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ABSTRACT: Bacteroides vulgatus&Anti-hyperlipidaemia

PROVIDER: PRJNA846135 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19548370_1.fastq.gz	Fastqsanger.gz
	SRR19548370_2.fastq.gz	Fastqsanger.gz
	SRR19548371_1.fastq.gz	Fastqsanger.gz
	SRR19548371_2.fastq.gz	Fastqsanger.gz
	SRR19548372_1.fastq.gz	Fastqsanger.gz

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Project description:We previously found that mice deficient in the CD susceptibility gene Nod2 develop small intestinal abnormalities including impaired mucus production by goblet cells and susceptibility to injury, which were associated with interferon-gamma producing intraepithelial lymphocytes. These abnormalities were caused by a striking expansion of a common member of the microbiota, Bacteroides vulgatus. Remarkably, infection of Nod2-deficient mice with the helminth Trichuris muris led to a TH2 response that eliminated B. vulgatus colonization and intestinal abnormalities. In addition, treatment with recombinant IL13 (rIL13) or recombinant IL4 reduced B. vulgatus levels and eliminated goblet cell defects, suggesting that type 2 cytokines alone can reverse intestinal abnormalities in the absence of helminth infection. To determine the mechanism by which type 2 cytokines protected Nod2-/- mice from intestinal abnormalities, we performed RNA-seq on small intestinal tissue from WT, Nod2-/- and rIL13 treated Nod2-/- mice. We found that rIL13 treatment induced a wound healing response characterized by M2 macrophage activation genes. Hence, type 2 cytokines can reverse inflammatory imbalances in the composition of the gut microbiota that occurs in a genetically susceptible host.

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