Immunobiology最新文献

{"title":"Complement system during infectious diseases.","authors":"Angela S Barbosa, Lourdes Isaac","doi":"10.1016/j.imbio.2026.153242","DOIUrl":"https://doi.org/10.1016/j.imbio.2026.153242","url":null,"abstract":"","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":" ","pages":"153242"},"PeriodicalIF":3.1,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral blood exosomal Hsa-miR-335-3p alleviates burn-induced acute lung injury by targeting TLR4 and the PI3K/AKT/NF-κB pathway","authors":"Xu-Dong Tang, Rui Ding, Xu-Lin Chen","doi":"10.1016/j.imbio.2026.153236","DOIUrl":"10.1016/j.imbio.2026.153236","url":null,"abstract":"<div><h3>Introduction</h3><div>Due to the incessant advancements in burn treatment technology, the cure rate among patients with severe burns has significantly improved. However, acute lung injury/acute respiratory distress syndrome secondary to severe burns remains one of the challenges in the treatment of severe burns. Exosomes play a role in information and material exchange by transporting lipids, miRNA, proteins, mtDNA, and other substances to target cells. This study primarily explores the role and molecular mechanism of exosomal miRNA in peripheral blood after burn injury in acute lung injury.</div></div><div><h3>Method</h3><div>From September 2021 to August 2023, data on severely burned patients treated in our hospital were collected. Based on the new global criteria for ARDS, these severely burned patients were divided into the ARDS group and the non-ARDS group. Exosomes from peripheral blood of severely burned patients collected 4–7 days post-injury were extracted using ultracentrifugation; Exosomes were identified using transmission electron microscopy, NTA, and exosome marker proteins CD63 and CD9. The Hsa-miR-335-3p in the two groups of exosomes were analyzed using RT-qPCR. After labeling exosomes with PKH 67 dye and co-culturing them with BEAS-2B cells, the uptake of exosomes by the cells was observed using confocal microscopy. The dual-luciferase gene reporter assay verified the specific binding of Hsa-miR-335-3p to the 3’-UTR region of TLR4 mRNA. The expression levels of proteins such as TLR4, Bcl-2, BAX, and C-caspase 3 were detected using Western blot. After Annexin V/PI double staining, flow cytometry was used to measure the apoptosis rate of cells in each group. TNF-α, IL-1β, and IL-6 in the cell supernatant were determined by ELISA.</div></div><div><h3>Result</h3><div>A positive correlation between TBSA, III°, and BI and Hsa-miR-335-3p. A strong correlation between inhalation injury and mechanical ventilation and Hsa-miR-335-3p. Furthermore, a negative correlation between PaO2/FiO2 and Hsa-miR-335-3p. Among ARDS patients undergoing mechanical ventilation, PaO2/FiO2 still showed a negative correlation with Hsa-miR-335-3p. The results of ROC curve analysis showed that Hsa-miR-335-3p had high sensitivity and specificity (0.944 and 0.819) for the diagnosis of post-burn ARDS, with an area under the curve of 0.907. Exosomes could be uptake by BEAS-2B cells. Exosomes delivered Hsa-miR-335-3p, which inhibited the expression of TLR4 protein in BEAS-2B cells. The results of the dual-luciferase gene reporter assay suggest that Hsa-miR-335-3p specifically binds to the 3’-UTR region of TLR4 mRNA, promoting the degradation of TLR4 mRNA and inhibiting its expression. In the burn microenvironment, Hsa-miR-335-3p protects against BEAS-2B cells apoptosis and mitigates inflammatory responses. Modulating TLR4 affects Hsa-miR-335-3p in protecting against cell apoptosis and reducing inflammatory responses. Hsa-miR-335-3p protects against burn lung","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153236"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864850","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":"m6A writer METTL14 restricts Mycobacterium tuberculosis infection by promoting TAX1BP1-mediated autophagy in macrophages","authors":"Nueramina Tieliwaerdi,&nbsp;Zhenzhen Pan,&nbsp;Nigela Elihamu,&nbsp;Limei Han","doi":"10.1016/j.imbio.2026.153240","DOIUrl":"10.1016/j.imbio.2026.153240","url":null,"abstract":"<div><div>N6-methyladenosine (m6A) modification plays a crucial role in regulating immune responses against <em>Mycobacterium tuberculosis</em> (Mtb) infection, but the underlying mechanisms remain unclear. Here, we