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Effect of Helicobacter pylori on gastric epithelial cells

World Journal of Gastroenterology 2014年第36期20卷 12767-12780页

作者： Shatha Alzahrani Taslima T Lina jazmin gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes Department of Microbiology and Immunology University of Texas Medical Branch Galveston TX 77555 United States MSIII School of Medicine University of Texas Medical Branch Galveston TX 77555 United States Department of Internal Medicine University of Texas Medical Branch Galveston TX 77555 United States Departments of Molecular Genetics and Microbiology University of New Mexico Health Sciences Center Albuquerque NM 87131 United States Departments of Pediatricsand and Microbiology and Immunology University of Texas Medical Branch Galves-ton TX 77555 United States

The gastrointestinal epithelium has cells with features that make them a powerful line of defense in innate mucosal immunity. Features that allow gastrointestinal epithelial cells to contribute in innate defense include cell barrier integrity, cell turnover, autophagy, and innate immune responses. Helicobacter pylori (H. pylori) is a spiral shape gram negative bacterium that selectively colonizes the gastric epithelium of more than half of the world’s population. The infection invariably becomes persistent due to highly specialized mechanisms that facilitate H. pylori’s avoidance of this initial line of host defense as well as adaptive immune mechanisms. The host response is thus unsuccessful in clearing the infection and as a result becomes established as a persistent infection promoting chronic inflammation. In some individuals the associated inflammation contributes to ulcerogenesis or neoplasia. H. pylori has an array of different strategies to interact intimately with epithelial cells and manipulate their cellular processes and functions. Among the multiple aspects that H. pylori affects in gastric epithelial cells are their distribution of epithelial junctions, DNA damage, apoptosis, proliferation, stimulation of cytokine production, and cell transformation. Some of these processes are initiated as a result of the activation of signaling mechanisms activated on binding of H. pylori to cell surface receptors or via soluble virulence factors that gain access to the epithelium. The multiple responses by the epithelium to the infection contribute to pathogenesis associated with H. pylori.

关键词： Helicobacter pylori Apoptosis Gastric epithelial cells Proinflammatory cytokines Chronic inflammation Gastric diseases Gastric cancer

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Immune evasion strategies used by Helicobacter pylori

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World Journal of Gastroenterology 2014年第36期20卷 12753-12766页

作者： Taslima T Lina Shatha Alzahrani jazmin gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes Department of Microbiology and Immunology University of Texas Medical Branch Galveston TX 77555 United States MS-III School of Medicine University of Texas Medical Branch Galveston TX 77555 United States Department of Internal Medicine University of Texas Medical Branch Galveston TX 77555 United States Departments of Molecular Genetics and Microbiology University of New Mexico Health Sciences Center Albuquerque NM 87131 United States Departments of Pediatrics and Microbiology and Immunology University of Texas Medical Branch Galveston TX 77555 United Statest

Helicobacter pylori(H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival.

关键词： Helicobacter pylori Immune response Pattern recognition receptors Phagocytes T cells Antigen presenting cells Gastric epithelial cells Vacuolating cytotoxin T4SS

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The Impulsivity and Drinking Motives as Predictor of the Alcohol Consumption in College Students

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Psychology Research 2014年第1期4卷 40-47页

作者： Diana Betancourt Ocampo Sahid Rafael Garcia Campos jazmin Garcia Zarate Laura Alejandra Corona Guevara Alejandro gonzalez-Gonzfilez Universidad Anahuac Mexico Norte Huixquilucan Mexico Universidad Nacional Autonoma de Moxico Mexico City Mexico

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