Helicobacter Pylori Report

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Introduction Helicobacter pylori, a spiral-shaped, Gram-negative bacterium that colonizes the stomach, is the most common bacterial infection causing peptic ulcer disease secondary to chronic gastritis and represents a major risk factor in the development of gastric cancer (1, 2). Although this bacterium colonizes approximately 50% of the population worldwide, only 15% of those infected will develop gastric disease (2, 5). Therefore, the manifestation of disease depends on the specific strain of H. pylori present and its interactions with host genetic factors and environmental factors. Due to the increasing development of H. pylori antibiotic resistance and its classification as a group I carcinogen, increased understanding of H. pylori transmission …show more content…
pylori survival within this hostile environment is facilitated through its motility and ability to sense urea as well as its production of urease (2, 8). The multiple flagella exhibited by H. pylori allow migration through the thick mucous lining of the stomach to the more neutral epithelial cells underneath via urea-mediated chemotaxis (1, 2, 8). This urea can then be converted into ammonia and carbon dioxide by urease, an enzyme produced by H. pylori. This local production of ammonia results in the local neutralization of stomach acid, providing a more amenable environment for H. pylori migration. Flagellar motility and local ammonia production by H. pylori confer this bacterium with resistance to acid, which is essential to the extracellular adherence of bacteria to the underlying gastric epithelial cells and thus, the establishment of infection via a variety of mechanisms, such as secretion of exotoxins (1, 2, …show more content…
pylori contain vacuolating cytotoxin gene A, which encodes for a 140kDa precursor to VacA (6, 7). Proteolytic processing of this precursor upon exocytosis yields the mature 88kDa toxin, which is activated by the characteristically low pH of the stomach. This mature, active toxin oligomerizes within the plasma membrane of gastric epithelial cells and subsequently causes the formation of anion-selective channels. The presence of these channels enhances the efflux of chloride and bicarbonate ions from the gastric mucosa, which is conducive to H. pylori proliferation. Furthermore, VacA augments paracellular permeability by disrupting tight junctions joining adjacent gastric epithelial cells. This increases the availability of Fe3+ and Ni2+; ions necessary for metabolic functions and urease production, respectively. Since these ions are crucial for the growth of H. pylori, VacA disruption of tight junctions facilitates the development of H. pylori infection. VacA also stimulates apoptosis through an unknown mechanism, which may lead to tissue damage (9). In addition to the effects within gastric epithelial cells, VacA may modulate the functioning of immune cells, thus permitting H. pylori infection to persist. For example, VacA binding and internalization via β2 integrin and LFA-1 on activated T cells inhibits proliferation of these cells through suppressing IL-2 production and downregulating IL-2 receptors on the surface of these immune cells. VacA may
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