Immunobiology最新文献

{"title":"Immunological profile of acute Chagas disease patients infected via oral transmission and treated with Benznidazole: a two-year follow-up of immune responses","authors":"Luciane de Freitas Firmino ,&nbsp;Victor Vaitkevicius-Antão ,&nbsp;Amanda Vasconcelos Nascimento ,&nbsp;Cíntia Nascimento Costa-Oliveira ,&nbsp;Michelle da Silva Barros ,&nbsp;Diego José Lira Torres ,&nbsp;Claudeir Dias Silva-Junior ,&nbsp;Byannca de Carvalho Torreão ,&nbsp;Maria Beatriz Araújo Silva ,&nbsp;Carolina de Araújo de Medeiros ,&nbsp;Tayne Fernanda Lemos da Silva ,&nbsp;Maria Aucineide Basílio Albuquerque ,&nbsp;Milena Maria de Morais Silva ,&nbsp;Filipe Prohaska Batista ,&nbsp;Demetrius Montenegro ,&nbsp;Wilson de Oliveira-Júnior ,&nbsp;Cristina Carrazzone ,&nbsp;Silvia Marinho Martins ,&nbsp;Ana Karine Araújo Soares ,&nbsp;Virginia Maria Barros de Lorena","doi":"10.1016/j.imbio.2026.153169","DOIUrl":"10.1016/j.imbio.2026.153169","url":null,"abstract":"<div><div>The state of Pernambuco, Brazil, reported its biggest outbreak of Acute Chagas disease (ACD) caused by oral transmission, in 2019. During the acute phase, timely access to treatment must be quick and performed in all cases, regardless of the transmission route, as approximately 70–80% of cases are cured. Monitoring the immunological profile after Benznidazole (BZ) treatment in ACD patients may help identify tools to support disease progression assessment. This study aimed to evaluate the immune response, especially cytokines and antibodies levels, in patients with ACD and treated with BZ. A total of 28 laboratory-confirmed patients from the outbreak were included. Th1 and Th2 cytokines were quantified in serum samples using flow cytometry, and antibody levels were assessed by indirect immunofluorescence. Our findings indicate that BZ reduced the inflammatory response, as evidenced by decreased levels of Th1-type cytokines (IFN-γ, TNF, IL-2 and IL-6). Anti-inflammatory cytokines (IL-4 and IL-10) also showed a decline following treatment. Only IgM antibody titers were reduced, with no consistent pattern observed for IgG. These results support the use of BZ in acute phase and suggest the potential use of cytokines as auxiliary biomarkers for therapeutic monitoring.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153169"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305475","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":"Clinical characteristics and risk factors of dyslipidemia in patients with rheumatoid arthritis","authors":"Jia Liu,&nbsp;Yehua Jin,&nbsp;Sihan Wang,&nbsp;Xinchun Zheng","doi":"10.1016/j.imbio.2026.153171","DOIUrl":"10.1016/j.imbio.2026.153171","url":null,"abstract":"<div><h3>Background</h3><div>Dyslipidemia is highly prevalent in patients with rheumatoid arthritis (RA) and may be closely associated with systemic inflammation and disease activity. However, its clinical characteristics and predictive factors remain unclear.</div></div><div><h3>Methods</h3><div>We retrospectively enrolled 312 RA patients and stratified them into dyslipidemia group (<em>n</em> = 168) and a normolipidemia group (<em>n</em> = 144) based on serum lipid profiles. Correlation analyses were performed to examine associations between lipid levels and inflammatory markers. Multivariate logistic regression was used to identify independent predictors of dyslipidemia. Receiver operating characteristic (ROC) curves were applied to evaluate the predictive performance of individual and combined models.</div></div><div><h3>Results</h3><div>Patients with dyslipidemia had higher levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), alongside reduced high-density lipoprotein cholesterol (HDL<img>C). The dyslipidemia group also showed higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and Disease Activity Score in 28 joints (DAS28). TC, TG, and LDL-C were positively correlated with inflammatory markers and DAS28, while HDL-C correlated negatively. Age, body mass index (BMI), female gender, smoking history, glucocorticoid use, and higher DAS28 were identified as independent risk factors for dyslipidemia. Elevated CRP and IL-6 further increased risk, whereas higher TNF-α levels were protective. Among predictive models, the combined Integrated Model achieved superior discriminative performance, outperforming any single clinical or inflammatory indicator.