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
. 2009 Dec;9(6):680-7.
doi: 10.1016/j.coph.2009.09.006. Epub 2009 Oct 12.

Pathogen recognition receptors, cancer and inflammation in the gut

Masayuki Fukata  1 , Maria T Abreu
Affiliations
Review

Pathogen recognition receptors, cancer and inflammation in the gut

Masayuki Fukata et al. Curr Opin Pharmacol. 2009 Dec.

Abstract

The pathogen recognition receptors (PRRs) initiate immediate responses against infection and tissue damage to protect the host from microbial invasion. In response to mucosal damage, intestinal PRR signaling initiates damage repair processes. Recent advances appear to link PRR abnormalities and inflammatory as well as neoplastic intestinal disorders. Emerging evidence suggests a dual role of PRRs, in which they may simultaneously induce tumorigenesis and antitumor immunity. PRR may induce tumor cell proliferation by activating cell survival signaling mainly via NF-kappaB, but this signal can activate dendritic cells to promote antitumor immunity. TLR signaling within the tumor cells may result in evasion of immune surveillance, propagation of metastatic growth, or rather, induction of tumor cell apoptosis depending on ligands. Epithelial cells induce endogenous PRR ligands when damaged or during neoplastic transformation. Targeted manipulation of PRR signaling may provide emerging opportunities for the development of new therapeutic strategies for many gastrointestinal diseases.

PubMed Disclaimer

Conflict of interest statement

There are no conflicts of interest.

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abreu MT, Fukata M, Arditi M. TLR signaling in the gut in health and disease. J Immunol. 2005;174:4453–4460. - PubMed
    1. Kufer TA, Banks DJ, Philpott DJ. Innate immune sensing of microbes by Nod proteins. Ann N Y Acad Sci. 2006;1072:19–27. - PubMed
    1. Brown SL, Riehl TE, Walker MR, Geske MJ, Doherty JM, Stenson WF, Stappenbeck TS. Myd88-dependent positioning of Ptgs2-expressing stromal cells maintains colonic epithelial proliferation during injury. J Clin Invest. 2007;117:258–269. Using Myd88- and prostaglandin-endoperoxide synthase 2 (Ptgs2)-deficient mice, the authors demonstrate an important role of MyD88- dependent signaling in relocation of a Ptgs2-expressing lamina propria stromal cells in response to mucosal injury, which is involved in the regulation of epithelial proliferation and cellular organization within the crypts. - PMC - PubMed
    1. Fukata M, Chen A, Klepper A, Krishnareddy S, Vamadevan AS, Thomas LS, Xu R, Inoue H, Arditi M, Dannenberg AJ, et al. Cox-2 is regulated by Toll-like receptor-4 (TLR4) signaling: Role in proliferation and apoptosis in the intestine. Gastroenterology. 2006;131:862–877. - PMC - PubMed
    1. Fukata M, Chen A, Vamadevan AS, Cohen J, Breglio K, Krishnareddy S, Hsu D, Xu R, Harpaz N, Dannenberg AJ, et al. Toll-like receptor-4 promotes the development of colitis-associated colorectal tumors. Gastroenterology. 2007;133:1869–1881. The authors demonstrate an increased expression of TLR4 in human and murine model of colitis-associated dysplasia. TLR4-deficient mice show significantly lower incidence and size of colorectal tumors in the colitis-associated cancer model. - PMC - PubMed

Publication types

MeSH terms