Journal of Inflammation Research最新文献

{"title":"Clinical and Immunological Associations of Anti-Ro52 Antibody Positivity in Primary Sjögren Disease: A Retrospective Cross-Sectional Study.","authors":"Wanting Hao, Yang Zhang, Rui Xue, Yue Wang, Peng Yang, Kai Feng","doi":"10.2147/JIR.S645648","DOIUrl":"10.2147/JIR.S645648","url":null,"abstract":"<p><strong>Purpose: </strong>To characterize the clinical and immunological correlates of anti-Ro52/TRIM21 antibody positivity in primary Sjögren disease (pSjD), focusing on prevalent interstitial lung disease (ILD), hematological abnormalities, and peripheral immune features.</p><p><strong>Patients and methods: </strong>This single-center retrospective cross-sectional study included 122 adults fulfilling the 2016 ACR/EULAR classification criteria (81 anti-Ro52-positive; 41 anti-Ro52-negative). Prespecified outcomes were prevalent ILD and hematological abnormalities. Anti-Ro52/anti-Ro60 profiles, lymphocyte subsets, absolute lymphocyte counts, and 12 circulating cytokines were assessed. Multiple immune comparisons were controlled using Benjamini-Hochberg false discovery rate (FDR) correction. Firth penalized logistic regression adjusted for age, sex, disease duration, and anti-Ro60 status; modified Poisson models estimated adjusted prevalence ratios (PRs).</p><p><strong>Results: </strong>ILD occurred in 19/81 (23.5%) anti-Ro52-positive and 3/41 (7.3%) anti-Ro52-negative patients (P=0.044); hematological abnormalities occurred in 16/81 (19.8%) and 2/41 (4.9%), respectively (P=0.032). In adjusted Firth models, anti-Ro52 positivity was not statistically associated with ILD (OR 2.95, 95% CI 0.91-12.26; P=0.074), whereas the association with hematological abnormalities remained evident (OR 5.05, 95% CI 1.28-30.44; P=0.018). Modified Poisson estimates were directionally similar. Anti-Ro52-positive patients had higher CD19+ B-cell percentages and lower natural killer-cell percentages; both remained significant after FDR correction. Absolute B-cell counts did not differ, whereas absolute natural killer-cell counts were lower. No cytokine remained significant after FDR correction.</p><p><strong>Conclusion: </strong>Anti-Ro52 positivity was associated with distinct clinical and peripheral immune features in hospitalized patients with pSjD. The ILD association was attenuated after adjustment for anti-Ro60 and demographic factors, whereas the hematological association remained statistically evident but imprecise. These findings support interpretation of anti-Ro52 within a broader serological and immunological context.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"645648"},"PeriodicalIF":4.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Topical Remibrutinib Attenuates LL37-Induced Rosacea-Like Dermatitis by Inhibiting BTK Activation, NF-κB Signaling and Mast Cell Activation.","authors":"Wangchao Li, Huiping Fan, Hua Liu, Qingsong Ma, Chengqi Liu, Dong Zhang, Weiyuan Ma","doi":"10.2147/JIR.S643728","DOIUrl":"10.2147/JIR.S643728","url":null,"abstract":"<p><strong>Background: </strong>Rosacea is a chronic inflammatory skin disorder in which LL37-driven mast cell activation contributes to cutaneous inflammation. Bruton's tyrosine kinase (BTK) is a key regulator of canonical IgE-dependent mast cell responses; however, its role in LL37-induced, IgE-independent mast cell activation remains unclear. This study investigated the involvement of BTK activation and nuclear factor-κB (NF-κB) signaling in LL37-induced mast cell activation and evaluated the therapeutic effects of topical remibrutinib in experimental rosacea-like dermatitis.</p><p><strong>Methods: </strong>Transcriptomic data from rosacea lesions (GSE65914) were analyzed to identify dysregulated inflammatory pathways. LL37-stimulated LUVA mast cells and an LL37-induced mouse model of rosacea-like dermatitis were used for in vitro and in vivo evaluation, respectively. Cell viability, mast cell degranulation, and inflammatory mediator production were assessed using the Cell Counting Kit-8 assay (CCK-8) and enzyme-linked immunosorbent assays (ELISA). Cutaneous inflammation and dermal mast cell accumulation were evaluated by histopathological examination and toluidine blue staining. BTK and NF-κB phosphorylation were examined by Western blotting and immunofluorescence.</p><p><strong>Results: </strong>Consistently, gene set enrichment analysis demonstrated enrichment of the NF-κB signaling pathway, with BTK included among the leading-edge genes contributing to this transcriptional signature. LL37 increased BTK and p65 phosphorylation in LUVA cells and mouse skin, accompanied by enhanced mast cell degranulation and inflammatory mediator release. Topical treatment with 1% remibrutinib reduced BTK and p65 phosphorylation, mast cell accumulation and degranulation, and inflammatory mediator levels. These changes were accompanied by reductions in erythema, epidermal thickening, and histopathological inflammation in mice.