</div></div><div><h3>Conclusion</h3><div>The integrated predictive model combining clinical and inflammatory markers improves risk discrimination, providing a useful tool for early identification of dyslipidemia in RA patients.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153171"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354808","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":"Cytokine-induced killer (CIK) cells inhibit Plasmodium falciparum parasitemia through cytolytic effector activity in vitro","authors":"Rohulla Vaseq ,&nbsp;Berthila Ferkamchwi ,&nbsp;Hans Weiher ,&nbsp;Veronika Lukacs-Kornek ,&nbsp;Nahid Mahleqa ,&nbsp;Marc P. Hübner ,&nbsp;Amit Sharma ,&nbsp;Ingo G.H. Schmidt-Wolf","doi":"10.1016/j.imbio.2026.153159","DOIUrl":"10.1016/j.imbio.2026.153159","url":null,"abstract":"<div><div>Cytokine-induced killer (CIK) cells, with dual traits resembling natural killer (NK) and T cells, have shown a promising clinical efficacy against cancer in clinical application leading to licensing of CIK cells in many countries. Here, we demonstrated that CIK cells can also inhibit the growth of <em>Plasmodium falciparum</em> in vitro, leading to a significant reduction in parasitemia levels after 24 h. We found that CIK cells cytotoxicity against infected RBCs is mostly dependent on their secretions rather than cell to cell communication, as they are a substantial repository of lytic agents, including granzyme B, granulysin, as well as perforin. We found that these components in the recombinant form acted synergistically, with granulysin and perforin facilitating granzyme B entry into target cells, resulting in parasite death. Moreover, we observed that priming CIK cells with dendritic cells pulsed with <em>P. falciparum</em> lysate antigen led to diminished CIK cell cytotoxicity against pRBCs. And finally, we found that although combination of CIK cells with chloroquine cannot be synergistic, CIK cells showed a comparable efficacy to chloroquine. Artemisinin combined with effector cells exhibited a slight enhancement in cytotoxicity compared to artemisinin alone. These results propose CIK cells as a potential alternative cell therapeutic approach in the preclinical and clinical setting against malaria and potentially other infections.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153159"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036478","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":"Altered CD163 and tweak expression in dendritic cells is associated with cardiac function post-acute myocardial infarction","authors":"Marín-Jáuregui Laura Sherell ,&nbsp;Martínez-Shio Elena Berenice ,&nbsp;Cárdenas-Hernández Ángel Martín ,&nbsp;Ramírez-Torres Ricardo ,&nbsp;Trujillo-Martíneza Aron Iván ,&nbsp;Escobedo-Uribe Carlos David ,&nbsp;Monsiváis-Urenda Adriana Elizabeth","doi":"10.1016/j.imbio.2026.153166","DOIUrl":"10.1016/j.imbio.2026.153166","url":null,"abstract":"<div><div>The activation of the innate immune system is crucial for myocardial recovery after acute myocardial infarction (AMI). Dendritic cells (DCs) and macrophages regulate inflammation and healing of the ischemic heart. This study aims to evaluate the levels of DCs and macrophages expressing CD163 and TWEAK in patients with acute ST-elevation myocardial infarction (STEMI). We decided to evaluate the frequency of CD163+ TWEAK+ DCs and macrophages in patients with STEMI within the first 72 h, as well as at 3 and 6 months after the acute event. We observed that expression of CD163 and TWEAK in myeloid DCs was higher in STEMI patients at 3-month follow-up, and this was associated with worse cardiac function. sTWEAK levels were higher in STEMI patients within 72 h after AMI and positively correlated with a better left ventricular ejection fraction (LVEF). Finally, in M2 Macrophages, rh-TWEAK administration resulted in a dose-dependent decrease in CD163 expression. mDC, pDC, as well as M1/M2 macrophages express CD163 and TWEAK. ages. Our results indicate that TWEAK and CD163 may be promoting an inflammatory milieu after AMI. Thus, an imbalance in the expression of these molecules can then lead to chronic inflammation, tissue damage, and heart failure.