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IBV is a key pathogenic agent in poultry, causing significant respiratory and renal diseases. This study investigated NLRP3 inflammasome and pyroptosis involvement in IBV-infected chicken macrophage HD11 cells. IBV infection triggered a time-dependent increase in the release of IL-1β/IL-18, along with the upregulation of inflammasome-related genes. MCC950 treatment, an NLRP3 inhibitor, notably decreased inflammatory markers while enhancing viral replication, highlighting the NLRP3 inflammasome's function in restricting viral proliferation and mediating immunopathology. Experiments with UV-inactivated IBV demonstrated that active viral replication was essential for inflammasome activation. Pyroptosis was confirmed in IBV-infected HD11 cells through increased LDH release, characteristic ultrastructural damage, and upregulation of pyroptosis-related genes. Additionally, transfection with the IBV nucleocapsid (N) gene alone induced inflammasome activation and pyroptosis, indicating that the N protein is a key viral factor in this process. Our study offers a new understanding of IBV pathogenesis mechanisms and indicates that targeting the NLRP3 inflammasome may serve as a therapeutic approach.
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http://dx.doi.org/10.3390/biology14081049 | DOI Listing |
FASEB J
September 2025
Department of Hematology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Epilepsy is a common chronic nervous system disease that threatens human health. However, the role of FOXC1 and its relations with pyroptosis have not been fully studied in epilepsy. Sprague-Dawley rats were obtained for constructing temporal lobe epilepsy (TLE) models.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
September 2025
Department of Anesthesiology, Qianjiang Maternal and Child Health and Family Planning Service Centre, Qianjiang, Hubei, China.
Acute lung injury (ALI) is a major contributor to the high morbidity and mortality associated with intestinal ischemia-reperfusion (II/R). Despite its severity, current clinical management of ALI remains limited to supportive care without addressing the cause of the disease, underscoring the urgent need to investigate the underlying mechanism and develop targeted therapies. In this study, we employed both in vitro and in vivo models to explore ALI in the setting of II/R.
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Immune cell metabolism is essential for regulating immune responses, including activation, differentiation, and function. Through glycolysis and oxidative phosphorylation (OXPHOS), metabolism supplies energy and key intermediates for cell growth and proliferation. Importantly, some metabolites generated during these processes act as signaling molecules that influence immune activity.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
August 2025
Anhui Provincial Key Laboratory of Immunology in Chronic Diseases, Bengbu Medical University, Bengbu 233030, China.
Objectives: To investigate the effect of avitinib for suppressing NLRP3 inflammasome activation and alleviating septic shock and explore the underlying mechanism.
Methods: Mouse bone marrow-derived macrophages (BMDM), human monocytic leukemia cell line THP-1, and peripheral blood mononuclear cells (PBMC) isolated from healthy volunteers were pre-treated with avitinib, followed by activation of the canonical NLRP3 inflammasome using agonists including nigericin, monosodium urate (MSU) crystals, or adenosine triphosphate (ATP). Non-canonical NLRP3 inflammasome activation was induced intracellular transfection of lipopolysaccharide (LPS).
Nan Fang Yi Ke Da Xue Xue Bao
August 2025
Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.
Objectives: To investigate the therapeutic mechanism of 2,6-dimethoxy-1,4-benzoquinone (DMQ) for alleviating dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice.
Methods: Eighteen male C57BL/6J mice were equally randomized into control group, DSS group and DMQ treatment group. In DSS and DMQ groups, the mice were treated with DSS in drinking water to induce UC, and received intraperitoneal injections of sterile PBS or DMQ (20 mg/kg) during modeling.