authors propose an innovative approach for treating BD through individualized and precise therapy using anti-inflammatory monoclonal antibody drugs. To support this proposal, the authors compile information on pharmacological effects and relevant studies, including trials of various anti-inflammatory therapeutic monoclonal antibody drugs (e.g. infliximab, tocilizumab, and canakinumab) for the potential treatment of BD and its associated side effects in psychiatry. The authors categorize these anti-inflammatory monoclonal antibody drugs into levels I-IV through a comprehensive analysis of their advantages and disadvantages. Their potential is examined, and the need for further exploration of their pharmaceutical effects is established.

BACKGROUND: Although a large number of trials have observed an anti-inflammatory property of acarbose, the currently available research remains controversial regarding its beneficial health effects. Hence, the purpose of this study was to examine the effect of acarbose on inflammatory cytokines and adipokines in adults.
METHODS: PubMed, Web of Science, and Scopus were systematically searched until April 2023 using relevant keywords. The mean difference (MD) of any effect was calculated using a random-effects model. Weighted mean difference (WMD) and 95% confidence intervals (CIs) were calculated via the random-effects model.
RESULTS: The current meta-analysis of data comprised a total of 19 RCTs. Meta-analysis showed that acarbose significantly decreased tumor necrosis factor-alpha (TNF-α) (weighted mean difference [WMD]) = - 4.16 pg/ml, 95% confidence interval (CI) - 6.58, - 1.74; P = 0.001) while increasing adiponectin (WMD = 0.79 ng/ml, 95% CI 0.02, 1.55; P = 0.044). However, the effects of acarbose on TNF-α concentrations were observed in studies with intervention doses ≥ 300 mg/d (WMD = - 4.09; 95% CI - 7.00, - 1.18; P = 0.006), and the adiponectin concentrations were significantly higher (WMD = 1.03 ng/ml, 95%CI 0.19, 1.87; P = 0.016) in studies in which the duration of intervention was less than 24 weeks. No significant effect was seen for C-reactive protein (CRP; P = 0.134), interleukin-6 (IL-6; P = 0.204), and leptin (P = 0.576).
CONCLUSIONS: Acarbose had beneficial effects on reducing inflammation and increasing adiponectin. In this way, it may prevent the development of chronic diseases related to inflammation. However, more studies are needed.

Leptin is a peptide hormone that regulates energy balance, immune inflammatory response, and bone metabolism. Several studies have demonstrated a relationship between leptin and periodontitis, a local inflammatory disease that progressively weakens the supporting structures of the teeth, eventually leading to tooth loss. This article reviews the existing literature and discusses leptin\'s basic characteristics, its relationship with periodontitis, and its effects on periodontal tissue metabolism.

Cardiovascular disorders (CVDs) represent a global challenge and are regarded as one of the leading causes of mortality. The role of inflammation as a risk factor in these disorders has been studied, with the accelerated atherosclerotic process being a crucial factor in the pathogenesis. Several inflammatory biomarkers such as C-reactive protein (CRP), Interleukins (ILs), Tumor Necrosis Factor-alpha (TNF-α), and others have been identified that play a role in the atherosclerotic process, thus linking systemic inflammatory conditions with CVDs, including acute myocardial infarction (AMI), chronic heart failure (CHF), venous thromboembolism (VTE) and others. These markers could be used to predict the risk of CVDs. Understanding the precise mechanisms can lead to therapeutic strategies targeted at pro-inflammatory processes. We aim to provide an overview of the existing literature on the role of inflammation in various cardiovascular disorders and identify different inflammatory biomarkers and therapeutic targets in this comprehensive literature review. We reviewed 190 references published between 2013 and August 3, 2023, in well-reputed journals and analyzed eight selected papers in-depth. We describe the pathophysiologic pathways that lead to atherosclerosis and other cardiovascular pathologies. Several inflammatory cytokines encompassing various groups were identified to be causing endothelial dysfunction, leading to an increased risk for CVDs. Polymorphisms in the genes for different cytokines also led to different levels of susceptibility to CVDs. Nevertheless, future research detailing the inflammatory pathways and their link with CVDs would lead to better outcomes for patients with preexisting and new onset of CVDs as well as chronic inflammatory disorders.

BACKGROUND: Both acute exercise and environmental hypoxia may elevate inflammatory cytokines, but the inflammatory response in the hypoxic exercise is remaining unknown.
OBJECTIVE: We performed this systematic review and meta-analysis to examine the effect of exercise in hypoxia on inflammatory cytokines, including IL-6, TNF-α and IL-10.
METHODS: PubMed, Scopus and Web of Science were searched to identify the original articles that compared the effect of exercise in hypoxia with normoxia on IL-6, TNF-α and IL-10 changes, published up to March 2023. Standardized mean differences and 95% confidence intervals (CIs) were calculated using a random effect model to (1) determine the effect of exercise in hypoxia, (2) determine the effect of exercise in normoxia and (3) compare the effect of exercise in hypoxia with normoxia on IL-6, TNF-α and IL-10 responses.
RESULTS: Twenty-three studies involving 243 healthy, trained and athlete subjects with a mean age range from 19.8 to 41.0 years were included in our meta-analysis. On comparing exercise in hypoxia with normoxia, no differences were found in the response of IL-6 [0.17 (95% CI - 0.08 to 0.43), p = 0.17] and TNF-α [0.17 (95% CI - 0.10 to 0.46), p = 0.21] between the conditions. Exercise in hypoxia significantly increased IL-10 concentration [0.60 (95% CI 0.17 to 1.03), p = 0.006] compared with normoxia. In addition, exercise during both hypoxia and normoxia increased IL-6 and IL-10, whereas TNF-α was increased only in hypoxic exercise condition.
CONCLUSIONS: Overall, exercise in both hypoxia and normoxia increased inflammatory cytokines; however, hypoxic exercise may lead to a greater inflammatory response in adults.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory disease of the nose and paranasal sinuses characterized by the presence of nasal polyps. The symptoms produced by the presence of nasal polyps such as nasal obstruction, nasal discharge, facial pain, headache, and loss of smell cause a worsening in the quality of life of patients. The source of the nasal polyps remains unclear, although it seems to be due to a chronic inflammation process in the sinonasal mucosa. Fibroblasts, the main cells in connective tissue, are intimately involved in the inflammation processes of various diseases; to this end, we carried out a systematic review to evaluate their inflammatory role in nasal polyps. Thus, we evaluated the main cytokines produced by nasal polyp-derived fibroblasts (NPDF) to assess their involvement in the production of nasal polyps and their involvement in different inflammatory pathways. The results of the review highlight the inflammatory role of NPDF through the secretion of various cytokines involved in the T1, T2, and T3 inflammatory pathways, as well as the ability of NPDF to be stimulated by a multitude of substances. With these findings, the fibroblast is positioned as a new potential therapeutic target in the treatment of CRSwNP.