Inflammation Research最新文献

{"title":"Integrative genomics and functional immunology reveal Clostridia species as modulators of neuroinflammation in amyotrophic lateral sclerosis.","authors":"Shuyu Wang, Hongquan Jiang, Ting Yao","doi":"10.1007/s00011-025-02105-5","DOIUrl":"https://doi.org/10.1007/s00011-025-02105-5","url":null,"abstract":"<p><strong>Objective: </strong>This multiomics study investigated causal relationships between the gut microbiota (GM), immune dysregulation, and amyotrophic lateral sclerosis (ALS) pathogenesis using Mendelian randomization (MR) with experimental validation.</p><p><strong>Materials: </strong>Analyses incorporated genome-wide data from 87,347 participants (GM: n = 7738; ALS: 20,806 patients, 59,804 controls; immune phenotypes: n = 3757), transcriptomic data from 71 subjects (56 ALS patients, 15 controls), and experimental validation in matched cohorts (n = 6 subjects per group).</p><p><strong>Methods: </strong>Two-sample bidirectional MR and mediation analysis were used to evaluate associations. Experimental validation employed flow cytometry for myeloid-derived suppressor cell quantification, enzyme-linked immunosorbent assay for cytokines, and real-time polymerase chain reaction for bacterial validation. Statistical analyses included inverse variance weighted methods with Cohen's d calculations.</p><p><strong>Results: </strong>Sixteen bacterial taxa, including p_Firmicutes.c_Clostridia, displayed protective associations with the risk of ALS, whereas sixteen showed harmful associations. Mediation analysis suggested that p_Firmicutes.c_Clostridia may confer protection through CD33+HLA-DR-myeloid-derived suppressor cell upregulation (23.8% mediation effect). Experimental validation confirmed fewer myeloid-derived suppressor cells in ALS patients (4.0 ± 0.8% vs. 7.5 ± 1.0%, p < 0.001, Cohen's d = 1.4) and lower levels of anti-inflammatory cytokines (TGF-β1: Cohen's d = 1.8, p < 0.001).</p><p><strong>Conclusions: </strong>These findings support causal associations between gut microbial taxa and the ALS risk, which are mediated through immunoregulatory mechanisms, highlighting therapeutic targets within the gut‒immune‒brain axis.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"136"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212665","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}

{"title":"Peripheral inflammation in spinocerebellar ataxia type 3: associations with genetic and clinical manifestations.","authors":"Jia-Yi Zhang, Qiu-Ni Su, Han Lin, Wei Lin, Mao-Lin Cui, Zhuo-Ying Huang, Bei-Ning Ye, Ying-Xin Ye, Yi-Lin Jia, Qing-Ying Zhu, Zhi-Han Li, Min-Ting Lin, Ning Wang, Bing-Long Wang, Shi-Rui Gan","doi":"10.1007/s00011-025-02102-8","DOIUrl":"https://doi.org/10.1007/s00011-025-02102-8","url":null,"abstract":"<p><strong>Background: </strong>Neuroinflammation plays a recognized role in the pathogenesis of Spinocerebellar Ataxia Type 3 (SCA3). However, the involvement of systemic inflammatory responses in SCA3 remains poorly defined.</p><p><strong>Objectives: </strong>Our study aimed to characterize peripheral inflammation in patients with SCA3, examine the relationship between peripheral inflammatory biomarkers and clinical/genetic features, and evaluate the diagnostic utility of these markers.</p><p><strong>Methods: </strong>The cross-sectional study enrolled 101 patients with SCA3 and 101 healthy controls (HCs). The differences in peripheral inflammatory markers between patients with SCA3 and HCs were assessed. Multivariate linear regressions were used to analyze the associations between blood cell count-derived indices, C-reactive protein (CRP), and clinical/genetic features of SCA3. ROC curves were conducted to assess the potential of these markers to distinguish patients with SCA3 from HCs.</p><p><strong>Results: </strong>Compared to HCs, patients with SCA3 exhibited significantly higher levels of leukocytes, neutrophils, monocytes, platelets, neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), systemic inflammatory index (SII), systemic inflammatory composite index (AISI), and CRP (adj. p < 0.05). Age influenced lgCRP, NLR, MLR, and lg(neutrophil-to-platelet ratio) (p < 0.05). CAG affected MLR and AISI (p < 0.05). The combination of BMI, monocytes, NLR, and SII differentiated patients with SCA3 from HCs (AUC = 0.779).</p><p><strong>Conclusion: </strong>Patients with SCA3 display distinct peripheral inflammatory profiles, which correlate with clinical/genetic factors. These peripheral inflammatory markers hold promise as potential tools for diagnosing and monitoring SCA3.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"137"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212668","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}

