Mediators of Inflammation最新文献

{"title":"Impaired Meningeal Lymphatic Drainage Aggravates LPS-Induced Neuroinflammation and Depression-Like Behaviors in Mice.","authors":"Chonglong Shi, Yin Zhou, Qiang Zhang, Wenjie Jin, Hongquan Dong","doi":"10.1155/mi/4288671","DOIUrl":"10.1155/mi/4288671","url":null,"abstract":"<p><p><b>Background:</b> The role of meningeal lymphatic vessels (mLVs) in neurodegenerative diseases has been increasingly recognized. However, their involvement in lipopolysaccharide (LPS)-induced neuroinflammation and associated depression-like behaviors remains poorly understood. Given that impaired clearance of neurotoxic substances can prolong central nervous system (CNS) inflammation, investigating the function of mLVs in this context may offer new insights into the mechanisms underlying acute neuroinflammation and provide potential therapeutic targets. <b>Methods:</b> First, the impact of intracerebral injection of LPS on the function of mLVs was investigated. Subsequently, the MAZ51, a VEGFR3 antagonist, was administered via intraperitoneal injection for 1 month to inhibit the development and function of mLVs, and to evaluate whether the impaired drainage function of mLVs exacerbates inflammation in the CNS caused by LPS. Finally, VEGFR3 ligand VEGF-C was administered preemptively to assess whether enhancing the function of mLVs mitigates LPS-induced inflammation and depression-like behavior. <b>Results:</b> The mice with intracerebral injection of LPS demonstrated a substantial reduction in the transport of OVA-647 to the deep cervical lymph nodes (dCLNs) and in the coverage of Lyve-1 within the mLVs, suggesting LPS impaired the development and drainage of mLVs. Pretreatment with MAZ51 further damages the drainage function of mLVs and intensify LPS-induced activation of microglia and astrocytes. Additionally, MAZ51 led to a decrease in the protein levels of PSD95 as well in the hippocampus, which was paralleled by an elevation in TNF-α and IL-6 levels, and aggravated depression-like behavior. On the contrary, pretreatment with VEGFR3 ligand VEGF-C attenuated LPS-induced neuroinflammation, as indicated by a decrease in TNF-α, IL-6, Iba1, and GFAP expression in the hippocampus. VEGF-C treatment also significantly increased the level of PSD95 and improved depression-like behavior. <b>Conclusion:</b> The drainage function of mLVs is pivotal in inflammation of the CNS. Enhancing meningeal lymphatic improves the development of neuroinflammation and inflammation-induced depression-like behaviors. VEGFR3 could serve as a potential therapeutic target for CNS inflammation.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"4288671"},"PeriodicalIF":4.2,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12350002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Fentanyl Abuse on the Gut Microbiota Pattern, Inflammation, and Metabolic Alterations in a Fentanyl Dependance Rat Model.","authors":"Kianoosh Ferdosnejad, Parvaneh Maghami, Mohammad-Reza Zarrindast, Seyed Davar Siadat","doi":"10.1155/mi/6661864","DOIUrl":"10.1155/mi/6661864","url":null,"abstract":"<p><p><b>Introduction:</b> This study examines the effects of fentanyl misuse on gut microbiota, inflammation, and metabolic pathways using a rat model. As the opioid crisis, driven by synthetic opioids like fentanyl, escalates, identifying new biomarkers, and therapeutic strategies becomes crucial to mitigate its negative impacts and rising overdose cases. <b>Methods:</b> This study was done using species-specific 16S rRNA gene profiling through absolute real-time PCR techniques, alongside relative real-time PCR analysis for inflammatory and metabolic markers and liquid chromatography-mass spectrometry (LC-MS) for metabolite quantification. To visualize the correlations between microbial abundance and inflammatory/metabolic markers, Spearman/Pearson correlation analyses were performed. <b>Results:</b> Fentanyl treatment increased <i>Clostridium sensu stricto</i> (<i>p</i>=0.69) and <i>Bacteroides fragilis</i> (<i>p</i>=0.04), while <i>Faecalibacterium prausnitzii</i> (<i>p</i>=0.14) and <i>Lacticaseibacillus rhamnosus</i> (<i>p</i>=0.14) showed a tendency to decrease. Additionally, fentanyl-treated rats exhibited heightened levels of pro-inflammatory cytokines (<i>IL-1β</i>, <i>p</i>=0.01; <i>TNF-α</i>, <i>p</i>=0.083; <i>IL-6</i>, <i>p</i>=0.17) and increased expression of toll-like receptors (<i>TLR-2</i>, <i>p</i>=0.005; <i>TLR-4</i>, <i>p</i>=0.001), indicating intestinal inflammation. Metabolic pathway analysis revealed significant alterations, including increased <i>BCoAT</i> expression (<i>p</i>  < 0.001) and decreased <i>tph1</i> expression (<i>p</i>  < 0.001) in fentanyl-treated rats. LC-MS analysis indicated a significant reduction in butyrate levels (45.49 ± 7.82; 73.52 ± 5.4 µM; <i>p</i>  < 0.001), suggesting impaired short-chain fatty acid production and potential gut barrier integrity issues. Tryptophan levels were also significantly lower (14.96 ± 1.3; 22.38 ± 2.1 µM; <i>p</i>  < 0.001), indicating possible disruptions in serotonin synthesis, while deoxycholic acid levels increased (106.1 ± 7.3; 77.35 ± 3.5 µM; <i>p</i>  < 0.001), suggesting altered bile acid metabolism contributing to gut inflammation. Leucine levels (31.8 ± 1.5; 30.67 ± 1.6 µM; <i>p</i>=0.15) remained comparable between groups. <b>Conclusion:</b> This study reveals complex relationships between fentanyl consumption, gut microbiota alterations, gut inflammation, and metabolic functions. The identified changes in specific bacterial species and inflammatory markers suggest a potential mechanism by which fentanyl may exacerbate gut inflammation and disrupt metabolic pathways, highlighting the importance of these dynamics in understanding the microbiota importance and opioid dependance.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"6661864"},"PeriodicalIF":4.2,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunophenotyping of Patients With Rheumatoid Arthritis Reveals Difference in CD27⁺IgD⁺ Unswitched Memory B Cell Profiles.","authors":"Bérénice Hansen, Raul Da Costa, Dominique Revets, Fanny Hedin, Maria Konstantinou, Eduardo Rosales Jubal, Franck Ngangom, Cédric C Laczny, Kirsten Roomp, Viacheslav Petrov, Andreas Michalsen, Etienne Hanslian, Daniela A Koppold, Anika Rajput Khokhar, Nico Steckhan, Michael Jeitler, Brit Mollenhauer, Sebastian Schade, Michel Vaillant, Antonio Cosma, Paul Wilmes, Jochen G Schneider","doi":"10.1155/mi/9675331","DOIUrl":"10.1155/mi/9675331","url":null,"abstract":"<p><p><b>Objectives:</b> Over the past decades, the prevalence of noncommunicable diseases has surged significantly, including the systemic autoimmune disorder rheumatoid arthritis (RA). Despite extensive research and advancement of RA therapy, effective prevention strategies or cures remain elusive, and the mechanisms underlying RA pathogenesis unclear. It is crucial to gain deeper insights into RA pathophysiology. The objective of this study is to provide a comprehensive immunophenotyping of patients with RA. <b>Methods:</b> We generated and analyzed deep immunophenotyping data from 52 patients with RA and 47 healthy controls (HCs). Whole blood samples were stained with extracellular markers, and intracellular antibodies and analyzed for 32 different cell markers using mass cytometry by time of flight. The acquired data was analyzed by both manual and automatic unsupervised tools and subsequently complemented with anthropometric data and clinical-laboratory parameters. <b>Results:</b> We observed a significant disparity in immune cell profiles between patients with RA and HC, notably a reduced frequency of CD27⁺IgD⁺ unswitched memory B (_mB) cells in patients with RA (<i>p</i>-value < 0.01), with the disease RA being the primary and only significant factor explaining up to 17.9% of the variance of these cells. <b>Conclusion:</b> Our results reveal, for the first time, that a reduced frequency of unswitched _mB cells in patients with RA is the only significant abnormality distinguishing patients with RA from HC in a complex immunophenotyping panel of 72 different cell populations. This provides important information to further individualize various interventions and possibly help to design novel therapeutic interventions.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"9675331"},"PeriodicalIF":4.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12324914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Inflammatory Factors and Calcium Metabolism With Arthritis in Patients With Inflammatory Bowel Disease: Evidence From Mediated Mendelian Randomization.","authors":"Sinan Xiao, Kairong Su, Hongliang Gao, Chenyang Qiao, Sumei Sha, Xin Liu, Haitao Shi","doi":"10.1155/mi/1675577","DOIUrl":"10.1155/mi/1675577","url":null,"abstract":"<p><p><b>Background:</b> Beyond intestinal inflammation, inflammatory bowel disease (IBD) is associated with many extraintestinal manifestations, particularly arthritis. However, systematic evidence regarding causal relationships between IBD and clinically prevalent arthritis subtypes remains limited. <b>Methods:</b> We conducted bidirectional two-sample Mendelian randomization (MR) analyses to assess causal associations between IBD (Crohn's disease [CD], ulcerative colitis [UC]) and seven arthritis subtypes: rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PsA), osteoarthritis (OA), reactive arthritis (ReA), gout and pyogenic arthritis (PA). A two-step MR (TSMR) analyses was subsequently performed to evaluate potential mediators across four domains: metabolites of gut microbiota, serum biochemical indicators, inflammatory/immune factors, and nutritional/metabolic indicators in IBD-AS/PsA/ReA pathways. <b>Results:</b> MR analysis revealed that IBD increased the risk of AS (OR = 1.21, 95% CI: 1.11-1.32, <i>P</i> _IVW < 0.001), PsA (OR = 1.18, 95% CI: 1.05-1.33, <i>P</i> _IVW = 0.007), and ReA (OR = 1.11, 95% CI: 1.04-1.18, <i>P</i> _IVW = 0.003). Subgroup analyses revealed CD increased the risk of AS (OR = 1.16, 95% CI: 1.07-1.27, <i>P</i> _IVW < 0.001) and UC increased the risk of ReA (OR = 1.14, 95% CI: 1.04-1.24, <i>P</i> _IVW = 0.005). The first step of the mediation MR showed that IBD was associated with increased butyrate levels, decreased serotonin levels, increased C-reactive protein (CRP), increased interleukin-6 (IL-6), increased percentage of neutrophils, decreased percentage of lymphocytes, and decreased total body bone mineral density, but the second step of the analysis revealed no significant evidence that the above factors were mediators of the causal effects of IBD on AS, PsA, and ReA. <b>Conclusion:</b> This study establishes the causal effect of IBD on AS, PsA, and ReA. The absence of significant mediation effects suggests that IBD-associated gut dysbiosis, systemic inflammation, and calcium metabolic disturbances may not directly drive arthritis pathogenesis, challenging their utility as predictive biomarkers for arthritis development in IBD patients.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"1675577"},"PeriodicalIF":4.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determination of Serum Alpha-1-Acid Glycoprotein Concentration and the Influence of Physiological and Gynecological Factors in Women Attending in Tertiary-Care Center in Mexico: A Pilot Study.","authors":"Liliana García-Ortiz, Mariana Téllez-Araiza, José Gutiérrez-Salinas, Liliana Hernández-Figueroa, Juana Arellano-García, Erasmo Cordero-Martínez","doi":"10.1155/mi/9998286","DOIUrl":"10.1155/mi/9998286","url":null,"abstract":"<p><p>Alpha 1-acid glycoprotein (AGP1) is recognized as a protein with an important immunomodulatory activity, which under certain circumstances its serum concentration is altered as a result of acute metabolic stress (e.g., infections) or chronic (e.g., obesity). This quality of altering its concentration according to the immunological circumstances of the individuals, for example, in women, in which hormonal variables, nutritional states, and/or pregnancy, has led to think that one protein can be used as a biomarker in cancer, immunological diseases, and other pathologies. The aim of the present study was to determine the concentration of AGP1 protein in serum samples of apparently healthy women and to associate this concentration with several variables, such as age, body weight, and other physiological variables, that may affect the concentration of this protein. A total of 656 apparently healthy women were included according to their clinical history, physical examination, and laboratory tests. The determination of AGP1 concentration was performed by nephelometry in serum samples. The results show that the overall mean serum concentration of AGP1 was 76.82 ± 18.63 mg/dL (range 37.95-175 mg/dL). This concentration is observed to be altered in women who presented morbid obesity (83.79 mg/dL; <i>p</i>  < 0.001); as well as in women who have had children (gestation). Our work reports for the first time the serum levels of AGP1 in Mexican women, as well as several physiological circumstances in which its concentration is modified, which should be considered if AGP1 is required as a biomarker, both in physiological and pathological circumstances.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"9998286"},"PeriodicalIF":4.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HBP21 Alleviates Sepsis-Induced Acute Kidney Injury by Targeting PI3K/AKT-Mediated M1 Macrophage Polarization.","authors":"Na An, Mingzhi Xu, Ruman Chen, Cuijuan Wang, Yafei Bai","doi":"10.1155/mi/9021628","DOIUrl":"10.1155/mi/9021628","url":null,"abstract":"<p><p><b>Background:</b> Sepsis-induced acute kidney injury (S-AKI), a life-threatening complication of systemic infection, is driven by macrophage-mediated inflammatory dysregulation. This study explores the role of heat shock binding protein 21 (HBP21) in attenuating renal injury through PI3K/AKT pathway modulation, employing cellular and animal models to dissect its therapeutic mechanisms and clinical