Abstract
Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1) in gastric epithelial cells plays an important role in innate immune responses against H. pylori. The detection of H. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense against H. pylori infection of the stomach.
Highlights
Helicobacter pylori is a microaerophilic, gram-negative bacterium that colonizes human gastric mucosa [1, 2]
It is well established that the gastric mucosa of patients with H. pylori infection is characterized by adaptive Th1 responses, the innate immune responses leading to such Th1 responses are poorly understood
In in vitro studies we found that H. pylori infection of AGS cells led to a massive increase of IFN-β and IP10 production, which was accompanied by the activation of both Stat1 and Stat2, suggesting that cag+ H. pylori organisms do activate epithelial cells via the IFNβ-IFN-stimulated gene factor 3 (ISGF3) pathway
Summary
Helicobacter pylori is a microaerophilic, gram-negative bacterium that colonizes human gastric mucosa [1, 2]. On the other hand, TLR signaling may not necessarily play a major role since gastric ECs have been shown to be hyporesponsive to TLR ligands [12] Another possibility is that epithelial cell signaling occurs through Nucleotide-binding oligomerization domain, Leucine-rich Repeat-containing (NLR) proteins, that is, a rapidly emerging family of innate immune regulatory molecules that function much like TLRs but with different signaling mechanisms [13]. Viala et al has shown that eradication of H. pylori requires the sensing of PGN by cytosolic NOD1 expressed in gastric ECs [15] Since this latter discovery, several mechanisms regarding NOD1-mediated mucosal host defense against H. pylori have been proposed. We focus on these mechanisms with the aim of explaining just how NOD1 signaling contributes to gastric inflammation and host defense against H. pylori
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