Inflammation Research最新文献_第2页

Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy. 芳烃受体（Aryl hydrocarbon receptor, AhR）通过激活PINK1/ parkinson介导的线粒体自噬，缓解lps诱导的IPEC-J2细胞炎症反应。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02063-y

Mengfei Ma, Jianxun Guo, Xiaoying Su, Baocai Ma, Xiufen Wang, Mingyu Wangshao, Kai Zhong, Yueying Wang, Guoyu Yang, Yingqian Han

{"title":"Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy.","authors":"Mengfei Ma, Jianxun Guo, Xiaoying Su, Baocai Ma, Xiufen Wang, Mingyu Wangshao, Kai Zhong, Yueying Wang, Guoyu Yang, Yingqian Han","doi":"10.1007/s00011-025-02063-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02063-y","url":null,"abstract":"Objective: This study investigates the role of the aryl hydrocarbon receptor (AhR) in lipopolysaccharide (LPS)-induced inflammatory responses in IPEC-J2 cells.Methods: Inflammatory responses were triggered in IPEC-J2 cells using 5 μg/ml LPS. AhR was activated with tryptophan or FICZ and knocked down via RNA interference. PINK1/Parkin-mediated mitophagy was activated using CCCP and inhibited by PINK1 knockdown. Inflammatory mediators and pathway proteins were analyzed through ELISA, RT-qPCR, western blot, and immunofluorescence. Mitochondrial function was assessed by measuring ROS, ATP, and mitochondrial membrane potential. The interaction between AhR and PINK1 was examined using dual-luciferase reporter assays.Results: The IDO1/AhR signaling axis was activated in LPS-stimulated IPEC-J2 cells. AhR activation was found to attenuate LPS-induced inflammatory responses, whereas AhR knockdown exacerbated these responses. Mechanistic investigations demonstrated that AhR activation alleviated LPS-induced mitochondrial damage. Activating PINK1/Parkin-mediated mitophagy successfully countered the increased inflammatory response in IPEC-J2 cells after AhR knockdown. Moreover, blocking PINK1 reversed the anti-inflammatory effects of FICZ. Dual-luciferase reporter assays revealed that AhR acts as a crucial transcription factor by directly binding to the promoter region, thereby initiating PINK1 transcription.Conclusions: AhR reduces LPS-induced inflammatory response in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy, with AhR directly engaging the PINK1 promoter to enhance its transcription. Targeting AhR may present a novel strategy for the prevention and management of Escherichia coli-induced diarrhea in piglets.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"98"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical outcomes of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease patients: a systemic review and meta-analysis of 37,056 individuals from 32 randomized trials. 抗炎疗法抑制冠心病患者NLRP3/IL-1β/IL-6/CRP通路的临床结果：一项来自32项随机试验的37,056人的系统评价和荟萃分析

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02058-9

Yannan Pan, Fangfang Fan, Jie Jiang, Yan Zhang

{"title":"Clinical outcomes of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease patients: a systemic review and meta-analysis of 37,056 individuals from 32 randomized trials.","authors":"Yannan Pan, Fangfang Fan, Jie Jiang, Yan Zhang","doi":"10.1007/s00011-025-02058-9","DOIUrl":"10.1007/s00011-025-02058-9","url":null,"abstract":"Background: Treatment effects of anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in coronary artery disease (CAD) had conflicting results. The study aims to evaluate efficacy and safety outcomes of treatments inhibiting this pathway.Methods: Cochrane Library, Embase, Pubmed, and ClinicalTrials.gov were searched for randomized controlled trials evaluating therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway in CAD patients. Relative risks (RR) with 95% confidence intervals (CI) were calculated.Results: 32 studies and 37,056 individuals were included. Anti-inflammatory therapies inhibiting the pathway reduced the risks of myocardial infarction (MI) (RR 0.85, 95% CI 0.78-0.93) and coronary revascularization (RR 0.80, 95% CI 0.74-0.86), with no benefits in major adverse cardiovascular events (MACE), heart failure (HF), stroke, cardiovascular or all-cause mortality. Colchicine reduced the risks of MACE, MI, and coronary revascularization. IL-1 inhibitors reduced the risks of coronary revascularization, with potential benefits in MI and HF. Increased risks of infections, gastrointestinal adverse effects, and injection site reactions were found. Meta-regression analysis demonstrated that post-treatment hsCRP/CRP was correlated with MACE (p < 0.001) and MI (p = 0.048) and post-treatment IL-6 was associated with MI (p = 0.033).Conclusion: Anti-inflammatory therapies inhibiting the NLRP3/IL-1β/IL-6/CRP pathway had satisfying safety profiles and were beneficial in preventing MI and coronary revascularization in CAD patients despite no benefits in stroke, cardiovascular, or all-cause mortality.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"99"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527776","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}

