Autophagy in the intestinal epithelium regulates Citrobacter rodentium infection

被引：35

作者：

Inoue, Jun ^{[1
]}

Nishiumi, Shin ^{[1
]}

Fujishima, Yoshimi ^{[1
]}

Masuda, Atsuhiro ^{[1
]}

Shiomi, Hideyuki ^{[1
]}

Yamamoto, Koji ^{[1
]}

Nishida, Masayuki ^{[1
]}

Azuma, Takeshi ^{[1
]}

Yoshida, Masaru ^{[1
,2
,3
]}

机构：

[1] Kobe Univ, Div Gastroenterol, Dept Internal Med, Grad Sch Med,Chu O Ku, Kobe, Hyogo 6500017, Japan

[2] Kobe Univ, Integrated Ctr Mass Spectrometry, Grad Sch Med, Kobe, Hyogo 6500017, Japan

[3] Kobe Univ, Div Metabol Res, Grad Sch Med, Kobe, Hyogo 6500017, Japan

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2012年 / 521卷 / 1-2期

关键词：

Autophagy; Intestinal epithelium; Citrobacter rodentium; Inflammation; Clearance; MURINE COLONIC HYPERPLASIA; MUCOSAL INFECTION; EFFACING PATHOGEN; CROHNS-DISEASE; MICE; CELLS; TUMORIGENESIS; CARDIOMYOPATHY; DEGRADATION; ACTIVATION;

D O I：

10.1016/j.abb.2012.03.019

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Autophagy, a ubiquitous degradation pathway, is important for the survival and homeostasis of cells. Previous studies have demonstrated the role of autophagy in host defense against bacterial infection, but the importance of autophagy in the intestinal epithelium for the regulation of bacterial infection has not been fully elucidated. In this study, we showed that the essential autophagy protein Atg7 is required for resistance to Citrobacter rodentium infection in the intestinal epithelium. Infected mice in which Atg7 had been conditionally deleted from the intestinal epithelium exhibited greater clinical evidence of disease and higher expression levels of pro-inflammatory cytokine mRNA in the large intestine. Moreover, C rodentium clearance was reduced in the Atg7 conditional knockout mice. These results demonstrate that autophagy in intestinal epithelial cells plays an important role in host defense against C. rodentium infection and the regulation of C. rodentium infectious colitis. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：95 / 101

页数：7

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