</p><p><strong>Conclusion: </strong>BTK and NF-κB are involved in LL37-induced, IgE-independent mast cell activation and rosacea-like inflammation. Topical remibrutinib attenuated experimental rosacea-like dermatitis by inhibiting BTK phosphorylation and NF-κB activation and mast cell activation, supporting topical BTK inhibition as a potential therapeutic strategy for rosacea.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"643728"},"PeriodicalIF":4.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell and Spatial Multi-Omics in Small-Intestinal Homeostasis and Ischemia/Reperfusion Injury: Current Advances, Applications, and Future Perspectives.","authors":"Jiaxi Zhu, Zhifeng Jiang, Gangze Li, Tianheng Gu, Lin Zhang","doi":"10.2147/JIR.S640336","DOIUrl":"10.2147/JIR.S640336","url":null,"abstract":"<p><p>The intestinal tract acts as a dynamic barrier between the external and internal environments, and intestinal homeostasis fundamentally influences human health. This homeostasis depends on complex interactions among the epithelium, immune cells, and microbiota. Intestinal ischemia/reperfusion (II/R) disrupts these interactions and can cause local barrier failure and distant organ injury. However, the transition of the intestinal microenvironment from homeostasis to injury and repair remains incompletely characterized. This narrative review summarizes single-cell RNA sequencing, single-cell multi-omics, spatial transcriptomics, and spatial multi-omics, including their underlying methods. We compare intestinal reference atlases with direct II/R studies and examine how these approaches complement bulk sequencing and histology. Human intestinal atlases reveal spatially organized epithelial states, whereas experimental II/R studies identify altered Paneth-cell states, endothelial regenerative signals, and epithelial stress responses. These findings differ in their model systems, sampling times, and degree of functional validation. Dissociation bias, batch effects, limited biological replication, spatial resolution, and uncertain integration across modalities constrain interpretation. Most disease-specific evidence remains preclinical, and inferred cell interactions should not be equated with demonstrated therapeutic mechanisms. Translation will require standardized human sampling, spatial and protein-level validation, causal perturbation, and prospective assessment of clinically accessible markers. Single-cell and spatial omics can therefore refine mechanistic hypotheses and guide validation in II/R, but currently do not constitute established clinical diagnostic or treatment pathways.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"640336"},"PeriodicalIF":4.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical Compression-Induced Peripheral Neuropathic Pain: From Astrocyte Mechanosensing and Phenotypic Reprogramming to CCL2-CCR2 Axis-Targeted Therapies.","authors":"Ying Shen, Min He, Binghao Wang, Zhen Liu, Shuang Wu, Long-Hao Chen, Keduo Ai, Hanzhe Lv, Wei Sheng, Ziyu Zhang, Zhizhen Lv, Lijiang Lv","doi":"10.2147/JIR.S634895","DOIUrl":"https://doi.org/10.2147/JIR.S634895","url":null,"abstract":"<p><p>Neuropathic pain (NP) arising from mechanical nerve compression is driven by central sensitization, in which reactive astrocytes and chemokine-mediated neuro-glial crosstalk act as master regulators. Among candidate chemokine axes, the C-C motif chemokine ligand 2 (CCL2) and its receptor, C-C chemokine receptor type 2 (CCR2), most directly couple astrocyte activation to nociceptive signaling, and aberrant activation of this axis is conserved across diverse compression paradigms. This review synthesizes current evidence on how mechanical compression is translated into persistent pain via astrocytes. We first outline the methodological foundations and anatomical diversity of compression models, together with advances and limitations in astrocyte profiling. We then trace how mechanosensitive receptors and ion channels initiate astrocytic activation and examine the multicellular origins of CCL2 and its intracellular and epigenetic regulation. Equally important are single-cell-resolved phenotypic heterogeneity beyond the A1/A2 dichotomy, sexual dimorphism in astrocytic versus microglial pathways and the collapse of homeostatic, non-inflammatory astrocyte functions. Downstream, astrocyte-derived CCL2 engages neuronal and microglial CCR2 and together with interleukin (IL) and tumor necrosis factor-α (TNF-α) cytokine cascades, drives feed-forward glial crosstalk and sensitization of spinal and supraspinal circuits. Building on this framework, we evaluate a range of strategies targeting the axis, spanning small-molecule inhibitors, natural products, gene-silencing and precision-delivery platforms, and combinatorial regimens. We also highlight the clinical translational gap, exemplified by the discontinued anti-CCL2 monoclonal antibody carlumab, the Phase II analgesic failure of the CCR2 antagonist AZD2423, the halted CCR2/CCR5 antagonist PF-04634817, and the absence of JAK inhibitors from pain randomized controlled trials. Finally, we identify three translational bottlenecks: limited tools for resolving astrocyte states in vivo, insufficient large-animal pharmacological validation, and compensatory chemokine-receptor redundancy. We further outline directions for next-generation, multi-modal interventions.