Journal
AUTOPHAGY
Volume 17, Issue 4, Pages 1057-1058Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2021.1904490
Keywords
Age-related barrier dysfunction; Drosophila; hippo pathway; host-microbe interaction; intestinal regeneration; Ref(2)P/p62; selective autophagy; symbiotic bacteria
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Funding
- Japan Society for the Promotion of Science [19K07061]
- Grants-in-Aid for Scientific Research [19K07061] Funding Source: KAKEN
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Research has shown that autophagy in Drosophila enterocytes suppresses a regenerative response triggered by ROS, with the lack of this suppression leading to excessive cytokine production, age-related barrier dysfunction, and systemic inflammation.
Intestinal epithelium functions as a barrier to protect the host from environmental microbes. Defects in macroautophagy/autophagy combined with intestinal microbes cause a disruption of homeostasis of the tissue, which is associated with the etiology of Crohn disease, an inflammatory bowel disease. However, the molecular mechanism of how autophagy interacts with microbes in the pathology are mostly unrevealed. Our recent findings using Drosophila as a model system showed that autophagy in enterocytes suppresses a regenerative response triggered by reactive oxygen species (ROS) secreted by the host epithelia toward commensal bacteria in the intestine. Without this suppression, accumulation of a receptor protein of selective autophagy, ref(2)P, continuously acts as a signaling platform to cause excessive regeneration via cytokine production by yki (yorkie) activation. This chronic response leads to the acceleration of age-dependent barrier dysfunction, systemic inflammation, and shorter lifespan. These results uncover a novel regulatory network linking commensal bacteria, autophagy, and gut homeostasis, represented by ROS, ref(2)P, and the hippo pathway.
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