Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 290, Issue 33, Pages 20511-20526Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.632257
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Funding
- Precursory Research for Embryonic Science and Technology
- Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology, Japan [24390018]
- Institute for Fermentation, Osaka
- Honjo International Scholarship Foundation
- [26-7438]
- Grants-in-Aid for Scientific Research [24390018, 15K14955] Funding Source: KAKEN
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Genome-wide association studies of inflammatory bowel diseases identified susceptible loci containing an autophagy-related gene. However, the role of autophagy in the colon, a major affected area in inflammatory bowel diseases, is not clear. Here, we show that colonic epithelial cell-specific autophagy-related gene 7 (Atg7) conditional knock-out (cKO) mice showed exacerbation of experimental colitis with more abundant bacterial invasion into the colonic epithelium. Quantitative PCR analysis revealed that cKO mice had abnormal microflora with an increase of some genera. Consistently, expression of antimicrobial or antiparasitic peptides such as angiogenin-4, Relm beta, intelectin-1, and intelectin-2 as well as that of their inducer cytokines was significantly reduced in the cKO mice. Furthermore, secretion of colonic mucins that function as a mucosal barrier against bacterial invasion was also significantly diminished in cKO mice. Taken together, our results indicate that autophagy in colonic epithelial cells protects against colitis by the maintenance of normal gut microflora and secretion of mucus.
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