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"634895"},"PeriodicalIF":4.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>TOX</i>-Related T-Cell Exhaustion as a Link Between Chronic Inflammation, Tumor Immunity, and Immunotherapy A Bibliometric and Mechanism-Oriented Review.","authors":"Yun Cong, Ziwei Ma, Kai Zhong, Yaoqiang Bao, Shitao Lei, Pingping Qiao, Tuerganaili Aji, Yingmei Shao","doi":"10.2147/JIR.S638869","DOIUrl":"10.2147/JIR.S638869","url":null,"abstract":"<p><strong>Background: </strong>Chronic inflammation and persistent antigen stimulation reshape T-cell fate and contribute to immune dysfunction in cancer, chronic infection, and inflammatory liver disease. <i>TOX</i> (<i>TOX1</i>) has emerged as a key transcriptional regulator linking these inflammatory contexts to T-cell exhaustion, immune checkpoint signaling, and immunotherapy response. However, existing reviews have mainly summarized molecular mechanisms and have not systematically connected the evolution of the field with its collaboration patterns, research hotspots, and emerging translational questions. A synthesis that combines bibliometric mapping with biological interpretation is needed to clarify how the field has evolved and where translational uncertainties remain.</p><p><strong>Methods: </strong>Web of Science Core Collection, PubMed, and Embase were searched for <i>TOX</i>-related T-cell exhaustion studies published from 2010 to 2026. After deduplication and relevance screening, 180 publications were included. Bibliometric analyses were performed with bibliometrix, VOSviewer, and CiteSpace, and the resulting knowledge structures were interpreted through a mechanism-oriented narrative review.</p><p><strong>Results: </strong>Annual output increased markedly after the landmark <i>TOX</i> studies of 2019, reaching a peak in 2025. The field was highly concentrated: Frontiers in Immunology was the most productive venue, whereas Nature, Immunity, and Nature Immunology contained the most influential foundational papers. The USA and China dominated publication output, and their centrality scores were comparable (0.12 vs 0.13). However, their collaboration structures differed by partner distribution, with the USA more connected to high-output European partners and China contributing strongly to recent disease-focused translational work. Keyword and co-citation analyses converged on four themes: transcriptional programming, immune-checkpoint-associated dysfunction, tissue microenvironmental regulation, and translational intervention.</p><p><strong>Conclusion: </strong><i>TOX</i>-related T-cell exhaustion should not be interpreted only as a binary marker of dysfunctional immunity. Instead, it represents a context-dependent regulatory interface between chronic inflammation, antigen persistence, tumor immune suppression, and therapeutic resistance. This perspective is essential for developing next-generation immunotherapies that modulate, rather than simply reverse, T-cell exhaustion in inflammatory and malignant microenvironments.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"638869"},"PeriodicalIF":4.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baseline Serum HMGB1 and the Composite of All-Cause Mortality or First Heart Failure Rehospitalization in Heart Failure with Preserved Ejection Fraction.","authors":"Haoran Chen, Xiaofei Miao, Liping Shen, Jin Han, Weizhang Li, Yukun Xu, Zhuo Chen, Lingyun Gu, Junyou Cui","doi":"10.2147/JIR.S633336","DOIUrl":"10.2147/JIR.S633336","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate the association between baseline serum high mobility group box 1 (HMGB1) and the composite of all-cause mortality or first heart failure rehospitalization in patients with heart failure with preserved ejection fraction (HFpEF).</p><p><strong>Patients and methods: </strong>This single-center prospective cohort included 224 patients with HFpEF. The primary endpoint was the first occurrence of all-cause mortality or heart failure rehospitalization.</p><p><strong>Results: </strong>During a median observation time of 58 months, 37 of 224 patients (16.5%) experienced the composite endpoint. Baseline HMGB1 was higher in patients with events than in those without events (8.76 ± 3.18 vs 5.99 ± 1.86 µg/L; P<0.001). After adjustment for NT-proBNP, age, and sex, each 1 µg/L increase in HMGB1 was associated with a higher risk of the composite endpoint (hazard ratio, 1.399; 95% confidence interval [CI], 1.242-1.576; P<0.001). Apparent areas under the curve were 0.753 (95% CI, 0.653-0.853) for HMGB1, 0.790 (95% CI, 0.708-0.872) for NT-proBNP, and 0.870 (95% CI, 0.793-0.947) for their combination. The combination did not significantly outperform NT-proBNP alone (ΔAUC, 0.080; 95% CI, -0.012 to 0.171; nominal P=0.088; Holm-adjusted P=0.176). The optimism-corrected Cox concordance index was 0.828, and sensitivity analyses showed associations in the same direction.