{"title":"The role of dietary fibre in lung inflammation: microbiota, metabolites, and immune crosstalk.","authors":"Aishat Azeez, John A Baugh","doi":"10.1007/s00011-025-02098-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02098-1","url":null,"abstract":"<p><strong>Background: </strong>Lung disease remains a leading cause of global morbidity and mortality, with prevalence strongly influenced by lifestyle factors, including dietary patterns such as the Western diet. Chronic lung inflammation, driven by dysregulated immune responses, is a hallmark of many pulmonary conditions and exacerbates disease progression and severity Emerging evidence highlights potentially critical role of for Dietary fibre and it's metabolites particularly short chain fatty acids (SCFAs), acetate, butyrate and propionate, in modulating the gut-lung axis and regulating pulmonary immune response.</p><p><strong>Objective: </strong>This review summarizes current evidence on how dietary fibre and SCFAs influence pulmonary immunity and inflammation through systemic and local mechanisms.MethodsLiterature on dietary fibre intake, SCFA production, and immune regulation in the context of lung disease was reviewed to identify key effects and mechanistic insights.</p><p><strong>Findings: </strong>SCFAs, including acetate, butyrate, and propionate, are produced by gut microbial fermentation of fibre and act via G-protein coupled receptor signalling and histone deacetylase inhibition. These metabolites modulate epithelial and immune cell function, reduce inflammation, and enhance lung immune protection. Beyond local effects, SCFAs influence hematopoietic cells in the bone marrow, altering their recruitment and activity in the lung.</p><p><strong>Conclusions: </strong>Dietary fibre intake and SCFA-mediated gut-lung immune regulation represent a promising area for therapeutic development. A deeper understanding of these pathways may support novel strategies for the prevention and treatment of respiratory diseases.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"135"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212595","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}

{"title":"Apolipoprotein E promoted the proliferation and function of group 2 innate lymphoid cells through low density lipoprotein receptor in allergic rhinitis.","authors":"Qingxiang Zeng, Xiangqian Qiu, Yinhui Zeng, Xi Luo, Jing Ma, Wenlong Liu","doi":"10.1007/s00011-025-02107-3","DOIUrl":"https://doi.org/10.1007/s00011-025-02107-3","url":null,"abstract":"<p><strong>Background: </strong>Apolipoprotein E (ApoE) promoted neutrophilic airway inflammation in mice with allergic asthma. Although group 2 innate lymphoid cells (ILC2s) have been established as pivotal mediators in allergic rhinitis (AR) pathogenesis, endogenous mechanisms regulating their hyperactivity are undefined. Whether ApoE has effects in ILC2s in AR is still unknown.</p><p><strong>Objective: </strong>The aim of this investigation is to identify the crucial function of the suppressor modulator ApoE in regulating ILC2-mediated allergic airway inflammation.</p><p><strong>Methods: </strong>A cohort comprising 15 pediatric AR patients and matched healthy controls was enrolled to assess serum ApoE messenger RNA (mRNA) expression and protein levels and their relationship with interleukin (IL)-5, IL-13 and total nasal symptoms scores (TNSS). In vitro experiments employing flow cytometry and enzyme-linked immunosorbent assay (ELISA) validated the regulatory effects of ApoE on ILC2s expansion capacity and cytokine secretion. Transcript levels of GATA binding protein 3 (GATA3) and retinoid acid receptor related orphan receptor alpha (RORα) was examined using quantitative reverse transcription polymerase chain reaction (qRT-RCR). The changes of IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) levels after stimulation of human nasal epithelial cells (HNECs) by Dermatophagoides pteronyssinus (Der p), ApoE and anti-Low-Density Lipoprotein Receptor (LDLR) were determined by ELISA. The effects of ApoE and anti-LDLR in vivo were using the ovalbumin (OVA)-induced murine model.</p><p><strong>Results: </strong>Clinical analyses indicated elevated serum ApoE mRNA and protein levels in AR patients, positively correlating with TNSS. Recombinant ApoE effectively promoted ILC2 activation in PBMCs from AR patients, inducing GATA3 and RORα expression and IL-5, IL-13 secretion, while these effects of ApoE were eliminated by anti-LDLR. Mechanistically, ApoE augmented the epithelial-ILC2 crosstalk by inducing nasal epithelial TSLP/IL-25/IL-33 release. Additionally, our studies have revealed that the anti-LDLR effectively reversed the effects of ApoE on those cytokine production. In vivo, administering anti-LDLR to AR mice effectively alleviates OVA and ApoE induced allergic airway inflammation, reducing eosinophilic infiltration and nasal symptoms, as well as OVA specific immunoglobulin E (IgE) and ILC2 proliferation.</p><p><strong>Conclusions: </strong>As our findings demonstrate, targeting the ApoE-LDLR axis has considerable therapeutic promise in treating ILC2-dependent allergic airway inflammation.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"139"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212639","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}

