Immunity, Inflammation and Disease最新文献

{"title":"NLRP3 Inflammasome Activation Mediates Coronary Artery Lesions in Kawasaki Disease by Inducing Endothelial Cells Pyroptosis and Glycocalyx Injury","authors":"Ronghao Zheng,&nbsp;Jing Yue,&nbsp;Qianjun Chen,&nbsp;Jing Xie,&nbsp;Lintao Wen,&nbsp;Nana Duan,&nbsp;Jianping Shang,&nbsp;Songbai Zhu,&nbsp;Li Huang,&nbsp;Yang Zou,&nbsp;Xiaoxiang Song,&nbsp;Xiaolin Wu,&nbsp;Qihua Feng","doi":"10.1002/iid3.70433","DOIUrl":"https://doi.org/10.1002/iid3.70433","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>To investigate the mechanism by which NOD-like receptor heat protein domain-associated protein 3 (NLRP3) activation mediates coronary endothelial dysfunction at different stages of Kawasaki disease (KD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Blood samples were collected from patients in the acute stage and convalescent stage of KD, as well as healthy/febrile controls. The mRNA expression of NLRP3 and Caspase-1 were detected by qRT-PCR. Serum levels of IL-1β, syndecan-1 (SDC-1), hyaluronic acid (HA), metalloproteinase-9 (MMP-9), and metalloproteinase-1 (TIMP-1) were quantified via ELISA, and Spearman correlation analysis was conducted. In vitro, human coronary artery endothelial cells (HCAECs) were treated with KD patient serum combined with NLRP3 activator/inhibitor treatment. Cell viability (CCK-8) and cell migration (Transwell) were assessed. The relative protein expression of pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD-N) were detected by Western blot. The concentrations of cytokine secretion (IL-1β/IL-18), matrix metabolism (MMP-9/TIMP-1), glycocalyx components (SDC-1/HA) were evaluated by ELISA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The levels of NLRP3 mRNA, Caspase-1 mRNA, IL-1β, MMP-9, TIMP-1, SDC-1 and HA in patients with acute KD were significantly higher than those in the healthy/febrile control group (<i>p</i> &lt; 0.01), and these indicators were positively correlated with NLRP3 activation (<i>p</i> &lt; 0.01). KD serum significantly suppressed the proliferation/migration of HCAEC (<i>p</i> &lt; 0.01), induced pyroptosis (upregulated NLRP3/Caspase-1/GSDMD-N), and increased IL-1β/IL-18 secretion with concomitant elevated levels of MMP-9/TIMP-1/SDC-1/HA. NLRP3 inhibitors can reverse the above-mentioned damaging effects (<i>p</i> &lt; 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>NLRP3 inflammasome activation during the progression of KD can cause coronary endothelial injury by inducing inflammatory imbalance, endothelial cells pyroptosis, and glycocalyx injury. Targeting NLRP3 represents a promising therapeutic strategy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147668400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Features and Associated Factors of Lupus Myocarditis: A Case-Control Study","authors":"Dong Yan,&nbsp;Siping Li,&nbsp;Mengxue Yan,&nbsp;Zhichun Liu,&nbsp;Leixi Xue","doi":"10.1002/iid3.70436","DOIUrl":"https://doi.org/10.1002/iid3.70436","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to explore the clinical characteristics of patients with lupus myocarditis (LM) and to evaluate the efficacy of rituximab (RTX) in LM treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The medical records of all patients with LM admitted to our hospital between January 2012 and March 2025 were retrospectively analyzed. Two control groups were established by randomly matching patients by sex and age at a 1:1 ratio: patients with systemic lupus erythematosus (SLE) without LM and patients with non-SLE myocarditis. The SLE disease activity index 2 K (SLEDAI 2 K) score and Systemic Lupus Erythematosus Disease Activity Score (SLE-DAS) were calculated to evaluate SLE disease activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 22 patients with LM were enrolled. Patients with LM had a higher incidence of lupus nephritis and a higher positivity rate for anti-SSB antibodies than those with SLE without LM. Furthermore, patients with SLE with LM had significantly higher SLE-DAS than those without LM, although no statistical difference in SLEDAI 2 K score was observed between the groups. Wall motion abnormalities, valvular regurgitation, and decreased left ventricular ejection fraction (LVEF) were more frequent in patients with LM than in those with non-SLE myocarditis. All patients with LM received corticosteroid treatment, with three of them receiving RTX in addition to standard therapy. With a median follow-up of 4 (range, 1–24) months, 2 patients (9.1%) died due to heart failure, and the remaining 20 achieved symptom remission. Moreover, 13 patients underwent follow-up echocardiography, which showed a significant improvement in LVEF. The three patients treated with RTX achieved clinical improvement within a mean of 2 weeks, enabling rapid glucocorticoid tapering.