</p><p><strong>Conclusion: </strong>Higher baseline serum HMGB1 was associated with the composite of all-cause mortality or first heart failure rehospitalization in this exploratory HFpEF cohort. Incremental discrimination beyond NT-proBNP and clinical utility remain unestablished. Independent prospective multicenter validation is required.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"633336"},"PeriodicalIF":4.6,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD74 as a Potential Adjunctive Tissue Biomarker for Bullous Pemphigoid Lesions: A Retrospective Study Integrating Bioinformatics Analysis and Experimental Validation.","authors":"Yuanlin Zhang, Xiaolong Zhang, Fei Dong, Chenchen Zhang, Zhangsi Jin, Yiwen Mao, Huan Zhu, Qi Zhang, Dewang Yin, Chunjun Yang, Xiaole Mei","doi":"10.2147/JIR.S645596","DOIUrl":"10.2147/JIR.S645596","url":null,"abstract":"<p><strong>Background: </strong>Bullous pemphigoid (BP), an autoimmune blistering disorder that primarily afflicts the geriatric population, poses diagnostic and therapeutic challenges, particularly in patients with comorbidities. This retrospective study aimed to identify and validate potential adjunctive tissue biomarkers for BP and explore their association with immune-related mechanisms through integrated bioinformatics analysis and experimental validation.</p><p><strong>Methods: </strong>Transcriptomic data from the GEO dataset were analyzed to identify differentially expressed genes (DEGs), which were further cross-referenced with immune-related gene signatures. CD74 was selected as a candidate biomarker and its expression was validated by immunohistochemistry (IHC) in paraffin-embedded skin tissues from patients with BP, healthy controls (HC), and disease controls, including pemphigus vulgaris (PV), psoriasis (Pso), atopic dermatitis (AD), and systemic lupus erythematosus (SLE). Diagnostic performance was evaluated by ROC curve analysis. Single-cell RNA sequencing and immunofluorescence staining were performed to investigate the cellular distribution and immune association of CD74.</p><p><strong>Results: </strong>CD74 was identified as an immune-related DEG associated with CCL13 expression. CD74 expression was increased in BP lesions and exhibited a characteristic linear distribution along the dermoepidermal junction. Quantitative ROC analysis based on CD74 expression area percentage showed moderate diagnostic performance, while the linear staining pattern demonstrated potential value as an adjunctive diagnostic feature. Single-cell RNA sequencing revealed predominant CD74 expression in MHC-II-enriched cells, and immunofluorescence confirmed CD74/HLA-DR colocalization. CD74 expression was positively correlated with peripheral blood eosinophil counts, suggesting an association with systemic immune activation in BP.</p><p><strong>Conclusion: </strong>CD74 may represent a promising adjunctive tissue biomarker for BP diagnosis. Its characteristic tissue distribution and association with immune-related features suggest that CD74 may reflect immune alterations within BP lesions. Further validation in larger independent cohorts is required.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"645596"},"PeriodicalIF":4.6,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Question-Driven Selection of Psoriasis Animal Models: A Structured Narrative Review of 48 Model Records.","authors":"Tong Zhao, Xianbin Zhao, Donglian Du, Zehua Qin, Songqi Tang, Min Xiao","doi":"10.2147/JIR.S641713","DOIUrl":"10.2147/JIR.S641713","url":null,"abstract":"<p><p>Animal models connect psoriasis mechanisms to preclinical testing, but no model is informative for every question. This structured narrative review used PubMed, supplemented by reference-list screening and manual checks, to identify 29 original studies contributing 48 model records. One reviewer conducted screening and extraction, with targeted verification by a second reviewer. Within the selected records, IMQ- and IL-23-induced models primarily addressed acute inflammatory pathways, genetically engineered and composite models tested defined perturbations, humanized models examined human immune responses, and relapse models examined post-resolution reactivation. Composite designs were the largest category (22/48, 45.8%), whereas TRM were experimentally assessed in 6/48 (12.5%). We integrated model construction, disease-stage suitability and mechanism-evidence patterns into a conceptual question-driven framework linking prespecified objectives to candidate initial models, complementary validation and interpretation boundaries. The framework is a hypothesis-generating planning aid that has not undergone independent validation. Focused questions may be addressed with a single model, whereas complex mechanistic or translational questions require complementary models and comparison with human data.