{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pruss KM"],"funding":["NIDDK NIH HHS"],"pagination":["261-265"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9067157"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["593(7858)"],"pubmed_abstract":["Several enteric pathogens can gain specific metabolic advantages over other members of the microbiota by inducing host pathology and inflammation. The pathogen Clostridium difficile is responsible for a toxin-mediated colitis that causes 450,000 infections and 15,000 deaths in the United States each year<sup>1</sup>; however, the molecular mechanisms by which C. difficile benefits from this pathology remain unclear. To understand how the metabolism of C. difficile adapts to the inflammatory conditions that its toxins induce, here we use RNA sequencing to define, in a mouse model, the metabolic states of wild-type C. difficile and of an isogenic mutant that lacks toxins. By combining bacterial and mouse genetics, we demonstrate that C. difficile uses sorbitol derived from both diet and host"],"journal":["Nature"],"pubmed_title":["C. difficile exploits a host metabolite produced during toxin-mediated disease."],"pmcid":["PMC9067157"],"funding_grant_id":["R01 DK085025"],"pubmed_authors":["Sonnenburg JL","Pruss KM"],"additional_accession":[]},"is_claimable":false,"name":"C. difficile exploits a host metabolite produced during toxin-mediated disease.","description":"Several enteric pathogens can gain specific metabolic advantages over other members of the microbiota by inducing host pathology and inflammation. The pathogen Clostridium difficile is responsible for a toxin-mediated colitis that causes 450,000 infections and 15,000 deaths in the United States each year<sup>1</sup>; however, the molecular mechanisms by which C. difficile benefits from this pathology remain unclear. To understand how the metabolism of C. difficile adapts to the inflammatory conditions that its toxins induce, here we use RNA sequencing to define, in a mouse model, the metabolic states of wild-type C. difficile and of an isogenic mutant that lacks toxins. By combining bacterial and mouse genetics, we demonstrate that C. difficile uses sorbitol derived from both diet and host","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2026-05-30T15:26:47.509Z","creation":"2025-04-04T10:02:06.837Z"},"accession":"S-EPMC9067157","cross_references":{"pubmed":["33911281"],"doi":["10.1038/s41586-021-03502-6"]}}