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A bile metabolite atlas reveals infection-triggered interorgan mediators of intestinal homeostasis and defense

ABSTRACT: A bile metabolite atlas reveals infection-triggered interorgan mediators of intestinal homeostasis and defense

PROVIDER: PRJNA943516 | ENA |

REPOSITORIES: ENA

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	SRR23823465_1.fastq.gz	Fastqsanger.gz
	SRR23823465_2.fastq.gz	Fastqsanger.gz
	SRR23823466_1.fastq.gz	Fastqsanger.gz
	SRR23823466_2.fastq.gz	Fastqsanger.gz

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A bile metabolite atlas reveals infection-triggered interorgan mediators of intestinal homeostasis and defense

Project description:An essential function of the liver is the formation of bile. This aqueous solution is critical for fat absorption and is transported to the duodenum via the common bile duct. Despite extensive studies of bile salts, other components of bile are less well-charted. Here, we characterized the murine bile metabolome and investigated how the microbiota and enteric infection influence bile composition. We discovered that the bile metabolome is not only substantially more complex than appreciated but is dynamic and responsive to the microbiota and enteric infection. Hepatic transcriptomics identified enteric infection-triggered pathways that likely underlie bile remodeling. Enteric infections stimulated elevation of four dicarboxylates in bile that modulated intestinal gut epithelial and microbiota composition, inflammasome activation, and host defense. Our data suggest that enteric infection-associated signals are relayed between the intestine and liver and induce transcriptional programs that shape the bile metabolome, modifying bile’s immunomodulatory and host defense functions.

2023-05-02 | GSE227180 | GEO

Project description:A bile metabolite atlas reveals infection-triggered interorgan mediators of intestinal homeostasis and defense

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Project description:The Arabidopsis Pathoarray 464_001 (GPL3638) was used to compare response of Col-0, pad4-1 (Zhou et al., 1998; Jirage et al., 1999) and sid2-2 (Wildermuth et al., 2001) to Pseudomonas syringae pv. tomato DC3000 hrcC mutant. SA production is drastically reduced in sid2 mutants. PAD4 is required for SA-mediated responses. The results suggested that the SA increase triggered by MAMPs is one major component in the MAMPs-triggered signaling mechanism. Keywords: Responses of Arabidopsis to Pseudomonas syringae pv. tomato DC3000 hrcC mutant

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Project description:Innate lymphoid cells (ILCs) are innate counterparts of adaptive T lymphocytes, contributing to host defense, tissue repair, metabolic homeostasis, and inflammatory diseases. ILCs have been considered to be tissue-resident cells, but whether ILCs move between tissue sites during infection has been unclear. We show here that interleukin-25- or helminth-induced inflammatory ILC2s are circulating cells that arise from resting ILC2s residing in intestinal lamina propria. They migrate to diverse tissues based on sphingosine 1-phosphate (S1P)-mediated chemotaxis that promotes lymphatic entry, blood circulation, and accumulation in peripheral sites, including the lung, where they contribute to anti-helminth defense and tissue repair. This ILC2 expansion and migration is a behavioral parallel to the antigen-driven proliferation and migration of adaptive lymphocytes to effector sites and indicates that ILCs complement adaptive immunity by providing both local and distant tissue protection during infection.

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