{"title":"Quantitative temporal analysis of pancreatic islet T lymphocyte and macrophage infiltration heralded by serum IgE in congenic BioBreeding (BB) Gimap5^-/^- rats at risk for insulitis and acute onset diabetes.","authors":"Josefine Jönsson, Linda Faxius, Jeanette Tångrot, Krysten Vance, Stephanie Jerman, Doug Bowman, Marika Bogdani, Peter Ericsson, Rasmus Bennet, Anita Ramelius, Åke Lernmark","doi":"10.1007/s00011-025-02101-9","DOIUrl":"https://doi.org/10.1007/s00011-025-02101-9","url":null,"abstract":"<p><strong>Objective and design: </strong>The objective was to determine the association between serum IgE levels and the infiltration order of T lymphocytes and macrophages in pancreatic islets in relation to the loss of insulin and glucagon cells in presymptomatic congenic BB Gimap5-DP (Diabetes Prone) rats.</p><p><strong>Material: </strong>Congenic prediabetes BB Gimap5-DP and control Gimap5-DR (Diabetes Resistant) rats were followed every other day from 29 to 32 days of age until peak serum IgE (≤ 55 days of age).</p><p><strong>Methods: </strong>Serum IgE was measured using ELISA. The HALO™ platform facilitated quantitative image analysis of infiltrating T lymphocytes, macrophages, and target organ insulin and glucagon cells. Whole genome sequencing (WGS) was employed to identify candidate type 1 diabetes genes.</p><p><strong>Results: </strong>Serum IgE levels increased with age in normoglycemic BB Gimap5-DP rats. Quantification of infiltrating cells per mm² in and around the islets indicated that T lymphocytes are the initial infiltrators, followed by macrophages. Elevated serum IgE levels inversely correlated with beta-cell mass (total mg insulin/mg pancreas). WGS refined the risk segment for islet inflammation to 1.02 Mbp, leaving 10 candidate genes, including Gimap4 and Gimap5.</p><p><strong>Conclusions: </strong>Elevated IgE levels herald T lymphocyte and macrophage infiltration. Pancreatic islet inflammation was linked to Gimap4, Gimap5, and other potential candidate genes on rat chromosome 4.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"134"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212573","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}