analyzed m6A regulatory gene expression in GEO dataset <span><span>GSE139825</span><svg><path></path></svg></span> and validated the finding in THP-1-derived macrophages. Bioinformatics analysis showed that METTL14, ALKBH5, and YTHDC1 were significantly downregulated, while METTL3 was upregulated in Mtb-infected alveolar macrophages compared to controls. In vitro experiments confirmed METTL14 expression was dose-dependently reduced with Mtb infection in macrophages, and METTL14 overexpression reversed Mtb-induced decreases in cell viability, reduced LDH release, and diminished intracellular Mtb burden. Mechanistically, METTL14 overexpression restored Mtb-suppressed autophagy, evidenced by increased LC3II/I ratio and Beclin1 expression as well as decreased p62 levels, which was abrogated by the autophagy inhibitor 3-MA. Further, as validated by bioinformatic prediction, RIP assay and actinomycin D experiment, METTL14 directly bound to TAX1BP1 mRNA and enhanced its m6A modification, thereby stabilizing TAX1BP1 mRNA and upregulating its expression. TAX1BP1 knockdown abolished the protective effects of METTL14 overexpression on macrophage viability, autophagy, and anti-Mtb capacity. Collectively, our findings demonstrate that METTL14, downregulated by Mtb infection, promotes macrophage autophagy and antibacterial activity via m6A-mediated stabilization of TAX1BP1. This METTL14-TAX1BP1-m6A pathway provides a novel therapeutic target for tuberculosis treatment.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153240"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911658","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 anti-leukemia drug ponatinib attenuates NLRP3 inflammasome activation in macrophages","authors":"Abigail H. Evered,&nbsp;Daniel C. Shippy,&nbsp;Jaidynne N. Lash,&nbsp;Sophia F. Oliai,&nbsp;Tyler K. Ulland","doi":"10.1016/j.imbio.2026.153241","DOIUrl":"10.1016/j.imbio.2026.153241","url":null,"abstract":"<div><div>The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is an established driver of inflammation in diseases such as diabetes, Alzheimer's disease, and gout. Previously, we screened 875 FDA-approved drugs for NLRP3 inhibitors and identified ponatinib as one of the five candidates that reduced NLRP3 inflammasome activation without causing cytotoxic effects in bone marrow-derived macrophages (BMDMs). Therefore, we hypothesize that ponatinib may be an effective NLRP3 inflammasome inhibitor. We performed dose curves and cytotoxicity assays to determine an effective <em>in vitro</em> concentration of ponatinib in BMDMs (1 μM) and primary microglia (0.5 μM) that reduced IL-1β secretion without inducing cytotoxicity. In BMDMs, ponatinib inhibited <em>Nlrp3-</em> and <em>Caspase-1</em>-dependent IL-1β and IL-18 secretion and significantly reduced caspase-1 processing. Ponatinib also reduced IL-1β secretion by microglia, indicating possible NLRP3 inflammasome inhibition in this cell type, but further testing is required. Although ponatinib has previously been demonstrated to drive cardiotoxicity-mediated inflammation, these data suggest that at specific doses, <em>in vitro</em> ponatinib can be non-cytotoxic and effective in attenuating NLRP3 inflammasome activation in macrophages and microglia.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153241"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897213","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":"ECMO-assisted whole lung lavage combined with GM-CSF inhalation for severe pulmonary alveolar proteinosis: a comparative cohort study","authors":"Qiong Li,&nbsp;Jingyu Wu,&nbsp;Hongmei Chen,&nbsp;Qin Huang,&nbsp;Jing Dong,&nbsp;Yue Zhang,&nbsp;Hong Zhou","doi":"10.1016/j.imbio.2026.153234","DOIUrl":"10.1016/j.imbio.2026.153234","url":null,"abstract":"<div><h3>Purpose</h3><div>This study evaluated the association of combining veno-venous extracorporeal membrane oxygenation (ECMO) with whole-lung lavage (WLL) and granulocyte-macrophage colony-stimulating factor (GM-CSF) nebulization in pulmonary alveolar proteinosis (PAP), focusing on pulmonary function, oxygenation, lipid metabolism, and inflammatory modulation.