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BioMed Research International
Volume 2017, Article ID 4101745, 11 pages
Research Article

A Type III Effector NleF from EHEC Inhibits Epithelial Inflammatory Cell Death by Targeting Caspase-4

1State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing 100071, China
2Institute of Health Sciences, Anhui University, Hefei, Anhui 230601, China

Correspondence should be addressed to Hongguang Ren; moc.361@neroib, Junjie Yue; moc.621@eijeuj_euy, and Long Liang;

Received 17 February 2017; Accepted 5 April 2017; Published 16 May 2017

Academic Editor: Yun-Peng Chao

Copyright © 2017 Ting Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Enterohemorrhagic E. coli (EHEC) is a highly pathogenic bacterial strain capable of inducing severe gastrointestinal disease. Here, we show that EHEC uses the T3SS effector NleF to counteract the host inflammatory response by dampening caspase-4-mediated inflammatory epithelial cell death and by preventing the production of IL-1β. The other two inflammatory caspases, caspase-1 and caspase-5, are not involved in EHEC ΔnleF-induced inflammatory cell death. We found that NleF not only interrupted the heterodimerization of caspase-4-p19 and caspase-4-p10, but also inhibited the interaction of caspase-1 and caspase-4. The last four amino acids of the NleF carboxy terminus are essential in inhibiting caspase-4-dependent inflammatory cell death.