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J Immunol:厦门大学俞春东教授课题组发表细菌性肠炎研究成果

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摘要 : 2017年1月4日,国际国际免疫学杂志《The Journal of Immunology》上在线发表了厦门大学生命科学学院俞春东教授课题组题为“Steroid Receptor Coactivator 3 Contributes to Host Defense against Enteric Bacteria by Recruiting Neutrophils via Upregulation of CXCL2 Expression”的研究论文。

2017年1月4日,国际国际免疫学杂志《The Journal of Immunology》上在线发表了厦门大学生命科学学院俞春东教授课题组题为“Steroid Receptor Coactivator 3 Contributes to Host Defense against Enteric Bacteria by Recruiting Neutrophils via Upregulation of CXCL2 expression”的研究论文。陈文博博士为论文第一作者,俞春东教授为通讯作者。

细菌性肠炎是一种能够造成人类,尤其是婴幼儿,腹泻和其它并发症的传染性疾病,是当今严重的全球性公共卫生问题之一。小鼠柠檬酸杆菌(C.rodentium)感染小鼠肠道是常常被用来研究细菌性肠炎的动物模型。俞春东教授课题组发现C.rodentium小鼠肠道感染后,与野生型小鼠相比,SRC-3敲除小鼠表现出对C.rodentium清除的缺陷以及严重的肠道组织损伤。进一步的研究发现SRC-3敲除小鼠肠道中对C.rodentium清除起重要作用的中性粒细胞的募集延迟了。相应地,在SRC-3敲除小鼠结肠上皮细胞中负责募集中性粒细胞的趋化因子CXCL2和CXCL5的诱导表达也延迟了。SRC-3是通过激活NF-kB信号通路在转录水平上促进CXCL2的表达。综上所述,在细菌性肠炎中SRC-3对肠道的保护作用至少是通过上调CXCL2的表达来募集中性粒细胞进而清除细菌的。

原文链接:

Steroid Receptor Coactivator 3 Contributes to Host Defense against Enteric Bacteria by Recruiting Neutrophils via Upregulation of CXCL2 Expression

原文摘要:

Steroid receptor coactivator 3 (SRC-3) is a transcriptional coactivator that interacts with nuclear receptors and some other transcription factors to enhance their effects on target gene transcription. We reported previously that SRC-3–deficient (SRC-3−/−) mice are extremely susceptible to Escherichia coli–induced septic peritonitis as a result of uncontrolled inflammation and a defect in bacterial clearance. In this study, we observed significant upregulation of SRC-3 in colonic epithelial cells in response to Citrobacter rodentium infection. Based on these findings, we hypothesized that SRC-3 is involved in host defense against attaching and effacing bacterial infection. We compared the responses of SRC-3−/− and wild-type mice to intestinal C. rodentium infection. We found that SRC-3−/− mice exhibited delayed clearance of C. rodentium and more severe tissue pathology after oral infection with C. rodentium compared with wild-type mice. SRC-3−/−mice expressed normal antimicrobial peptides in the colons but exhibited delayed recruitment of neutrophils into the colonic mucosa. Accordingly, SRC-3−/− mice showed a delayed induction of CXCL2 and CXCL5 in colonic epithelial cells, which are responsible for neutrophil recruitment. At the molecular level, we found that SRC-3 can activate the NF-κB signaling pathway to promote CXCL2 expression at the transcriptional level. Collectively, we show that SRC-3 contributes to host defense against enteric bacteria, at least in part via upregulating CXCL2 expression to recruit neutrophils.

doi:10.4049/​jimmunol.1600300

作者:俞春东 点击:

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