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153166"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146219110","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":"Lymphocyte subpopulations in healthy Ukrainian men: local reference ranges, long temporal stability, and exercise-induced variability","authors":"Dariia Zabara ,&nbsp;Iryna Kozeretska ,&nbsp;Ivan Klapoushenko ,&nbsp;Yaroslava Anoshko ,&nbsp;Ievgen Dubrovskyi ,&nbsp;Boris Dons'koi","doi":"10.1016/j.imbio.2026.153170","DOIUrl":"10.1016/j.imbio.2026.153170","url":null,"abstract":"<div><div>Reliable interpretation of lymphocyte immunophenotyping depends on population-specific reference ranges that account for demographic and environmental factors. However, such reference data are currently lacking for the Ukrainian population. This study aimed to establish local reference ranges for lymphocyte subpopulations in healthy adult men and to assess their temporal stability and variability following physical exercise.</div><div>Peripheral blood samples from 100 clinically healthy men aged 22–55 years were analyzed by flow cytometry to quantify T lymphocytes (CD3⁺, CD3⁺CD4⁺, CD3⁺CD8⁺), B lymphocytes (CD3⁻CD19⁺), and NK cells (CD3⁻CD56⁺, CD3⁻CD56⁺NKp46⁺). Temporal stability was evaluated in 24 participants monitored during a one-year Antarctic expedition, while acute immune responses were assessed in 19 men before and after a modified Cooper test. The established reference ranges were as follows: CD3⁺ (54.0–82.2%), CD3⁺CD4⁺ (29.3–54.0%), CD3⁺CD8⁺ (11.2–39.6%), CD3⁻CD19⁺ (3.7–20.1%), CD3⁻CD56⁺ (4.2–30.0%), and CD3⁻CD56⁺NKp46⁺ (2.7–24.3%).</div><div>Comparison with published studies revealed differences in several parameters, whereas discrepancies relative to reference values used by local laboratories were observed across multiple measures. Following a one-year Antarctic expedition, lymphocyte subset distributions remained largely stable despite a significant expansion of monocytes, whereas short-term physical exercise elicited pronounced, subset-selective increases in NK cells and monocytes, accompanied by concurrent elevations in cortisol and testosterone levels. The differences observed across populations and laboratories underscore the need for harmonized, population-based reference intervals.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153170"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305414","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":"Clinical value of CTCs combined with serum tumor markers/inflammatory cytokines for the early diagnosis of non-small cell lung cancer","authors":"Xiuxue Gu ,&nbsp;Lingling Wan","doi":"10.1016/j.imbio.2026.153161","DOIUrl":"10.1016/j.imbio.2026.153161","url":null,"abstract":"<div><div>Objective: This study investigates the clinical utility of circulating tumor cells (CTCs) in combination with serum tumor markers/inflammatory cytokines for the diagnosis of early-stage non-small cell lung cancer (NSCLC). Methods: A retrospective analysis was conducted on the clinical data of 43 NSCLC patients (stage I-IIA) who underwent surgical treatment at the Fourth Hospital of Hebei Medical University between November 2021 and December 2022. A control group of 50 healthy individuals was also included. Comparative analyses of CTCs, serum tumor markers, and inflammatory cytokine levels were performed between the two groups. The clinical diagnostic value was assessed using receiver operating characteristic (ROC) curve analysis. Results: The median concentrations of CTCs, carcinoembryonic antigen (CEA), Cytokeratin 19 fragment (CYFRA21-1), neuron-specific enolase (NSE), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and interleukin-17 A (IL-17 A) were significantly elevated in the NSCLC cohort compared to the healthy control cohort, while interleukin-2 (IL-2) levels were reduced (<em>P</em> &lt; 0.05). ROC curve analysis revealed that CTCs exhibited a sensitivity of 65.12%, specificity of 100.00%, and an area under the curve (AUC) of 0.826 for the diagnosis of early-stage NSCLC. The combined