| Relationship between Helicobacter pylori Virulence Factors and Clinical Outcomes |
| Helicobacter pylori 독성인자와 위장관 질환과의 연관성 |
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김성국 |
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경북대학교 의과대학 소화기내과 |
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| Abstract |
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Helicobacter pylori is a Gram-negative bacterium that colonizes the human stomach. H. pylori infects over half of the world population. Infection with the bacterium causes gastritis and peptic ulcer disease and is associated with the development of gastric cancers. However, only a small proportion of individuals develop these complications of infection. The ability of H. pylori to cause this spectrum of diseases depends on host, bacterial, and environmental factors. Of the bacterial factors, there is continuing interest in identifying H. pylori virulence factors that might predict the risk for symptomatic clinical outcomes. It has been proposed that cagA, vacA, iceA, oipA and babA genes are such markers and can identify patients with gastric diseases. CagA gene is a considered to be a marker for a pathogenicity island containing several genes. CagPAI enhance the inflammatory responses such as interleukin(IL)-8 production in gastric epithelial cells. VacA gene is composed of a hypervariable signal sequence and a mid-region alle. Of the vacA subtypes, s1c/m1 subtype is most common without association with clinical outcomes in Korea. A new candidate gene designated iceA has 2 main allelic variants, iceA1 and iceA2 and was suggested to have an association with peptic ulcer. One study suggested that the addition of iceA genotyping might provide a better discrimination. But We can't confirm an association between the iceA allele and clinical outcome in Korea. Several lines of evidence suggest that the presence of babA is related to the occurrence of peptic ulcer. However, the incidence of the babA was low and was not related to peptic ulcer disease in Korean strains. Functional oipA was significantly associated with high H. pylori density, severe neutrophil infiltration, and high mucosal IL-8 levels. Among the factors, oipA functional status was only related to clinical presentation and histologic change until now. (Korean J Helicobacter Res Prac 2002;2:219-223) |
| Key Words:
Virulence factor, Helicobacter pylori, CagA, VacA, IceA, BabA |
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