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
. 2013 Jan;29(1):15-22.
doi: 10.1097/MOG.0b013e32835a68ea.

Nod-like receptors in intestinal host defense: controlling pathogens, the microbiota, or both?

Affiliations
Review

Nod-like receptors in intestinal host defense: controlling pathogens, the microbiota, or both?

Susan J Robertson et al. Curr Opin Gastroenterol. 2013 Jan.

Abstract

Purpose of review: Nod-like receptors (NLRs) are intracellular innate immune sensors of microbes and danger signals that control multiple aspects of inflammatory responses. We review the evidence that highlights the critical importance of NLRs in the host response to intestinal pathogens. Moreover, we discuss the potential roles played by NLRs in the dynamic control of the intestinal microbiota and how commensal microorganisms may affect host susceptibility to enteric bacterial pathogens through interactions with NLRs as well as with invading pathogens.

Recent findings: Recent studies targeting the intestinal microbiota in the context of NLR deficiencies suggest inherent alterations in bacterial density or abundance may underlie the development of inflammatory diseases. As commensal microorganisms may also affect host susceptibility to enteric bacterial pathogens, NLRs might promote intestinal innate immune defense through mechanisms more complex than previously anticipated.

Summary: The inclusion of the intestinal microbiota as a critical parameter in innate immunity represents an exciting new dimension for understanding NLR functioning and the clinical implications for human health.

PubMed Disclaimer

Similar articles

Cited by

Publication types

Substances

LinkOut - more resources