relevance. <b>Methods:</b> In vitro, RAW264.7 cells underwent LPS-induced M1 polarization, and HBP21 expression was manipulated to evaluate its role in macrophage phenotype and PI3K/AKT signaling activation. M1/M2 macrophage polarization was quantified by flow cytometry, while coculture with NRK-52E cells evaluated tubular epithelial cell viability (CCK-8) and apoptosis (flow cytometry). An S-AKI rat model was induced via cecal ligation and puncture (CLP). Renal function (serum creatinine [Scr]/blood urea nitrogen [BUN]), tissue damage (hematoxylin and eosin [H&E]/terminal dUTP nick-end labeling [TUNEL]), and inflammation (Western blot/IHC) were systematically analyzed. <b>Results:</b> HBP21 overexpression promoted M2 macrophage polarization and activated PI3K/AKT signaling in LPS-stimulated macrophages. Knockdown of HBP21 obtained the opposite data. Inhibition with LY294002 or activation with 740 Y-P reversed these effects, confirming pathway involvement. Cocultured NRK-52E cells exposed to conditioned medium from HBP21-overexpressing macrophages showed a 62.32% increase in viability and a 56.11% reduction in apoptosis under LPS challenge. HBP21 overexpression in vivo lowered Scr (38.5%) and BUN (47.4%), alleviated tubular damage, and shifted renal macrophages toward an M2 anti-inflammatory phenotype with concurrent TNF-α/IL-6 downregulation. <b>Conclusion:</b> These findings suggest that HBP21 mitigates S-AKI pathogenesis via PI3K/AKT-mediated M2 macrophage polarization, underscoring its translational potential in renal injury therapy.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"9021628"},"PeriodicalIF":4.2,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12318628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Serum Total Bilirubin Level With Abdominal Aortic Calcification: A Population-Based Cross-Sectional Study.","authors":"Chunjiang Liu, Kuan Li, Guohua Wang, Ziqian He, Suyan Cao","doi":"10.1155/mi/5229580","DOIUrl":"10.1155/mi/5229580","url":null,"abstract":"<p><p><b>Objective:</b> The purpose of our study was to examine the association between serum total bilirubin level and abdominal aortic calcification (AAC) in the general United States population. <b>Methods:</b> We analyzed data from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) to assess the association of total bilirubin levels with AAC and severe AAC (SAAC). Restricted cubic spline (RCS) plots, weighted multivariable logistic regression (odds ratios [ORs] and 95% confidence intervals [CIs]), and stratified subgroup analyses (by age, sex, hypertension, diabetes mellitus, and body mass index [BMI]) were conducted. <b>Results:</b> Our analysis included a total of 3016 participants. First, the RCS plots showed the U-shaped curve association of serum total bilirubin level with prevalence of AAC and SAAC. RCS analysis revealed a U-shaped association between serum total bilirubin levels and the prevalence of both AAC and SAAC. Serum total bilirubin levels were categorized into quartiles: Q1 (0.10-0.50 mg/dL), Q2 (0.51-0.60 mg/dL), Q3 (0.61-0.80 mg/dL), and Q4 (0.81-2.20 mg/dL). Second, after adjusting for potential confounders, compared with the Q1 group, the ORs with 95% CI for the association of total bilirubin level with AAC and SAAC across Q2, Q3, and Q4 were (0.71 (0.61, 0.98), 1.11 (0.90, 1.38), and 1.36 (1.07, 1.73) and 0.78 (0.58, 1.21), 1.12 (0.77, 1.65), and 1.28 (0.87, 1.77)), respectively. Finally, this U-shaped correlation was found among participants in age ≥60 years, with hypertension, with DM and with BMI of ≥30 kg/m². <b>Conclusions:</b> Our study identified a significant U-shaped association between serum total bilirubin levels and both AAC and SAAC. These findings suggested that monitoring and optimizing total bilirubin levels may offer potential preventive benefits against AAC development.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"5229580"},"PeriodicalIF":4.2,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12318627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Roles of Prostaglandin E2 (PGE2) in Bone Remodeling and Pain Management: Bridging the Gap in Osteoarthritis Research.","authors":"Yulian Zhang, Wenzhi Wu, Zhuo Chen","doi":"10.1155/mi/8882429","DOIUrl":"10.1155/mi/8882429","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a bone disease mainly treated with nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain. However, the exact mechanisms underlying this disease remain elusive, which creates an attractive opportunity to explore the mechanisms and provide intentional treatments for OA. In this narrative review, we selected articles discussing advancements and applications of