Helicobacter pylori is a spiral gram-negative urease-producing bacterium that can be found in the mucus coating the gastric mucosa or between the mucous layer and gastric epithelium. Multiple factors enable the bacterium to live in the hostile stomach acid environment, including its ability to produce urease, which helps alkalize the surrounding pH. Helicobacter pylori infection is most commonly acquired in childhood and results in a chronic active gastritis that is usually lifelong without specific treatment. Risk factors for acquiring H pylori include low socioeconomic status, household crowding,as well as country of origin.The prevalence of H pylori varies among different countries and is significantly higher in developing than in industrialized countries.The majority of infected persons remain asymptomatic, but approximately 10–15% develop peptic ulcer disease during their lifetime. In addition to causing chronic gastritis and peptic ulcers, H pylori has been associated with the development of gastric adenocarcinoma and gastric mucosa– associated lymphoid tissue (MALT) lymphoma.In 1994,the International Agency for Research on Cancer classified H pylori as a group 1 carcinogen and a definite cause of gastric cancer in humans.
Infection with H pylori increases the risk of peptic ulcers and GI bleeding from threefold to sevenfold. Depending on the population, H pylori is present in up to 70–90% of patients with duodenal ulcers and up to 30–60% of gastric ulcers. Multiple clinical studies show that H pylori eradication reduces ulcer recurrence to less than 10% as compared with recurrences of 70% with acid suppression alone. Helicobacter pylori generally causes mucosal injury and ulcer complications through inflammation and cytokines.Despite a vigorous systemic and mucosal humoral response,antibody production does not lead to eradication of the infection.
A combination of microbial and host factors determines the outcome of H pylori infection. These include the virulence of the organism, host genetics, as well as environmental factors that affect the distribution and severity of gastric inflammation and level of acid secretion. Helicobacter pylori that express the cytotoxin-associated gene A (Cag A–positive strains) reportedly represents virulent strains having greater interactions with humans. Several genes in a genomic fragment that make up a Cag pathogenicity island encode components of a type IV secretion island that translocates Cag A in host cells and affects cell growth and cytokine production.
Cag A is a highly antigenic protein that is associated with a prominent inflammatory response by eliciting interleukin-8 production. Helicobacter pylori strains that also express the vacuolating cytotoxin or the outer membrane protein OipA are similarly associated with a higher risk of diseases,including gastric cancer.
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