diagnostic sensitivity of CTCs, CEA, CYFRA21-1, and NSE reached 86.05%, with 100.00% specificity and an AUC of 0.945. Among the seven inflammatory cytokines evaluated, IL-17 A exhibited the highest diagnostic efficacy for early-stage NSCLC, with an AUC of 0.871, sensitivity of 93.02%, and specificity of 75.00%. The combination of IL-17 A and CTCs achieved an AUC of 0.953, with a sensitivity of 86.05% and specificity of 90.00%. Conclusion: The integration of CTCs with serum tumor markers and/or inflammatory cytokines provides high sensitivity and specificity for the diagnosis of early-stage NSCLC, highlighting its significant clinical potential.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153161"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131788","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":"BCL3 drives an immunosuppressive tumor microenvironment in esophageal cancer by promoting M2 macrophage polarization via STAT3 activation","authors":"Yushuai Geng ,&nbsp;Haowen Ma ,&nbsp;Minghang Liu ,&nbsp;Tairan Feng ,&nbsp;Yang Lv ,&nbsp;Zhiqiang Li ,&nbsp;Shujun Ma ,&nbsp;Hui Wang ,&nbsp;Yuna Niu","doi":"10.1016/j.imbio.2026.153164","DOIUrl":"10.1016/j.imbio.2026.153164","url":null,"abstract":"<div><h3>Introduction</h3><div>The progression of esophageal cancer is closely linked to the establishment of an immunosuppressive tumor microenvironment. Although B-cell leukemia/lymphoma 3 (BCL3) is dysregulated in various cancers, its specific role and mechanism in shaping the immune microenvironment of esophageal cancer, particularly in macrophage polarization, remain elusive.</div></div><div><h3>Results</h3><div>BCL3 was significantly overexpressed in esophageal cancer tissues, demonstrated good diagnostic value (AUC = 0.75, <em>P</em> &lt; 0.01), and its high expression was significantly associated with poor patient prognosis (<em>P</em> &lt; 0.05). Immune infiltration analysis revealed that high BCL3 expression correlated with increased M2 macrophage infiltration. In vitro experiments confirmed that knocking down BCL3 suppressed M2 macrophage polarization. Mechanistic studies indicated that BCL3 drives M2 polarization by enhancing the phosphorylation of STAT3.</div></div><div><h3>Conclusion</h3><div>Our study unveils a novel mechanism whereby BCL3 promotes an immunosuppressive tumor microenvironment in esophageal cancer by facilitating M2 macrophage polarization via the STAT3 signaling pathway. BCL3 represents a potential prognostic biomarker and a promising therapeutic target for immunotherapy in esophageal cancer.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153164"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197513","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":"Preface to the special issue for the 30th International Complement Workshop Brisbane 2025","authors":"Barbara E. Rolfe ,&nbsp;John D. Lee ,&nbsp;Trent M. Woodruff","doi":"10.1016/j.imbio.2025.153149","DOIUrl":"10.1016/j.imbio.2025.153149","url":null,"abstract":"<div><div>This <em>Immunobiology</em> special issue commemorates the 30th International Complement Workshop, held for the first time in Australia. Reflecting the global reach of complement research, the Workshop brought together delegates from 24 countries and showcased a diverse range of topics including: Structural insight into complement function; Mechanisms of activation and regulation; Cell-autonomous and intracellular complement; Novel and non-canonical roles; Complement in infection and disease; and Biomarkers, diagnostics and therapeutics<em>.</em> In addition to invited reviews and an original research article, this issue includes all accepted abstracts from the Workshop. Together, these contributions provide a compelling snapshot of a rapidly evolving field, one that continues to expand in scope and deepen mechanistic understanding. They highlight the dynamic, interdisciplinary and collaborative nature of complement research, and set the stage for future discoveries that will translate into clinical benefit.