{"title":"Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.","authors":"Xuan Miao, Xue Li, Zuokuan He, Guiying Xu, Yu Li, Youwei Wang, Junping Wu, Qi Wu, Huaiyong Chen","doi":"10.1007/s00011-025-02106-4","DOIUrl":"https://doi.org/10.1007/s00011-025-02106-4","url":null,"abstract":"<p><strong>Objective: </strong>Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a significant global health burden, characterized by complex host-pathogen interactions that drive heterogeneous clinical outcomes. While pulmonary epithelial cells are increasingly recognized as active participants in innate immunity during Mtb infection, how host defense are altered when the epithelial barrier is compromised remains unclear.</p><p><strong>Methods: </strong>In this study, we developed a murine model combining naphthalene-induced pulmonary epithelial injury with Mtb infection and mapped the pulmonary cells landscape through single-cell RNA sequencing (scRNA-seq), followed by in vitro stimulation assays to validate macrophage functional changes.</p><p><strong>Results: </strong>Notably, we found a pronounced impairment in pulmonary bacterial clearance. Transcriptomic analysis revealed a widespread suppression of epithelial immune functions and showed that macrophages transitioned from an antimicrobial to an antigen-presenting phenotype, indicating waning pulmonary innate defenses and heightened adaptive immune activation. In vitro experiments further suggested that this macrophage transition may be linked to epithelial cell alterations.</p><p><strong>Conclusions: </strong>These findings indicate that pulmonary epithelial integrity may influence early host immune responses to Mycobacterium tuberculosis and provide a transcriptomic framework for exploring epithelial-immune crosstalk as a potential therapeutic target.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"138"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212644","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}

{"title":"Renal denervation alleviates neuroinflammation by suppressing the microglial Ifi27l2a/cGAS-STING signaling axis.","authors":"Yiting Xu, Xin Shi, Donghuo Gong, Hongjin Chen, Ming Wang, Wenzheng Han","doi":"10.1007/s00011-025-02103-7","DOIUrl":"https://doi.org/10.1007/s00011-025-02103-7","url":null,"abstract":"<p><strong>Objective: </strong>Hypertension remains a global health crisis, with conventional therapies failing in 40% of patients. Renal denervation (RDN) has emerged as a promising therapeutic alternative for resistant hypertension; however, the mechanisms underlying its antihypertensive effects remain unclear. Ifi27l2a, an interferon-stimulated gene, is implicated in neuroinflammatory processes. Therefore, we investigated the hypertensive mechanisms of RDN, focusing on its effects on Ifi27l2a expression.</p><p><strong>Methods: </strong>Cells from the single-cell RNA sequencing datasets were analyzed via clustering and cell type identification to delineate microglial populations impacted by RDN. In vivo experiments were conducted to validate changes in Ifi27l2a expression and cyclic GMP-AMP synthase (cGAS)-STING pathway activation. In vitro, siRNA-mediated Ifi27l2a knockdown in BV2 microglia was employed to evaluate its effects on cGAS-STING pathway activation and cytokine release.</p><p><strong>Results: </strong>Single-cell RNA sequencing revealed significant Ifi27l2a downregulation in microglia following RDN. In vivo, cGAS-STING signaling was significantly downregulated, as indicated by decreased cGAS, p-STING, and p-IRF3 expression, which correlated with attenuated neuroinflammatory responses. In vitro validation with Ifi27l2a-knockdown BV2 cells demonstrated coordinated downregulation of inflammatory cytokines and attenuated cGAS-STING pathway activity, confirming its regulatory role in neuroinflammation.</p><p><strong>Conclusions: </strong>Ifi27l2a is a crucial link between RDN and neuroinflammation resolution, offering a therapeutic target for resistant hypertension.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"140"},"PeriodicalIF":5.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212660","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}

{"title":"Dysregulation of PKM2 promotes inflammatory response in allergic rhinitis.","authors":"Duo Guo, Huiqin Zhou, Xiaomin Wu, Yu Xu","doi":"10.1007/s00011-025-02097-2","DOIUrl":"https://doi.org/10.1007/s00011-025-02097-2","url":null,"abstract":"<p><strong>Objective and design: </strong>This study aimed to investigate the role of pyruvate kinase muscle isoform 2 (PKM2) in macrophage-driven allergic rhinitis (AR) pathogenesis using both in vivo and in vitro experimental models.</p><p><strong>Material or subjects: </strong>Myeloid-specific PKM2 knockout (PKM2^mye-KO) and littermate control (PKM2^WT) mice were used, along with human nasal mucosa samples from AR patients and bone marrow-derived macrophages (BMDMs).</p><p><strong>Treatment: </strong>BMDMs were treated with the PKM2 activator TEPP-46 (100 µM) or vehicle prior to house dust mite (HDM) stimulation.</p><p><strong>Methods: </strong>Histological and immunological analyses were performed on human and murine tissues. Cytokine expression, nuclear translocation, and metabolic markers were assessed in BMDMs following HDM stimulation. Statistical significance was evaluated using appropriate tests (e.g., Student's t-test or ANOVA).</p><p><strong>Results: </strong>PKM2 levels and macrophage infiltration were elevated in AR patient nasal mucosa. PKM2^mye-KO mice showed reduced allergic inflammation, decreased pro-inflammatory cytokines (e.g., IL-6, TNF-α), and suppressed STAT3 activation compared to controls. TEPP-46 treatment attenuated HDM-induced cytokine release and nuclear PKM2 translocation.</p><p><strong>Conclusions: </strong>PKM2 regulates macrophage-mediated inflammation in AR via STAT3-dependent pathways, suggesting its nuclear translocation and interaction with STAT3 as potential therapeutic targets for allergic diseases.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"132"},"PeriodicalIF":5.4,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124581","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}