引用次数: 0

Identification of key genes and development of an identifying machine learning model for sepsis. 关键基因的鉴定和败血症识别机器学习模型的开发。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02068-7

Zhonghao Li, Shengsong Chen, Nan Gao, Jie Chen, Ying Qin, Guoqiang Zhang

{"title":"Identification of key genes and development of an identifying machine learning model for sepsis.","authors":"Zhonghao Li, Shengsong Chen, Nan Gao, Jie Chen, Ying Qin, Guoqiang Zhang","doi":"10.1007/s00011-025-02068-7","DOIUrl":"https://doi.org/10.1007/s00011-025-02068-7","url":null,"abstract":"Objective and design: This study aims to identify key genes of sepsis and construct a model for sepsis identification through integrated multi-organ single-cell RNA sequencing (scRNA-seq) and machine learning.Material or subjects: Datasets downloaded from the Gene Expression Omnibus (GSE207363, GSE207651, GSE185263, GSE69063 and GSE134347) were used.Methods: ScRNA-seq data extracted from heart (GSE207363) and lung tissues (GSE207651) of septic mice were processed and analyzed using the Seurat package in R. Key genes were identified as present in both heart and lung tissues, resulting from the overlap of three analyses along with differential expression analyses. We then used support vector machine recursive feature elimination to construct a model for sepsis identification based on these key genes. The GSE185263 dataset was used for training, while GSE69063 and GSE134347 were used for testing. The accuracy of the model in identifying of sepsis was validated by analyzing the area under the receiver operating characteristic curve (AUROC) using the test datasets.Results: Thirteen genes were initially identified as key genes, and after translation to their human homologs, ten genes remained. The optimal SVM-RFE model incorporated eight of these genes (CAMP, CD74, HLA-DQA1, HLA-DQB1, HLA-DMA, HLA-DRB5, and LYZ). In the two test datasets, the AUROC value for the accuracy of the model in identifying of sepsis was 0.904 and 0.924, respectively.Conclusions: We have identified several key genes and developed a machine learning model for sepsis identification. Further studies are needed to validate our findings.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"100"},"PeriodicalIF":4.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biological attributes of zinc-dependent endopeptidases in endothelial dysfunction associated with sepsis: a narrative review. 锌依赖性内肽酶在脓毒症相关内皮功能障碍中的生物学特性：一篇叙述性综述。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-30 DOI: 10.1007/s00011-025-02056-x

Óscar Gorgojo-Galindo, María Álvarez-Bardón, Adrián García-Concejo, Rocío López-Herrero, María Heredia-Rodríguez, Eduardo Tamayo, Hugo Gonzalo-Benito

引用次数: 0

MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner. MitoQ以柠檬酸合酶依赖的方式减轻脓毒症急性肺损伤中的线粒体损伤。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-24 DOI: 10.1007/s00011-025-02055-y

Jiaojiao Sun, Sihao Jin, Zhiqiang Wang

{"title":"MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner.","authors":"Jiaojiao Sun, Sihao Jin, Zhiqiang Wang","doi":"10.1007/s00011-025-02055-y","DOIUrl":"10.1007/s00011-025-02055-y","url":null,"abstract":"Sepsis is a systemic inflammatory disease caused by severe infection, involving multiple organs in the body, with the lungs being the most susceptible, leading patients to develop acute lung injury (ALI). Mitoquinone Mesylate (MitoQ) is an antioxidant specifically designed to target mitochondria, and it has anti-aging and antioxidant properties. This study aimed to investigate the protective effects of MitoQ on sepsis-induced ALI and its mechanisms. C57BL/6 mice were used to establish the cecal ligation and puncture (CLP) model of sepsis and were orally administered or not administered MitoQ for two weeks. MitoQ effectively alleviated sepsis-induced lung tissue damage, inflammatory responses, oxidative stress, and apoptosis. Furthermore, MitoQ significantly inhibited oxidative stress and mitochondrial damage in pulmonary macrophages. Mechanistically, MitoQ upregulated the mRNA and protein levels of citrate synthase (CS) in lung tissues and pulmonary macrophages. Silencing the CS gene with siRNA significantly reduced the protective effects of MitoQ against oxidative stress, inflammation, and cell apoptosis. In conclusion, MitoQ alleviates sepsis-induced ALI by preserving mitochondrial function.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"92"},"PeriodicalIF":4.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475062","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}