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153149"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827669","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":"Unraveling SLAN+/− monocytes transcriptomics in lupus and extracellular vesicles effects","authors":"Paula X. Losada ,&nbsp;Juan Antonio Villatoro-García ,&nbsp;Julio Jaramillo ,&nbsp;Lina Serrato ,&nbsp;Karen Álvarez ,&nbsp;Daniel Rodriguez ,&nbsp;Juan Camilo Diaz ,&nbsp;Ricardo Pineda ,&nbsp;Pedro Carmona-Saez ,&nbsp;Mauricio Rojas ,&nbsp;Gloria Vásquez","doi":"10.1016/j.imbio.2025.153153","DOIUrl":"10.1016/j.imbio.2025.153153","url":null,"abstract":"<div><h3>Objective</h3><div>Lupus Nephritis (LN) is a common and serious complication in patients with Systemic Lupus Erythematosus (SLE), an immune complex-mediated disease. Extracellular Vesicles (EVs) can carry autoantigens recognized by circulating antibodies, forming immune complexes (ICs) that may deposit in the kidney and be detected by inflammatory cells like monocytes in LN class III/IV. The SLAN marker identifies a subset of non-classical monocytes considered highly inflammatory and migratory. However, the interactions between these blood components in the context of LN remain incompletely understood. We aimed to analyze the transcriptional profiles of circulating SLAN+/− monocytes from LN patients and assess the influence of patient-derived EVs on SLAN− monocyte gene expression.</div></div><div><h3>Methods</h3><div>SLAN+/− monocytes were isolated from female LN patients, and controls were matched by similar age. Plasma-derived EVs from LN patients were co-incubated with SLAN-monocytes from controls. Next-generation RNA sequencing was employed to evaluate gene expression profiles and changes induced by EVs, followed by bioinformatic analysis to identify differential gene expression and functional pathways.</div></div><div><h3>Results</h3><div>Monocytes from LN patients exhibited an inflammatory profile characterized by elevated interferon response genes. The SLAN+ fraction displayed biological processes relevant to renal pathology, including cellular stress response, differentiation, and migration pathways. EVs elicited an inflammatory response with differentiation potential in non-SLAN monocytes.</div></div><div><h3>Conclusions</h3><div>These findings suggest that EVs transport antigenic molecules and induce transcriptional changes in monocytes toward inflammatory and migratory states, implicating them in LN pathogenesis and highlighting their potential as therapeutic targets.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153153"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976249","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":"Chlamydia psittaci inclusion membrane protein CPSIT_0844 elicits inflammatory IL-6 and IL-8 production in human monocytes via TLR2/TLR4 signaling pathways","authors":"Xiaoliang Yan ,&nbsp;Buwei Wang ,&nbsp;Kang Zheng ,&nbsp;Dan Luo ,&nbsp;Yumeng Li ,&nbsp;Jian Xiao ,&nbsp;Yuqing Chen ,&nbsp;Zhangping He ,&nbsp;Yating Wen ,&nbsp;Chuan Wang ,&nbsp;Yimou Wu","doi":"10.1016/j.imbio.2026.153160","DOIUrl":"10.1016/j.imbio.2026.153160","url":null,"abstract":"<div><div>The respiratory disease caused by <em>Chlamydia psittaci</em> (<em>C. psittaci</em>) infection is often characterized by significant inflammation. In the present study, we demonstrated that the <em>C. psittaci</em> inclusion membrane protein CPSIT_0844 induced THP-1 cells to express IL-6 and IL-8. However, silencing of the Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) genes by using small interfering RNA (siRNA) and transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) were found to reduce the expression of IL-6 and IL-8 in THP-1 cells stimulated with CPSIT_0844. Furthermore, CPSIT_0844 induces IL-6 and IL-8 production by signaling pathways involving JNK, p38, and NF-κB in monocytes. Collectively, our findings identify CPSIT_0844 as a proinflammatory virulence factor that triggers IL-6 and IL-8 expression via a TLR2/TLR4-MyD88-dependent mechanism, culminating in the activation of MAPK and NF-κB pathways. This work provides crucial molecular insight into the inflammatory pathogenesis of <em>C. psittaci</em> infection.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153160"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036477","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}