{"title":"taVNS alleviates preeclampsia-induced vascular endothelial dysfunction via α7nAChR- IP3R1/GRP75/VDAC1 signal pathway.","authors":"Jing Zhao, Yuman Lei, Chengcheng Mu, Yuwei Wu, Rourou Fang, Dongdong Wu, Shouzhu Xu, Haifa Qiao","doi":"10.1007/s00011-025-02100-w","DOIUrl":"https://doi.org/10.1007/s00011-025-02100-w","url":null,"abstract":"<p><strong>Background: </strong>Endothelial dysfunction is considered to play a pivotal role in the pathogenesis of preeclampsia (PE). Transcutaneous auricular vagus nerve stimulation (taVNS) is a potential non-pharmaceutical alternative treatment for PE. This study aimed to explore the mechanisms of taVNS on endothelial dysfunction.</p><p><strong>Methods: </strong>We used the reduced uterine perfusion pressure method to establish PE model and TNF-α to establish endothelial dysfunction model in HUVECs. In vivo, we detected blood pressure, vascular proteomics and morphology, ACh and receptor α7nAChR, and inflammatory factors (IL-6, IL-1β, and TNF-α). In vitro, we checked cell viability, mitochondrial membrane potential, apoptosis rate, calcium levels, HUVECs morphology, and Endoplasmic reticulum (ER) and mitochondria (MITO) interaction.</p><p><strong>Results: </strong>taVNS promoted the release of ACh, which decreased Ca²⁺ inflow from ER to MITO through the IP3R1/GRP75/VDAC1 complex, presumably through α7nAChR. This reduced the release of pro-apoptotic proteins (cleaved caspase-3, HSC70, and cytochrome C) and helped preserve the morphological and functional integrity of mitochondria, thus reducing the apoptosis of HUVECs, improving endothelial function, and relieving PE.</p><p><strong>Conclusion: </strong>taVNS may exert an anti-PE effect through ER-MITO interaction. These findings offer preliminary insights into PE pathogenesis, and suggest that the ACh/α7nAChR axis and IP3R1/GRP75/VDAC1 complex could be promising targets for future therapeutic investigation.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"133"},"PeriodicalIF":5.4,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124573","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}

{"title":"Exosomes in primary Sjögren's disease: diagnostic and therapeutic perspectives from emerging evidence.","authors":"G Pagnoni, A Vicenzi, F Coppi","doi":"10.1007/s00011-025-02099-0","DOIUrl":"10.1007/s00011-025-02099-0","url":null,"abstract":"<p><p>This correspondence comments on the recent review \"Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease,\" emphasizing the dual role of exosomes in primary Sjögren's disease (pSD). On one side, lymphocyte-derived vesicles contribute to epithelial dysfunction through pathogenic microRNA transfer; on the other, mesenchymal stromal cell-derived exosomes show promising immunomodulatory and regenerative properties. Salivary and tear-derived exosomes emerge as attractive diagnostic tools, although their clinical adoption remains hindered by methodological variability. The discussion extends to systemic involvement, including pulmonary hypertension and cardiovascular risk, highlighting exosomes as potential predictive biomarkers. Overall, the letter underscores the translational opportunities of exosome research in pSD while calling for advances in standardization, targeted delivery, and large-scale production to facilitate clinical integration.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"131"},"PeriodicalIF":5.4,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124612","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}