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Autophagy controls an intrinsic host defense to bacteria by promoting epithelial cell survival: a murine model

Authors
 Sun-Young Chang  ;  Se-Na Lee  ;  Jin-Young Yang  ;  Dong Wook Kim  ;  Joo-Heon Yoon  ;  Hyun-Jeong Ko  ;  Michinaga Ogawa  ;  Chihiro Sasakawa  ;  Mi-Na Kweon 
Citation
 PLOS ONE, Vol.8(11) : e81095, 2013 
Journal Title
PLOS ONE
Issue Date
2013
MeSH
Animals ; Apoptosis ; Autophagy/genetics* ; Bacterial Load ; Cell Survival ; Dysentery, Bacillary/immunology* ; Dysentery, Bacillary/microbiology ; Dysentery, Bacillary/pathology ; Gene Expression Profiling ; Gene Expression Regulation ; Host-Pathogen Interactions ; Immunity, Innate* ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Mice ; Mice, Inbred C57BL ; Paneth Cells/immunology ; Paneth Cells/microbiology ; Paneth Cells/pathology* ; Peyer's Patches/immunology ; Peyer's Patches/microbiology ; Peyer's Patches/pathology* ; Shigella flexneri/immunology*
Keywords
Animals ; Apoptosis ; Autophagy/genetics* ; Bacterial Load ; Cell Survival ; Dysentery, Bacillary/immunology* ; Dysentery, Bacillary/microbiology ; Dysentery, Bacillary/pathology ; Gene Expression Profiling ; Gene Expression Regulation ; Host-Pathogen Interactions ; Immunity, Innate* ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Mice ; Mice, Inbred C57BL ; Paneth Cells/immunology ; Paneth Cells/microbiology ; Paneth Cells/pathology* ; Peyer's Patches/immunology ; Peyer's Patches/microbiology ; Peyer's Patches/pathology* ; Shigella flexneri/immunology*
Abstract
Cell death is a critical host response to regulate the fate of bacterial infections, innate immune responses, and ultimately, disease outcome. Shigella spp. invade and colonize gut epithelium in human and nonhuman primates but adult mice are naturally resistant to intra-gastric Shigella infection. In this study, however, we found Shigella could invade the terminal ileum of the mouse small intestine by 1 hour after infection and be rapidly cleared within 24 h. These early phase events occurred shortly after oral infection resulting in epithelial shedding, degranulation of Paneth cells, and cell death in the intestine. During this process, autophagy proceeded without any signs of inflammation. In contrast, blocking autophagy in epithelial cells enhanced host cell death, leading to tissue destruction and to inflammation, suggesting that autophagic flow relieves cellular stress associated with host cell death and inflammation. Herein we propose a new concept of “epithelial barrier turnover” as a general intrinsic host defense mechanism that increases survival of host cells and inhibits inflammation against enteric bacterial infections, which is regulated by autophagy.
Files in This Item:
T201304086.pdf Download
DOI
10.1371/journal.pone.0081095
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
Yonsei Authors
Yoon, Joo Heon(윤주헌)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/88512
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