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Title 

NQO1-knockout mice are highly sensitive to Clostridium difficile toxin A-induced enteritis

Authors 

S T NamJung Hwan HwangD H KimL F LuJ HongP ZhangI N YoonJ S HwangH K ChungM ShongChul Ho LeeH Kim

Publisher 

The Korean Society for Applied Microbiology

Issue Date 

2016

Citation 

Journal of Microbiology and Biotechnology, vol. 26, no. 8, pp. 1446-1451

Keywords 

Bacterial toxinsBarrier functionClostridium difficileEnteritisGut epithelial cell tight junctionNQO1

Abstract 

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.

ISSN 

1017-7825

Link 

http://dx.doi.org/10.4014/jmb.1603.03041

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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