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Patients with LM more frequently present with lupus nephritis and positive anti-SSB antibodies, are more likely to have echocardiographic abnormalities, and exhibit a higher mortality rate. In addition, RTX is a promising drug for LM treatment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70436","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147668482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway","authors":"Tengfei He,&nbsp;Anni Zhang,&nbsp;Changxi Zhang","doi":"10.1002/iid3.70418","DOIUrl":"10.1002/iid3.70418","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Evidence supporting the therapeutic efficacy of Bufei Nashen pill (BFNSP) for chronic obstructive pulmonary disease (COPD) is currently limited. We evaluated BFNSP's effects on COPD progression and elucidated its potential mechanisms through LC/MS analysis of its active components.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Following the establishment of a rat COPD model, animals received graded BFNSP doses. Pulmonary function testing quantified respiratory parameters, while HE staining revealed histological changes in lung tissue. ELISA was used to measure TGF-β1, IL-6, IL-8, and IL-1β concentrations in BALF, as well as MDA, SOD, and GSH levels in lung tissue. Immunofluorescence staining was used to detect the levels of GRP78 and CHOP expression. Protein expression levels of GRP78, CHOP, p-PERK, p-eIF2α, and p-ATF4 in lung tissue were analyzed using Western blotting. The results were further confirmed through in vitro cellular assays.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study found that BFNSP improved pulmonary ventilation, reduced lung tissue damage, decreased inflammatory factor secretion, and alleviated oxidative and endoplasmic reticulum stress in COPD rats by inhibiting the PERK/eIF2α signaling pathway, potentially slowing COPD progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>BFNSP mitigates COPD progression by regulating endoplasmic reticulum stress via the suppression of the PERK/eIF2α signaling pathway.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70418","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147668503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prnp Deletion Mitigates Muscle Fiber Type-Specific Sarcopenia Induced by Prion Infection in Mice","authors":"Wenduo Liu,&nbsp;Yong-Chan Kim,&nbsp;Sae-Young Won,&nbsp;Thi Thu Trang Kieu,&nbsp;Sung Ho Kook,&nbsp;Byung-Hoon Jeong,&nbsp;Sang Hyun Kim","doi":"10.1002/iid3.70425","DOIUrl":"https://doi.org/10.1002/iid3.70425","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Recent studies have shown that significant expression of PrP^C protein is also present in skeletal muscle, and it plays a significant role in maintaining skeletal muscle homeostasis. Although the expression of PrP^C in skeletal muscle has been clarified, the effects of PrP^Sc-mediated prion protein infection on sarcopenia in mice and its potential regulatory mechanisms remain unclear. This study investigated the role of PrP^C in Prion-induced sarcopenia, using an animal model of prion disease based on intraperitoneal injection of the scrapie strain ME7 into wild-type mice and Prnp knockout mice. The results indicate that prion infection-induced sarcopenia exhibits muscle fiber type specificity, and that the lack of PrP^C can prevent prion protein infection-induced sarcopenia, although the lack of PrP^C may lead to reduced mitochondrial-endoplasmic reticulum homeostasis. These data provide novel evidence that prion infection affects skeletal muscle system health through myofiber-specific mechanisms.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70425","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147668491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship Between IL6/IL10 Serum Concentrations and Organ Function in Critically Ill Patients Based on Sepsis: A Prospective Study","authors":"Guang-Jian Wang,&nbsp;Hui Lian,&nbsp;Hong-Min Zhang,&nbsp;Ye-Cheng Liu,&nbsp;Xiao-Ting Wang","doi":"10.1002/iid3.70414","DOIUrl":"10.1002/iid3.70414","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Critical illnesses, particularly sepsis with accompanying organ dysfunction, significantly increase patient mortality. The imbalance between pro-inflammatory and anti-inflammatory responses is closely linked to the onset and progression of organ dysfunction in critical conditions. The ratio of interleukin-6 (IL6) to interleukin-10 (IL10) is a useful indicator of the pro- and