</div></div><div><h3>Methods</h3><div>This retrospective cohort study included 40 PAP patients, categorized into WLL + GM-CSF (<em>n</em> = 20) and ECMO + WLL + GM-CSF (<em>n</em> = 20) groups according to the treatment they received. Outcomes included pulmonary function [diffusing capacity for carbon monoxide (DLCO%), forced vital capacity (FVC%)], arterial blood gas parameters [partial pressure of oxygen (PaO₂), carbon dioxide (PaCO₂), oxygen saturation (SaO₂)], lipid profiles [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C)], inflammatory cytokines such as interleukin-6 (IL-6) and C-reactive protein, and functional assessments (Barthel Index score, 6-min walk distance). Correlations between lipids profiles, arterial blood gas parameters, pulmonary functional indicators, and inflammatory cytokines were evaluated using Pearson's or Spearman's correlation coefficients.</div></div><div><h3>Results</h3><div>The ECMO + WLL + GM-CSF group showed greater improvements in DLCO% and FVC%, significant increases in PaO₂ and SaO₂, and greater reductions in PaCO₂, pro-inflammatory markers (IL-6, CRP), and lipid levels (TC, TG, LDL-C) compared to the WLL + GM-CSF group. In the ECMO + WLL + GM-CSF group, negative correlations were observed between serum TG and PaO₂, DLCO%, and FVC%, and IL-6 inversely correlated with FVC%. The ECMO + WLL + GM-CSF group also achieved higher functional recovery based on the higher Barthel index scores and longer 6-min walk distance.</div></div><div><h3>Conclusion</h3><div>ECMO-assisted WLL combined with GM-CSF was associated with greater improvements in pulmonary function and oxygenation, as well as greater reductions in serum lipid levels and inflammatory markers.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153234"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887324","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":"Transcriptomic profiling reveals complement activation in chronic pancreatitis adjacent to pancreatic ductal adenocarcinoma","authors":"Arun Kumar Selvam,&nbsp;Ville N. Pimenoff,&nbsp;Carlos Fernández Moro,&nbsp;Soledad Pouso Elduayen,&nbsp;Joakim Dillner,&nbsp;Mikael Björnstedt,&nbsp;Mehran Ghaderi","doi":"10.1016/j.imbio.2026.153239","DOIUrl":"10.1016/j.imbio.2026.153239","url":null,"abstract":"<div><div>Chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) frequently coexist, yet distinguishing inflammatory changes secondary to malignancy from primary pancreatitis remains challenging. Here, we present an integrated multi-omics analysis of spatially distinct pancreatic tissue compartments obtained from a single patient undergoing pancreaticoduodenectomy for PDAC, combining histopathology, transcriptomics, immunofluorescence, and meta-transcriptomic microbial profiling. Morphological assessment identified tumor tissue, adjacent CP, and normal pancreas. Transcriptomic profiling of macro-dissected samples revealed differential gene expression and enrichment of the classical complement pathway in the CP compartment, which was qualitatively supported by immunofluorescent detection of C1q and C3 along the ductal epithelium. Meta-transcriptomic analysis detected a limited number of bacterial taxa and no viral RNA; these findings were interpreted conservatively given the constraints of low-biomass tissue profiling and the single-patient design. Although causal inference and generalizability are limited by the single-patient design, this study demonstrates the feasibility of integrating pathology with transcriptomic and microbial analyses to generate a hypothesis-generating, multi-omics framework for exploring inflammatory-malignant interactions in pancreatic disease.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153239"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873969","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":"Ketone ester alleviates sepsis-associated liver injury through β-hydroxybutyrylation of STAT1","authors":"Yaping Bai,&nbsp;Kai Li,&nbsp;Dan Zhu,&nbsp;Rui Li,&nbsp;Yisong Yan,&nbsp;Changjun Zhong,&nbsp;Lei Zha,&nbsp;Qihai Wang","doi":"10.1016/j.imbio.2026.153243","DOIUrl":"10.1016/j.imbio.2026.153243","url":null,"abstract":"<div><div>Sepsis-associated liver injury is characterized by excessive inflammation and macrophage activation. β-Hydroxybutyrate (β-OHB) has anti-inflammatory effects and induces lysine β-hydroxybutyrylation (Kbhb), but the role of site-specific Kbhb in septic liver injury remains unclear. This study examined the role of STAT1 K679 Kbhb in the protective effect