引用次数: 0

Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease. 外泌体作为自身免疫性炎症的免疫调节剂：对原发性Sjögren病的影响。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-13 DOI: 10.1007/s00011-025-02053-0

Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua

{"title":"Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.","authors":"Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua","doi":"10.1007/s00011-025-02053-0","DOIUrl":"https://doi.org/10.1007/s00011-025-02053-0","url":null,"abstract":"Primary Sjögren's disease (pSD) is a systemic autoimmune disorder characterized by exocrine gland dysfunction and lymphocytic infiltration, leading to dry mouth and eyes. Increasing evidence implicates extracellular vesicles, particularly exosomes, as critical mediators of immune regulation in pSD. This review outlines the biogenesis, molecular composition, and immunomodulatory functions of exosomes, and summarizes their emerging roles in the pathogenesis, diagnosis, and potential treatment of pSD. Exosomes derived from immune and glandular cells carry diverse cargoes, such as miRNAs, proteins, and nucleic acids, that modulate disease-relevant immune pathways. For example, exosomal miR-BART13-3p from Epstein-Barr virus-infected B cells suppresses STIM1 and AQP5, impairing salivary gland function, while PD-L1-enriched exosomes from mesenchymal stem cells inhibit T follicular helper cell polarization via the PI3K/AKT pathway, thereby modulating B-cell activation. Additional exosomal cargoes affect Th17/Treg balance, inflammasome activation, and type I interferon signaling. We also highlight the diagnostic potential of disease-specific exosomal markers in plasma and discuss advances in preclinical studies using exosomes as therapeutic agents. However, significant challenges remain, including cargo heterogeneity, lack of standardized isolation methods, and limited clinical data, all of which hinder the translation of exosome-based therapies into clinical practice. By integrating mechanistic and translational findings, this review provides a comprehensive perspective on the immunological and clinical relevance of exosomes in pSD. These insights may guide future development of diagnostic biomarkers and targeted therapies in autoimmune diseases.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"91"},"PeriodicalIF":4.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome. 神经发育障碍（ndd）与NLRP3炎性体的关系。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-03 DOI: 10.1007/s00011-025-02052-1

Abbas Shahi, Zahra Firoozi, Ghaidaa Raheem Lateef Al-Awsi, Ebrahim Mirzaei, Hojjat Shahbazi, Zahra Rezaee, Elham Mohammadisoleimani, Yaser Mansoori, Ali Moravej

{"title":"The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome.","authors":"Abbas Shahi, Zahra Firoozi, Ghaidaa Raheem Lateef Al-Awsi, Ebrahim Mirzaei, Hojjat Shahbazi, Zahra Rezaee, Elham Mohammadisoleimani, Yaser Mansoori, Ali Moravej","doi":"10.1007/s00011-025-02052-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02052-1","url":null,"abstract":"The brain's process of creating neural networks that affect functionality or performance is referred to as neurodevelopment. A person's capacity to learn and remember, pay attention, regulate their emotions, socialize, exercise and self-control are just a few of the cognitive and motor abilities that can be affected by abnormal brain development. Numerous neurodevelopmental diseases have been functionally related to abnormalities in innate immune signaling networks. Innate immunity is in charge of the defense of humans against pathogens and tissue damage by triggering inflammation, mainly through sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Some of these inflammatory processes have been shown to be mediated by large multiprotein complexes called inflammasomes which are present in cytosol and play important roles in the immune system. Due to its role in defense against infectious agents, bacteria, viruses, and fungi, NLRP3 is almost the most studied and well-known member of inflammasomes. The involvement of NLRP3 in inflammatory illnesses is evident due to the wide range of triggers and its intricate signaling pathways. In disorders with neurodevelopmental underpinnings, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia (SCZ), obsessive compulsive disorder (OCD), bipolar disorder (BD), Tourette syndrome (TS), etc., neuroinflammation plays a significant role in their pathophysiology. For these reasons, we reviewed the roles of NLRP3 in various neurodevelopmental disorders below.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"90"},"PeriodicalIF":4.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Successful treatment of refractory erythrodermic pemphigus foliaceus with low-dose rituximab and intravenous immunoglobulin. 小剂量利妥昔单抗联合静脉注射免疫球蛋白成功治疗难治性红皮病性天疱疮。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-03 DOI: 10.1007/s00011-025-02059-8

