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Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress [16S]

ABSTRACT: Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress [16S]

PROVIDER: PRJNA911803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22715428.fastq.gz	Fastqsanger.gz
	SRR22715429.fastq.gz	Fastqsanger.gz

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Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress super

Project description:Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress super

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Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress.

Project description:Colonic goblet cells are specialized epithelial cells that secrete mucus to physically separate the host and its microbiota, thus preventing bacterial invasion and inflammation. How goblet cells control the amount of mucus they secrete is unclear. We found that constitutive activation of autophagy in mice via Beclin 1 enables the production of a thicker and less penetrable mucus layer by reducing endoplasmic reticulum (ER) stress. Accordingly, genetically inhibiting Beclin 1-induced autophagy impairs mucus secretion, while pharmacologically alleviating ER stress results in excessive mucus production. This ER-stress-mediated regulation of mucus secretion is microbiota dependent and requires the Crohn's-disease-risk gene Nod2. Overproduction of mucus alters the gut microbiome, specifically expanding mucus-utilizing bacteria, such as Akkermansia muciniphila, and protects against chemical and microbial-driven intestinal inflammation. Thus, ER stress is a cell-intrinsic switch that limits mucus secretion, whereas autophagy maintains intestinal homeostasis by relieving ER stress.

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Cathelicidin deficiency disrupts goblet cell mucus secretion but not mucus associated proteins in Citrobacter rodentium-induced colitis

Project description:Colonic goblet cells respond to invading enteropathogens by secreting Muc2 mucin and other specific goblet cell proteins that physically entrap and expel microbes away from the epithelium. At present, it is unclear how innate effectors in the gut, including small cationic cathelicidin peptides secreted by the intestinal epithelium and leukocytes, contribute to mucus barrier defense during infections. In this study, we used cathelicidin-deficient (Camp-/-) mice, colonoids, and human colonic LS174T goblet cells to elucidate the mechanisms by which cathelicidin regulates goblet cell secretions in innate host defense against attaching/effacing Citrobacter rodentium. We showed that even though Camp-/- littermates infected with C. rodentium displayed increased fecal shedding and epithelial colonization, Muc2 mucin granules were retained in bloated colonic goblet cells that impaired mucus secretion and expressed less mucus-associated proteins, as quantified by proteomic analysis. C. rodentium infected Camp-/- littermates showed impaired reactive oxygen species (ROS) production and transcriptomic profiling associated with decreased ROS biosynthesis and an increase in ROS negative regulators. Camp-/- bone marrow derived macrophages produced less ROS than their wild-type counterparts. In LS174T goblet cells, human cathelicidin LL-37 promptly induced the secretion of goblet cell-associated TFF3 and RELMβ, which was dependent on ROS production. These findings demonstrate that cathelicidin signaling in colonic goblet cells regulates mucus and mucin-associated protein secretion via an ROS-dependent mechanism to clear bacterial infections and restore gut homeostasis.

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Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress super

Project description:This SuperSeries is composed of the SubSeries listed below.

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Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress [16S]

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