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空肠弯曲菌可激活Caco-2细胞单层以及体外感染的原代人结肠组织中的丝裂原活化蛋白激酶。

Campylobacter jejuni activates mitogen-activated protein kinases in Caco-2 cell monolayers and in vitro infected primary human colonic tissue.

作者信息

MacCallum Amanda, Haddock Graham, Everest Paul H

机构信息

Institute of Comparative Medicine, Sir Henry Wellcome Building, University of Glasgow Faculty of Veterinary Medicine, Bearsden Road, Glasgow G61 1QH, UK.

Department of Paediatric Surgery, Yorkhill Hospital, Glasgow G3 8SJ, UK.

出版信息

Microbiology (Reading). 2005 Aug;151(Pt 8):2765-2772. doi: 10.1099/mic.0.27979-0.

Abstract

The mitogen-activated protein kinases (MAPKs) play a central role in many host signalling pathways. These signalling proteins are known to be involved in host responses against invasive bacteria including generation of chemotactic and inflammatory cytokines. It was hypothesized that Campylobacter jejuni may activate MAPKs, as intestinal infection may induce a clinical and pathological picture of acute colonic inflammation. Infection of Caco-2 cell monolayers (human colonic epithelial cell line) and human colonic tissue with C. jejuni in vitro demonstrated increased MAPK activity for ERK 1/2 (p44/42 MAPK), JNK and p38 MAPKs. Kinase activity and phosphorylated forms were increased in infected Caco-2 cells and human colonic explants, suggesting that these pathways are important in inflammatory responses induced by C. jejuni in man.

摘要

丝裂原活化蛋白激酶(MAPKs)在许多宿主信号通路中起核心作用。已知这些信号蛋白参与宿主对侵袭性细菌的反应,包括趋化性和炎性细胞因子的产生。据推测,空肠弯曲菌可能激活MAPKs,因为肠道感染可能诱发急性结肠炎症的临床和病理表现。体外将空肠弯曲菌感染Caco-2细胞单层(人结肠上皮细胞系)和人结肠组织,结果显示ERK 1/2(p44/42 MAPK)、JNK和p38 MAPKs的MAPK活性增加。感染的Caco-2细胞和人结肠外植体中的激酶活性和磷酸化形式均增加,表明这些信号通路在空肠弯曲菌诱发的人类炎症反应中很重要。

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