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
. 2010 Mar 19;140(6):859-70.
doi: 10.1016/j.cell.2010.01.023.

Homeostasis and inflammation in the intestine

Wendy S Garrett  1 , Jeffrey I Gordon, Laurie H Glimcher
Affiliations
Review

Homeostasis and inflammation in the intestine

Wendy S Garrett et al. Cell. .

Abstract

The gut is home to our largest collection of microbes. The ability of the immune system to coevolve with the microbiota during postnatal life allows the host and microbiota to coexist in a mutually beneficial relationship. Failure to achieve or maintain equilibrium between a host and its microbiota has negative consequences for both intestinal and systemic health. In this Review, we consider the many cellular and molecular methods by which inflammatory responses are regulated to maintain intestinal homeostasis and the disease states that can ensue when this balance is lost.

PubMed Disclaimer

Figures

Figure 1
Figure 1. The gut landscape: Maintaining intestinal homeostasis
The mucus layer, sitting atop the intestinal epithelium, is a key component of the mucosal barrier and also is both a source of nutrients and a microhabitat for bacterial members of the microbiota. The epithelial crypt-villus axis differs between the small and large intestine. The populating enterocyte populations vary as well. M cells and Paneth cells are restricted to the small intestine. Intestinal immune cells that mediate tolerance-inducing responses and participate in host defense, localize to inductive sites. These sites include Peyers patches (small intestine), lymphoid follicles, and colonic patches (large intestine) and effector sites such as the epithelium and underlying lamina propria.
Figure 2
Figure 2. Regulators of host-microbial interactions in the gut
The commensal microbiota, intestinal epithelial cells, and intestinal immune cells engage in a complex crosstalk. Epithelial cells, M cells, and dendritic cells (DCs) can directly sense and sample the intestinal contents and communicate information about the microbiota to other subsets of immune cells. The Toll-like receptors are one class of microbe-sensing molecules expressed by epithelial cells, M cells and DCs. Cytokines, chemokines, and host and microbial metabolites are key molecular mediators of intestinal homeostasis that influence responses of both host and microbe.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Amit I, Garber M, Chevrier N, Leite AP, Donner Y, Eisenhaure T, Guttman M, Grenier JK, Li W, Zuk O, et al. Unbiased Reconstruction of a Mammalian Transcriptional Network Mediating Pathogen Responses. Science. 2009 epub. - PMC - PubMed
    1. Androulidaki A, Iliopoulos D, Arranz A, Doxaki C, Schworer S, Zacharioudaki V, Margioris AN, Tsichlis PN, Tsatsanis C. The kinase Akt1 controls macrophage response to lipopolysaccharide by regulating microRNAs. Immunity. 2009;31:220–231. - PMC - PubMed
    1. Antar AA, Konopka JL, Campbell JA, Henry RA, Perdigoto AL, Carter BD, Pozzi A, Abel TW, Dermody TS. Junctional adhesion molecule-A is required for hematogenous dissemination of reovirus. Cell Host Microbe. 2009;5:59–71. - PMC - PubMed
    1. Artis D. Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut. Nat Rev Immunol. 2008;8:411–420. - PubMed
    1. Atarashi K, Nishimura J, Shima T, Umesaki Y, Yamamoto M, Onoue M, Yagita H, Ishii N, Evans R, Honda K, et al. ATP drives lamina propria T(H)17 cell differentiation. Nature. 2008;455:808–812. - PubMed

Publication types