anti-inflammatory status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>To investigate the correlation between IL6/IL10 and various outcomes, including organ function, in critically ill patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This prospective study was conducted from 1 January to 31 May 2023 at Peking Union Medical College Hospital. Baseline characteristics, intensive care unit (ICU) parameters, laboratory test results, and outcome data were extracted from the electronic medical records system. Correlations between IL6/IL10 and various outcomes, including organ function, were analyzed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Result</h3>\u0000 \u0000 <p>In total, 208 patients were included in the study. Higher IL6/IL10 levels were associated with shorter in-hospital stay, ICU stay, and mechanical ventilation time in both univariate and multivariate models. The β values and 95% confidence intervals in the multivariate model were −0.526 (− 0.684, −0.369), −0.183 (− 0.245, −0.121), and −1.510 (− 2.565, −0.456), respectively. Significant positive associations between IL6/IL10 and all organ functions except the platelet count and PaO₂/FiO₂ ratio were found. Sensitivity analyses in the sepsis group revealed significant correlations with nearly every organ function (except liver function) in patients without tumors and those who underwent surgery.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study showed that in critically ill patients, particularly those with sepsis, IL6/IL10 is significantly associated with outcomes such as organ dysfunction (including coagulation, renal, cardiac, and pulmonary function). These findings are hypothesis-generating, suggesting that IL6/IL10 may serve as a valuable indicator associated with inflammation and severity changes in critical illness.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066732/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miR-1246 in Syphilis Serofast State: Diagnostic Value and NLRP3 Inflammasome Suppression","authors":"Yue Mou,&nbsp;Caifeng He,&nbsp;Fanxiang Wang,&nbsp;Wenhao Cheng,&nbsp;Chaochao Ji,&nbsp;Xinting Wang,&nbsp;Wenlong Hu,&nbsp;Hong Ren","doi":"10.1002/iid3.70434","DOIUrl":"10.1002/iid3.70434","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><b>S</b>erofast state (SF), defined as persistent low-titer antibodies after treatment, poses a diagnostic challenge because of the overlap with serologic features of active infection. Exosomal miRNAs are stable in body fluids and have potential as diagnostic markers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to identify plasma exosomal miR-1246 as a diagnostic biomarker for SF and elucidate its role in NLRP3 inflammasome suppression, providing mechanistic insights into SF pathogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using microarray analysis and reverse transcription quantitative polymerase chain reaction (RT-qPCR), differential miRNA expression was measured in the plasma samples of SF patients. Microarray analysis, target gene prediction, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to identify differentially expressed microRNAs (DEmiRNAs). The plasma levels of NLRP3 and related cytokines were quantified using enzyme-linked immunosorbent assay (ELISA), and the regulatory effect of miR-1246 on NLRP3 was measured in vitro. Diagnostic performance was assessed based on receiver operating characteristic (ROC) curve analysis for miR-1246 alone and in combination with the rapid plasma reagin (RPR) test.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Plasma exosomal miR-1246 was significantly upregulated in SF patients (<i>p</i> &lt; 0.001), whereas NLRP3 and its associated factors were downregulated (<i>p</i> &lt; 0.05). In vitro experiments confirmed that miR-1246 negatively regulated NLRP3 inflammasome activity. GO and KEGG analyses revealed that the target genes of DEmiRNAs were involved in multiple biological processes and signalling pathways. ROC analysis showed that miR-1246 alone yielded an area under the curve (AUC) of 0.760 (sensitivity 77.4%, specificity 62.9%). When combined with RPR, the AUC increased to 0.824 (sensitivity 83.3%, specificity 65.7%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Exosomal miR-1246 is elevated in SF and may contribute to its pathogenesis by inhibiting NLRP3 inflammasome. It demonstrates potential as a diagnostic biomarker, particularly when combined with RPR.