of ketone ester (KE) against LPS-induced liver injury. STAT1^p.K679R knock-in mice were generated, and liver injury was induced by lipopolysaccharide (LPS). KE pretreatment alleviated hepatic histopathological injury, reduced serum alanine aminotransferase and aspartate aminotransferase levels, and decreased the Bax/Bcl-2 ratio in wild-type mice. These effects were significantly attenuated in STAT1^p.K679R mice. KE increased hepatic STAT1 Kbhb, whereas the K679R mutation markedly reduced this modification. In RAW264.7 macrophages, K679R reduced β-OHB-induced STAT1 Kbhb, while no significant effect was observed in AML12 hepatocytes. KE also reduced hepatic M1 macrophage markers, IL-6 and IL-12 expression, and STAT1 Ser727 phosphorylation in LPS-treated wild-type mice, whereas these effects were attenuated by K679R. These results show that STAT1 K679 Kbhb contributes to the inhibition of macrophage M1 polarization by KE and is involved in its protective effect against LPS-induced liver injury.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153243"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963408","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 Sesn2/Nrf2 axis suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages","authors":"Qiong Zhang,&nbsp;Guanlin Zhou,&nbsp;Chunming Gao,&nbsp;Sen Jia,&nbsp;Zhihua Huang,&nbsp;Yuhan Zhou,&nbsp;Zong Ning","doi":"10.1016/j.imbio.2026.153238","DOIUrl":"10.1016/j.imbio.2026.153238","url":null,"abstract":"<div><h3>Background</h3><div>Pyroptosis is a key mechanism driving immune imbalance in sepsis, while the stress-induced protein Sestrin 2 (Sesn2) and Nuclear factor E2-related factor 2 (Nrf2) are core regulators of antioxidant defense. No existing studies have clarified the interactive regulatory effect of the Sesn2/Nrf2 axis on pyroptosis in alveolar macrophages. Therefore, this study aims to investigate the regulatory mechanism of the Sesn2/Nrf2 axis on pyroptosis and oxidative stress in LPS/nigericin-challenged alveolar macrophages, providing a theoretical basis for further understanding of sepsis.</div></div><div><h3>Methods</h3><div>Bioinformatics analysis involved screening differentially expressed genes in sepsis from the Gene Expression Omnibus dataset <span><span>GSE185263</span><svg><path></path></svg></span>, intersecting them with genes related to pyroptosis and ferroptosis, constructing a protein-protein interaction network, and identifying core genes. An inflammatory injury model was established in the mouse alveolar macrophage cell line MH-S by stimulating cells with LPS and nigericin. Interventions were performed using siRNA to knock down Sesn2 and plasmids to overexpress Nrf2. Cell viability, oxidative stress markers, expression of pyroptosis-related molecules, and secretion of inflammatory cytokines were measured.</div></div><div><h3>Results</h3><div>SESN2 as a key gene common to sepsis, pyroptosis, and ferroptosis. The Sesn2/Nrf2 signaling axis significantly enhanced the cell viability of MH-S cells after inflammatory injury, increased Superoxide Dismutase activity and Glutathione levels, and reduced reactive oxygen species and Lactate Dehydrogenase levels. Simultaneously, this axis suppressed the expression of pyroptosis-related inflammasomes (NOD-like receptor thermal protein domain associated protein 3, Absent in melanoma 2) and key execution proteins (Gasdermin D, Cleaved Caspase-1, Caspase-4), and reduced the secretion of inflammatory cytokines IL-1β, IL-18, and TNF-α. Sesn2 and Nrf2 exhibited mutual positive regulation in macrophages following inflammatory injury.</div></div><div><h3>Conclusion</h3><div>In vitro cell model studies indicate that the Sesn2/Nrf2 axis synergistically suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages, suggesting that this axis may represent a potential target warranting further investigation in in vivo models.