中国免疫学杂志Issue(10)：1313-1319,7.DOI:10.3969/j.issn.1000-484X.2014.10.004
UⅡ／UT系统对LPS刺激枯否细胞固有免疫炎症信号通路TLR4-IRF3的影响
Roles of UⅡ/UT system played in innate immune inflammatory signal pathway TLR4-IRF3 in LPS-stimulated primary Kupffer cells
摘要
Abstract
Objecitve:To investigate effects of urotensin Ⅱ( UⅡ)/UT system on innate immune inflammatory signal pathway TLR4-IRF3 in the lipopolysaccharide (LPS)-stimulated Kupffer cells (KCs).Methods: Rat KCs were isolated and cultured.Pro-in-flammatory cytokines including IL-6,IFN-βand IFN-γwere assayed by ELISA in culture supernatant of KCs.Cell surface TLR4 were tested with flow cytometry technique.Expression of IRF3 were tested with real-time PCR and Western blot.Results: Significant increases were showed in IL-6, IFN-βand IFN-γsecretion, TLR4-expressed positive rates and IRF3 mRNA levels in KCs after stimulated by LPS,but were inhibited via urantide pretreatment.In addition,LPS induced upregulation of nuclear IRF3 protein and downregulation of cytoplasm IRF3 protein in KCs,which were blocked by urantide pretreatment.Conclusion:UⅡ/UT system mediates immune inflammatory response in part through activating TLR 4-IRF3 pathway in LPS-stimulated KCs.关键词
枯否细胞/炎症/脂多糖/UrotensinⅡ/Urantide/Toll样受体4/干扰素调节因子3Key words
Kupffer cell/Inflammation/Lipopolysaccharide/Urotensin Ⅱ/Urantide/TLR4/IRF3分类
医药卫生引用本文复制引用
涂文娟,汪小庭,刘亮明,朱彤,梁冬雨,杨志文,高得勇..UⅡ／UT系统对LPS刺激枯否细胞固有免疫炎症信号通路TLR4-IRF3的影响[J].中国免疫学杂志,2014,(10):1313-1319,7.基金项目
国家自然科学基金项目（81070357、30660066）。 （）
