Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2007:2:401-29.
doi: 10.1146/annurev.pathol.1.110304.100128.

Body traffic: ecology, genetics, and immunity in inflammatory bowel disease

Affiliations
Review

Body traffic: ecology, genetics, and immunity in inflammatory bowel disease

Jonathan Braun et al. Annu Rev Pathol. 2007.

Abstract

The abundant bacteria and other microbial residents of the human intestine play important roles in nutrient absorption, energy metabolism, and defense against microbial pathogens. The mutually beneficial relationship of host and commensal microbiota represents an ancient and major coevolution in composition and mutual regulation of the human mucosa and the resident microbial community. Inflammatory bowel disease (IBD) is a set of chronic, relapsing inflammatory intestinal diseases in which rules of normal host-microbial interaction have been violated. This review considers the components of this host-microbial mutualism and the ways in which it is undermined by pathogenic microbial traits and by host immune and epithelial functions that confer to them susceptibility in patients with IBD. Recent advances in understanding the genetics of IBD and the immunology of host-microbial interaction are opening new strategies for treatments that target host susceptibility, candidate microbial pathogens, and intestinal ecology.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources