| Literature DB >> 29141885 |
Josephine Ni1, Ting-Chin David Shen1, Eric Z Chen2, Kyle Bittinger3, Aubrey Bailey4, Manuela Roggiani5, Alexandra Sirota-Madi6, Elliot S Friedman1, Lillian Chau1, Andrew Lin1, Ilana Nissim7, Justin Scott6, Abigail Lauder4, Christopher Hoffmann4, Gloriany Rivas8, Lindsey Albenberg9, Robert N Baldassano9, Jonathan Braun10, Ramnik J Xavier6,10,11, Clary B Clish6, Marc Yudkoff7, Hongzhe Li2, Mark Goulian5, Frederic D Bushman4, James D Lewis1,2, Gary D Wu12.
Abstract
Gut dysbiosis during inflammatory bowel disease involves alterations in the gut microbiota associated with inflammation of the host gut. We used a combination of shotgun metagenomic sequencing and metabolomics to analyze fecal samples from pediatric patients with Crohn's disease and found an association between disease severity, gut dysbiosis, and bacterial production of free amino acids. Nitrogen flux studies using 15N in mice showed that activity of bacterial urease, an enzyme that releases ammonia by hydrolysis of host urea, led to the transfer of murine host-derived nitrogen to the gut microbiota where it was used for amino acid synthesis. Inoculation of a conventional murine host (pretreated with antibiotics and polyethylene glycol) with commensal Escherichia coli engineered to express urease led to dysbiosis of the gut microbiota, resulting in a predominance of Proteobacteria species. This was associated with a worsening of immune-mediated colitis in these animals. A potential role for altered urease expression and nitrogen flux in the development of gut dysbiosis suggests that bacterial urease may be a potential therapeutic target for inflammatory bowel diseases.Entities:
Mesh:
Substances:
Year: 2017 PMID: 29141885 PMCID: PMC5808452 DOI: 10.1126/scitranslmed.aah6888
Source DB: PubMed Journal: Sci Transl Med ISSN: 1946-6234 Impact factor: 17.956