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 5","pages":"Article 153238"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860343","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":"Neuropilin-1 serves as a prognostic marker and a potential target of M2-polarized tumor-associated macrophages in gastric cancer","authors":"Jingya Wang,&nbsp;Cheng Lan,&nbsp;Zhebo Xia,&nbsp;Dawei Cui,&nbsp;Hang Lv,&nbsp;Na Qiang,&nbsp;Guiping Chen,&nbsp;Junjie Ao","doi":"10.1016/j.imbio.2026.153206","DOIUrl":"10.1016/j.imbio.2026.153206","url":null,"abstract":"<div><div>Neuropilin-1 (NRP1) has recently emerged as a promising immune checkpoint. However, its prognostic significance in gastric cancer (GC) and its association with the tumor immune microenvironment remain insufficiently understood. In this study, analysis of TCGA data revealed elevated NRP1 expression in GC tissues compared to normal controls. Based on NRP1 expression levels, TCGA GC samples were stratified into high- (<em>n</em> = 185) and low-expression (n = 185) groups. The high-expression group exhibited more advanced TNM and histological grade stages, along with a significantly shorter overall survival. Differential expression analysis between the two groups highlighted enrichment of genes involved in extracellular matrix (ECM)-related signaling pathways and cell chemotaxis. Notably, NRP1 expression showed the strongest positive correlation with the infiltration of M2-polarized tumor-associated macrophages (M2-TAMs) and the expression of the M2-TAMs marker CD163 in the TCGA cohort. Consistently, CD163 expression was higher in the NRP1 high-expression group. Furthermore, immunohistochemical analysis of 20 clinical GC specimens, scored for both NRP1 and CD163, demonstrated co-positivity in 14 cases (70%) and co-negativity in 3 cases (15%). Pearson correlation analysis confirmed a significant association between NRP1 staining intensity and both tumor grade and CD163 score. To explore causality, conditioned medium from GC cell lines with high or low NRP1 expression was used to treat THP-1 monocytic cells. The supernatant from NRP1-high cells promoted both CD163 expression and migration of THP-1 cells, effects that were abolished by the NRP1 inhibitor EG00229. In conclusion, our findings suggest that NRP1 serves as a prognostic biomarker and an immune-regulatory molecule warranting further investigation in GC, possibly through modulating M2-TAMs polarization and recruitment.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 4","pages":"Article 153206"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257556","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 potential diagnostic biomarkers for myocardial infarction using bioinformatics and machine learning","authors":"Ling Ren,&nbsp;Min Xu,&nbsp;Ronglu Jiang,&nbsp;Juying Li","doi":"10.1016/j.imbio.2026.153216","DOIUrl":"10.1016/j.imbio.2026.153216","url":null,"abstract":"<div><div>Acute myocardial infarction(<em>AMI</em>)is an important type of cardiovascular disease, which seriously threatens the lives of humans. In order to help patients receive timely clinical treatment and improve their survival rates, it is necessary to screen out related molecules in advance. To this end, we applied bioinformatics methods and machine learning algorithms to find possible biomarkers associated with AMI. When considering possible connections with dynamics of immune cells activation. Based on the RNA-seq results, differential expression analysis was performed followed by WGCNA to identify stably changed genes. The KEGG and GO enrichment analyses revealed that the identified genes are mainly related with inflammatory response, immune processes, apoptosis and immunomodulation. In our PPI network, some hub genes (e.g., FOS, JUN, TNF, IL1B, TLR2) were located in the center of the whole network. We found strong associations between the major genes and their interaction effects, we developed a predictive model for diagnosis using an artificial intelligence algorithm as follows: suggesting a substantially increased discriminative performance for AMI with the 4 hub genes NFKBIA, FCER1G, CD36 and ICAM1. The model achieved a high AUC score of 0.924.</div><div>External validation based on an independent single-cell sequencing dataset demonstrated that NFKBIA, FCER1G, and ICAM1 displayed consistent expression patterns in both the training and test cohorts, with the highest expression levels observed in cardiomyocytes. Accordingly, these three genes may serve as reliable biomarkers for AMI and are closely associated with the distribution of immune cells.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 4","pages":"Article 153216"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148446056","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}