title: Effect of Helicobacter pylori on gastric epithelial cells.
abstract: 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.
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Shatha
authors.initials: S
authors.lastname: Alzahrani
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Taslima T
authors.initials: TT
authors.lastname: Lina
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Jazmin
authors.initials: J
authors.lastname: Gonzalez
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Irina V
authors.initials: IV
authors.lastname: Pinchuk
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Ellen J
authors.initials: EJ
authors.lastname: Beswick
authors.affiliation: Shatha Alzahrani, Taslima T Lina, Irina V Pinchuk, Victor E Reyes, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, United States.
authors.forename: Victor E
authors.initials: VE
authors.lastname: Reyes
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D005753:Gastric Mucosa / Q000276:immunology / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D005838:Genotype; D016481:Helicobacter Infections / Q000276:immunology / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D018928:Immunity, Mucosal; D050296:Microbial Viability; D015398:Signal Transduction; D014774:Virulence
keywords: Apoptosis; Chronic inflammation; Gastric cancer; Gastric diseases; Gastric epithelial cells; Helicobacter pylori; Proinflammatory cytokines