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Autophagy down-regulates NLRP3-dependent inflammatory response of intestinal epithelial cells under nutrient deprivation
Yewon Yun1 (Graduate student), Ahreum Baek1 (Research worker), Dong-Eun Kim 1,* (Professor)
1Bioscience and Biotechnology, Konkuk University
Abstract
Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1モ, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1モ, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including proinflammatory cytokines IL-1モ and IL-17E/25, under nutrient deprivation.
Abstract, Accepted Manuscript(in press) [Submitted on September 25, 2020, Accepted on December 11, 2020]
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