Jiawen Zhang, Chengfeng Zhang, Zhongyi Xu, Jun Liang, Qinyuan Zhu

引用次数: 0

OptiStack classifier: optimized stacking framework with ensemble feature engineering for enhanced cardiovascular risk prediction. OptiStack分类器：采用集成特征工程优化的叠加框架，增强心血管风险预测。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-31 DOI: 10.1007/s00011-025-02039-y

M Dhilsath Fathima, S P Raja, K Jayanthi, R Hariharan

{"title":"OptiStack classifier: optimized stacking framework with ensemble feature engineering for enhanced cardiovascular risk prediction.","authors":"M Dhilsath Fathima, S P Raja, K Jayanthi, R Hariharan","doi":"10.1007/s00011-025-02039-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02039-y","url":null,"abstract":"Background: Cardiovascular diseases (CVD) are a leading cause of morbidity and mortality globally, highlighting the urgent need for accurate risk prediction to improve early intervention and management. Traditional models have difficulty capturing the complex interactions between risk factors, which limits their predictive power.Objective: This paper proposes the OptiStack Classifier, an optimized stacking framework developed to enhance CVD risk prediction through ensemble feature engineering and machine learning techniques.Methods: The model uses dimensionality reduction and ensemble feature engineering methods, including polynomial expansion, binning and domain-specific feature transformation, to improve data representation. Principal Component Analysis (PCA) is used to dimensionality reduction, improving computational efficiency. A stacking framework integrates multiple machine learning algorithms as base learners, with Logistic Regression acting as the meta-classifier. Bayesian Optimization is applied for hyperparameter tuning, further boosting predictive performance.Results: The proposed model shows significant improvements in predicting CVD risk, helping with early diagnosis and prevention, which can lead to better health outcomes for patients.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"88"},"PeriodicalIF":4.8,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation. 在脂多糖诱导的神经炎症中，白细胞介素-37通过MyD88/NF-κB通路调节小胶质细胞表型并抑制炎症反应。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-29 DOI: 10.1007/s00011-025-02048-x

Jingwen Zhang, Muhammad Abid Hayat, Yu Si, Tao Guo, Yinying Ni, Qian Wang, Yancheng Hong, Yudie Cao, Sijia He, Zijuan Weng, Fengmei Li, Hao Zuo, Xin Sun, Bo Chen, Jiabo Hu

{"title":"Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation.","authors":"Jingwen Zhang, Muhammad Abid Hayat, Yu Si, Tao Guo, Yinying Ni, Qian Wang, Yancheng Hong, Yudie Cao, Sijia He, Zijuan Weng, Fengmei Li, Hao Zuo, Xin Sun, Bo Chen, Jiabo Hu","doi":"10.1007/s00011-025-02048-x","DOIUrl":"https://doi.org/10.1007/s00011-025-02048-x","url":null,"abstract":"Objective: Interleukin-37 (IL-37), an anti-inflammatory cytokine within the interleukin-1 (IL-1) family, exhibits immunomodulatory properties. Here we evaluate the effects of IL-37 on microglia in neuroinflammation and its potential mechanisms.Methods: C57BL/6 mice were injected intraperitoneally with 1 µg of recombinant human IL-37 protein (rhIL-37), and 24 h later with lipopolysaccharide (LPS) (5 mg/kg) to induce neuroinflammation. After 2-h pretreatment of BV2 cells with rhIL-37 (100 ng/mL), an in vitro model was established by treating with LPS (100 ng/mL). Mice were assessed for behavioral tests, and neuronal damage was evaluated by Nissl staining and hematoxylin and eosin staining. The expression of Iba1, CD86, CD206, and NF-κB were detected by immunofluorescence staining, and inflammatory mediators and pathway proteins were evaluated by ELISA, qRT-PCR, and Western blot.Results: IL-37 significantly ameliorated LPS-induced behavioral deficits and protected mice from inflammatory injury. In vitro experiments suggested that IL-37 modulates polarization of microglia from M1 to M2 phenotype, along with reducing pro-inflammatory cytokine production. Moreover, IL-37 attenuated the production of NF-κB and MyD88.Conclusions: IL-37 regulates microglia against neuroinflammatory responses by blocking the MyD88/NF-κB pathway and shows for the first time how IL-37 influences the phenotype of microglia, suggesting a potential therapeutic target for neuroinflammation.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"87"},"PeriodicalIF":4.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0