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Review
. 2013 May;6(3):451-63.
doi: 10.1038/mi.2013.13. Epub 2013 Mar 20.

The role of pattern recognition receptors in intestinal inflammation

M Fukata  1 , M Arditi
Affiliations
Review

The role of pattern recognition receptors in intestinal inflammation

M Fukata et al. Mucosal Immunol. 2013 May.

"VSports在线直播" Abstract

Recognition of microorganisms by pattern-recognition receptors (PRRs) is the primary component of innate immunity that is responsible for the maintenance of host-microbial interactions in intestinal mucosa. Dysregulation in host-commensal interactions has been implicated as the central pathogenesis of inflammatory bowel disease (IBD), which predisposes to developing colorectal cancer. Recent animal studies have begun to outline some unique physiology and pathology involving each PRR signaling in the intestine. The major roles played by PRRs in the gut appear to be the regulation of the number and the composition of commensal bacteria, epithelial proliferation, and mucosal permeability in response to epithelial injury. In addition, PRR signaling in lamina propria immune cells may be involved in induction of inflammation in response to invasion of pathogens. Because some PRR-deficient mice have shown variable susceptibility to colitis, the outcome of intestinal inflammation may be modified depending on PRR signaling in epithelial cells, immune cells, and the composition of commensal flora. Through recent findings in animal models of IBD, this review will discuss how abnormal PRR signaling may contribute to the pathogenesis of inflammation and inflammation-associated tumorigenesis in the intestine VSports手机版. .

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Conflict of interest statement

The authors declared no conflict of interest.

Figures (V体育官网)

Figure 1
Figure 1
The pattern-recognition receptor pathway inducing production of mature interleukin (IL)-18 and IL-1β. Upon recognition of pathogens, Toll-like receptor (TLR) signaling (mainly TLR4) induces transcription of IL-18 and IL-1β. Expression of mRNA for these genes produces pro-forms of IL-18 and IL-1β protein within the cytosol. At the same time, TLR signaling induces reactive oxygen species (ROS) generation and following release of mitochondrial DNA, which activates nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). NLRs are also activated by detecting various ligands introduced via phagocytosis followed by lysosomal stabilization, bacterial type III secretion system, or intracellular metabolic and/or enzymatic activities. The activated NLRs are homo- or hetero-oligomalized to form multi-protein complex termed “inflammasome” that activate caspase-1. Activated caspase-1 induces proteolytic conversion of pro-IL-18 and pro-IL-1β to mature IL-18 and IL-1β to release the active form of these cytokines. ASC, apoptosis-associated speck-like protein; CARD, caspase activation and recruitment domain; CIITA, MHC class II transcription activator; HET-E, incompatibility locus protein from podospora anserina; MAPK, mitogen-activated protein kinase; Mt DNA, mitochondrial DNA; NACHT, neuronal apoptosis inhibitory protein; NBD, nucleotide-binding domain; NF, nuclear factor; NLRP3, NLR protein 3; PYD, pyrin domain; TP1, telomerase-associated protein. PowerPoint slide
Figure 2
Figure 2
Pattern-recognition receptors share immune signaling pathways. Most Toll-like receptors (TLRs) except for TLR3 induce nuclear factor (NF)-κB activation through the myeloid differentiation primary response gene 88 (MyD88) pathway. TLR3 exclusively induces IRF3 activation through the TIR-domain-containing adapter-inducing interferon (IFN)-β (TRIF) pathway. The TRIF pathway is shared by TLR4 and TLR5 (in intestinal epithelial cells). Nucleotide-binding oligomerization domain 1 (NOD1) and NOD2 also activate NF-κB via the RICK (receptor-interacting serine/threonine kinase) pathway. TLRs and NODs also induce activate mitogen-activated protein (MAP)-kinases. AP-1, activator protein 1; CARD, caspase activation and recruitment domain; IRF, interferon regulatory factor; TAK1, transforming growth factor-β-activated kinase 1; TRAF, tumor necrosis factor receptor-associated factor; TRAM, TRIF-related adapter molecule. PowerPoint slide
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