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"641713"},"PeriodicalIF":4.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13674558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 Obesity and Serum Uric Acid with Nail Involvement in Chinese Patients with Psoriasis: A Cross-Sectional Mediation Analysis.","authors":"Jingyue Ma, Zhimin Wang, Xinzu Tong, Yang Qiu, Yali Guo, Suju Luo, Yan Li, Huiping Wang","doi":"10.2147/JIR.S643317","DOIUrl":"10.2147/JIR.S643317","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a chronic immune-mediated systemic inflammatory disease often accompanied by metabolic comorbidities, most notably obesity. Although nail involvement is common in patients with psoriasis, its relationships with obesity and serum uric acid (SUA) remain insufficiently characterized.</p><p><strong>Aims: </strong>This study aimed to characterize the clinical, metabolic, and inflammatory profiles of patients with psoriasis across different body mass index (BMI) groups and to evaluate associations among obesity, SUA, and nail involvement, as well as the potential statistical mediating role of SUA.</p><p><strong>Methods: </strong>This single-center retrospective cross-sectional study stratified adult patients with plaque psoriasis by BMI into normal-weight, overweight, and obese groups. Patient characteristics were compared across BMI groups. Multivariable logistic regression was used to analyze factors associated with psoriatic nail involvement. An exploratory mediation analysis was conducted to assess the potential statistical mediating role of SUA in the association between overweight/obesity and psoriatic nail involvement.</p><p><strong>Results: </strong>A total of 189 patients were included (normal-weight, n = 62; overweight, n = 72; obese, n = 55), and 108 (57.1%) had nail involvement. The proportion of nail involvement increased across BMI groups (43.5%, 59.7%, and 69.1%, respectively; <i>P</i> = 0.018). SUA levels were higher in overweight and obese patients than in normal-weight patients (overall <i>P</i> < 0.001). Multivariable logistic regression analysis showed that both obesity [adjusted OR (aOR) = 2.857, 95% CI: 1.202-6.791] and elevated SUA (per 100 μmol/L increase, aOR = 1.712, 95% CI: 1.131-2.592) were associated with nail involvement. In exploratory mediation analysis, potential indirect statistical associations of overweight and obesity with nail involvement through SUA were observed.</p><p><strong>Conclusion: </strong>The observed statistical associations of overweight/obesity and elevated SUA with psoriatic nail involvement, together with the exploratory indirect association through SUA, provide further insight into the clinical and metabolic features associated with nail involvement in psoriasis. These findings warrant further confirmation in prospective studies.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"643317"},"PeriodicalIF":4.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13674557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria-Macrophage Interactions in Sepsis at Different Immune Stages: Integrating Immunometabolic Reprogramming, Organ Damage, and Therapeutic Strategies.","authors":"Jiaqi Li, Yuting Sun, Meilin He, Xueyi Liao, Qingfang Zou, Shuming Pan","doi":"10.2147/JIR.S641837","DOIUrl":"10.2147/JIR.S641837","url":null,"abstract":"<p><p>Sepsis is a life-threatening disorder caused by dysregulated host responses to infection, characterized by immune dysfunction, metabolic reprogramming, and multi-organ injury. Mitochondria, beyond their role in energy metabolism, act as central signaling hubs that integrate cellular metabolism, innate immunity, and inflammatory responses. Emerging evidence suggests that disrupted mitochondria-macrophage crosstalk forms a self-amplifying loop that drives excessive inflammation and organ dysfunction during sepsis. This review highlights recent advances in understanding how mitochondrial quality control and immunometabolic remodeling regulate macrophage activation and function. We discuss the impact of key metabolic pathways, including glycolysis, oxidative phosphorylation, tricarboxylic acid cycle remodeling, and fatty acid metabolism, on macrophage polarization, as well as the dynamic roles of mitophagy, mitochondrial biogenesis, and mitochondrial dynamics throughout sepsis progression. We further summarize current challenges and potential therapeutic strategies targeting the mitochondria-macrophage axis. Elucidating this regulatory network may provide new insights into precision medicine and the development of targeted therapies for sepsis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"641837"},"PeriodicalIF":4.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13674562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}