PGE2 to OA biology and pathology and discussed how PGE2 reacts during OA-associated pain, the resulting bone structural alterations, and the potential drugs or treatments for patients with OA. We aimed to summarize the accumulating evidence suggesting that prostaglandin E2 (PGE2) plays an important role in the central sensitization of OA-related pain, elucidating the precise mechanisms underlying the pain relief effects of NSAIDs. Additionally, we interpreted the potential mechanisms by which PGE2 influences bone repair and regeneration at different stages of bone remodeling in OA progression, which raises concerns regarding the side effects of NSAIDs in bone remodeling during disease progression. Finally, we discussed the potential therapeutic strategies for different stages of OA based on available evidence. This review focused on the newly found evidence for the novel functions of PGE2 in central sensitization and bone remodeling and provides possible future directions for the treatment of OA.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"8882429"},"PeriodicalIF":4.2,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12317822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drugs Used in the Treatment of Viral Infections for the Prevention of Airway Remodeling in Asthma.","authors":"Joanna Wieczfinska, Rafal Pawliczak","doi":"10.1155/mi/5526526","DOIUrl":"10.1155/mi/5526526","url":null,"abstract":"<p><p>One of the main causes of the exacerbation of chronic airway inflammatory diseases is respiratory virus infections. The most prevalent viruses that can infect humans multiple times a year are rhinovirus (RV) and respiratory syncytial virus (RSV). Because remodeling factors like matrix metalloproteinases (MMPs), which are released by infiltrating neutrophils, are present. Airway remodeling is a characteristic of the pathology of airway diseases such as bronchial asthma. In these circumstances, viral infections may result in increased neutrophilic activation, which would exacerbate asthma symptoms and modify the airway. Although a connection between viral infections and acute exacerbations of chronic inflammatory respiratory diseases has been established, anti-inflammatory medications are frequently used in conjunction with antiviral medications to treat viral infections. Although their modes of action differ, they all lessen inflammation, which is essential for the development of airway remodeling. This review addresses the potential role of anti-inflammatory and antiviral drugs in preventing airway remodeling.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"5526526"},"PeriodicalIF":4.2,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-429 Inhibits Microglial Inflammation by Targeting <i>IKKβ</i> Through the NF-κB Pathway.","authors":"Zhongling Ke, Yanhui Chen, Xiaoxia Lin, Jilong Jiang","doi":"10.1155/mi/7165782","DOIUrl":"10.1155/mi/7165782","url":null,"abstract":"<p><p>This study was designed to explore the specific mechanism of miR-429 in neuroinflammation of TS, to provide a theoretical basis for the etiology of TS and new targets for future treatment. Male SD rats were randomly divided into the normal control (CON) group and the Tourette syndrome (TS) group. The activation of microglia in the striatum was detected by immunohistochemistry and the concentration of interleukin (IL)-6 in the brain was measured by ELISA. The expression of miR-429 in brains was detected by quantitative real-time PCR (qPCR). Human microglia clone 3 (HMC3) cells were transfected, respectively, with double-stranded inactive miRNA; miR-429 mimics; miR-429 inhibitors. The levels of miR-429 and <i>IKKβ</i> mRNA were detected by qPCR. The expression levels of IKKβ, NF-κBp65 b, and IL-6 proteins were detected by western blot. MiR-429 and <i>IKKβ</i> targeted binding was verified by a double luciferase experiment. IL-6 in the brain of the TS rat group was higher than in the CON group. Furthermore, the relative expression of miR-429 in the TS group was several hundreds of times higher than in the CON group. The levels of IKKβ, NF-κBp65, and IL-6 protein in lipopolysaccharide (LPS)-induced microglia were lower in the miR-429 mimics group, but higher in the miR-429 inhibitor group, compared to those of the MiRNA negative control (miR-NC) group (<i>p</i> < 0.05). The miR-429 targeted <i>IKKβ</i> binding to regulate the NF-κB pathway and inhibit the release of pro-inflammatory factors, thus, controlling neuroinflammation in microglia, which may be the mechanism of action of miR-429 in TS.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"7165782"},"PeriodicalIF":4.2,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}