"Targeted disruption of the epithelial-barrier by Helicobacter pylori "
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“Targeted disruption of the epithelial-barrier by Helicobacter pylori“ Lydia E Wroblewski1* and Richard M Peek Jr1,2,3* Abstract Helicobacter pylori colonizes the human gastric epithelium and induces chronic gastritis, which can lead to gastric cancer. Through cell-cell contacts the gastric epithelium forms a barrier to protect underlying tissue from pathogenic bacteria; however, H. pylori have evolved numerous strategies to perturb the integrity of the gastric barrier. In this review, we summarize recent research into the mechanisms through which H. pylori disrupts intercellular junctions and disrupts the gastric epithelial barrier. Review The gastric epithelium and Helicobacter pylori
The gastric epithelium is comprised of a single layer of cells that invaginate to form highly organized gastric glands, populated by a distinct variety of cell types. The gastric epithelium can mediate digestive processes; however, an essential function of the gastric mucosal epithelium is to maintain a protective barrier that separates luminal contents containing pathogenic microorganisms such as Helicobacter pylori, from the underlying tissue compartments. H. pylori is a Gram-negative bacterial pathogen that selectively colonizes the gastric epithelium of approximately half of the world’s population [1]. The most common outcome of H. pylori infection is chronic asymptomatic gastritis [2]; however, long-term colonization with H. pylori significantly increases the risk of developing gastro-duodenal diseases. Among infected individuals, approximately 10% develop peptic ulcer disease, 1-3% develop gastric adenocarcinoma, and less than 0.1% develop mucosa associated lymphoid tissue (MALT) lymphoma [3]. Accordingly, H. pylori is classified as a Type I carcinogen, and is considered to be the most common etiologic agent of infection-related cancers, which represent 5.5% of the global cancer burden [4]. H. pylori strains are extremely diverse and have evolved sophisticated virulence strategies that affect host cell signaling pathways and play an important role in * Correspondence: [email protected]; Richard. [email protected] 1 Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA Full list of author information is available at the end of the article
determining the outcome of infection [1]. Disease-associated H. pylori strains possess the cag pathogenicity island (cag PAI), which encodes components of a bacterial type IV secretion apparatus, and functions to export the terminal product of the cag PAI, CagA, across the bacterial membrane and into host gastric epithelial cells [5-7]. There are two mechanisms reported through which H. pylori may translocate CagA into host cells. One mechanism requires the interaction of CagL, a pilus localized component of the type IV secretion apparatus, with integrin a5b1 on host epithelial cells [8]. An alternative mechanism is the type IV secretion apparatus induces externalization of phosphatidylserine,
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