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Nomogram Based on the Castelli Risk Index for Predicting Prognosis in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention: A Cohort Study","authors":"Yan Liu,&nbsp;Ge Song,&nbsp;Ying Zhang,&nbsp;Weichao Shan,&nbsp;Yuewen Qi,&nbsp;Xinchen Wang,&nbsp; Chen Wei,&nbsp;Jingyi Liu,&nbsp;Lixian Sun","doi":"10.1002/iid3.70431","DOIUrl":"10.1002/iid3.70431","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>Composite lipid indices are closely related to the risk and poor prognosis of diseases. However, there are no studies on the prognostic value of Castelli's risk indices-I and II (CRI-I, CRI-II) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). Therefore, the aim of this study was to investigate the association of CRI-I and CRI-II with the prognosis of patients with ACS undergoing PCI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Patients and Methods</h3>\u0000 \u0000 <p>A total of 1475 patients with ACS undergoing PCI were consecutively enrolled in this prospective cohort study from January 2016 to December 2018. The CRI-I and CRI-II were measured. The endpoints were MACEs, including all-cause mortality, requirement of rehospitalization for severe heart failure, recurrence of myocardial infarction, in-stent restenosis, and reaccept PCI. Follow-up data were collected via clinical visits or telephone calls at 1, 3, 6, and 12 months and annually thereafter.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Result</h3>\u0000 \u0000 <p>Multivariable Cox regression analysis revealed that the risk of MACEs increased gradually with increasing CRI-I and CRI-II. The cumulative survival rate in the CRI-I ≥ 3.350 and CRI-II ≥ 1.697 groups was significantly lower than that in the CRI-I &lt; 3.350 and CRI-II &lt; 1.697 groups, respectively (log-rank tests: all <i>p</i> &lt; 0.001). The nomogram demonstrated good predictive performance for the 1-, 2-, and 3-year survival probability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>CRI-I ≥ 3.350 and CRI-II ≥ 1.697 could serve as independent predictors of MACEs in patients with ACS undergoing PCI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13058236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-COVID-19 Area Postrema Syndrome With SARS-CoV-2 in CSF: A Dual-Case Report and Review of the Literature","authors":"Wan Zhu,&nbsp;Jing Qian,&nbsp;Min Peng,&nbsp;Yan Li,&nbsp;Jinghan Hu","doi":"10.1002/iid3.70421","DOIUrl":"10.1002/iid3.70421","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune astrocytopathy characterized by inflammatory demyelinating lesions in the central nervous system. Area postrema syndrome (APS), marked by intractable nausea, vomiting, and hiccups, is a recognized but less common initial manifestation. Post-infectious autoimmunity triggered by SARS-CoV-2 has been increasingly associated with NMOSD pathogenesis; however, the clinical significance of direct viral neuroinvasion and its relationship to divergent patient outcomes remains poorly understood.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We report two female patients who developed isolated APS shortly after COVID-19 infection. Both patients underwent comprehensive neurological evaluation, including brain and spinal magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) analysis with metagenomic next-generation sequencing (mNGS), and serological testing for aquaporin-4 immunoglobulin G (AQP4-IgG), myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG), and glial fibrillary acidic protein immunoglobulin G (GFAP-IgG) using cell-based assays. Clinical outcomes were compared in the context of antibody serostatus and treatment strategies. A review of the relevant literature on post-COVID NMOSD was also performed.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Both patients presented with intractable vomiting and hiccups following SARS-CoV-2 infection, and MRI demonstrated isolated T2/FLAIR hyperintense lesions in the dorsal medulla consistent with area postrema involvement. SARS-CoV-2 RNA sequences were detected in the CSF of both patients via mNGS, suggesting direct viral neuroinvasion or blood–brain barrier compromise. Despite similar initial presentations, their outcomes diverged dramatically. Patient 1 was AQP4-IgG negative, responded well to immunotherapy with intravenous immunoglobulin and corticosteroids followed by mycophenolate mofetil maintenance, and remained relapse-free at 12-month follow-up with significant lesion regression on MRI. Patient 2 was AQP4-IgG positive in both serum and CSF, and despite acute treatment, experienced a fatal relapse 6 months later with longitudinally extensive transverse myelitis while on low-dose prednisone monotherapy.