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Human oral metagenome

ABSTRACT: Comparative metagenomics reveals taxonomically idiosyncratic yet functionally congruent communities in periodontitis

PROVIDER: PRJNA508385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9641790_1.fastq.gz	Fastqsanger.gz
	SRR9641790_2.fastq.gz	Fastqsanger.gz
	SRR9641800_1.fastq.gz	Fastqsanger.gz
	SRR9641800_2.fastq.gz	Fastqsanger.gz
	SRR9641810_1.fastq.gz	Fastqsanger.gz

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Project description:At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrate that epithelial intrinsic production of IL-23 triggers an inflammatory loop in the prevalent oral disease, periodontitis. Epithelial IL-23 expression localized to areas proximal to the disease-associated microbiome, is evident both in experimental models and in patients with common and genetic forms of disease. Mechanistically, flagellated microbial species of the periodontitis microbiome, trigger epithelial IL-23 induction in a TLR5-dependent manner. Intriguingly, unlike other Th17-driven diseases, here non-hematopoietic cell-derived IL-23 serves as an initiator of pathogenic inflammation. Beyond periodontitis, analysis of publicly available datasets reveals expression of epithelial IL-23 in settings of infection, malignancy, and autoimmunity, suggesting a broader role for epithelial-intrinsic IL-23 in human disease. Collectively, this work highlights an unappreciated role for the barrier epithelium in the induction of IL-23-mediated inflammation.

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