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Isolated APS may represent an important yet under-recognized manifestation of post-COVID-19 autoimmune neuroinflammation. Detection of SARS-CoV-2 in CSF supports a role for direct viral neuroinvasion as a localized inflammatory stimulus. ","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperoside Modulates the Estrogen-PI3K/VEGF Axis to Ameliorate Oxidative Damage-Induced Inhibition of Bone Formation in MC3T3-E1 Cells","authors":"Shuo Wang,&nbsp;Wei Feng,&nbsp;Xueqin Feng,&nbsp;Peitong Wu,&nbsp;Nanxi Zhang,&nbsp;Xiaoqian Yang,&nbsp;Yawen Li,&nbsp;Chunnan Li,&nbsp;Jiaming Sun","doi":"10.1002/iid3.70412","DOIUrl":"10.1002/iid3.70412","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aims to investigate how hyperoside (HYP) alleviates oxidative stress-induced osteoporosis, its molecular mechanisms, and its impact on osteoblast differentiation, oxidative damage, and the estrogen-PI3K/VEGF signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The osteoblast differentiation model was induced using dexamethasone, and osteoblast-related markers like ALP, NO, GSH, MDA, and SOD were measured post-HYP intervention. A zebrafish model was used to assess HYP's impact on ROS and bone formation. Network pharmacology identified key oxidative stress and osteoporosis targets, with HYP's binding affinity confirmed via molecular docking and simulation. RT-qPCR verified the expression of key pathway targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>HYP can counteract dexamethasone-induced inhibition of osteoblast differentiation, boost ALP, NO, GSH, and SOD levels, and lower MDA levels in osteoblasts. It also reduces ROS accumulation and enhances bone formation in zebrafish. Network pharmacology identified a common oxidative stress and osteoporosis target, with molecular docking confirming HYP's stable binding. RT-qPCR showed HYP significantly upregulates SRC, PI3K, AKT1, and e-NOS, activating the estrogen-PI3K/VEGF pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>HYP plays an anti-oxidative stress effect through targeted regulation of estrogen-PI3K/VEGF signal axis, and then promotes osteoblast differentiation and bone formation, which provides a new potential candidate drug and experimental basis for the treatment of osteoporosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Prognostic Values of Neutrophil Extracellular Traps-Related Genes in Glioma Based on Bioinformatics","authors":"Xiaobing Guo,&nbsp;Xiaowen Li,&nbsp;Hengxi Li,&nbsp;Yan Cao,&nbsp;Pengfei Zhang,&nbsp;Ping Li","doi":"10.1002/iid3.70422","DOIUrl":"10.1002/iid3.70422","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Glioma is a highly invasive and drug-resistant malignant primary tumor. Increasing research is focusing on the function of neutrophil extracellular traps (NETs) in glioma progress. We aimed to explore the mechanism of NETs-related genes (NETs-RGs) in glioma to find potential biomarkers for glioma.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The GSE16011 data set was downloaded from the GEO database, and the gene expression matrix and clinical data of glioma patients were downloaded from the TCGA database, the cbioportal website, and the CGGA database, as the training and validation sets. The NETs-RGs were obtained from previous studies. Subsequently, differential expression analysis, WGCNA, GO enrichment, and GSEA analysis. The risk model was established for Cox, LASSO, survival, and independent prognostic analyses. The CIBERSORT algorithm was used for immune infiltration analysis, and pRRophetic was used for drug sensitivity analysis. Finally, the expression levels of genes were validated by data set, glioma patients' tissue samples, and glioma cells, and evaluating cell biological behavior.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 57 differential expression genes between Glioma and Normal samples were obtained. Then, two modules with the highest positive correlation with NETs-RGs by WGCNA, the NETs-RGs were obtained from previous studies. Six candidate genes were obtained for subsequent analysis. Then, we conducted functional enrichment of candidate genes and constructed a glioma prognosis model. The prognosis model was indicated as a good predictor of a patient's glioma risk. These genes were related to immune cells significantly. And drug sensitivity analysis predicted 128 differences in chemotherapy drugs and found that MICALL2 had a significant correlation with multiple drugs. Finally, only NFIL3 had the same trend of significantly high expression levels. Moreover, knockdown NFIL3 can inhibit glioma cell malignant growth, and promote apoptosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Three prognosis-related genes have better prognosis values for glioma patients and may be the potential biomarkers for the treatment of glioma.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}