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The Korean Journal of Helicobacter  and Upper Gastrointestinal Research 2006;6(1):1-10.
Published online June 1, 2006.
Host Defense System against Helicobacter pylori Infection
Helicobacter pylori 감염에 대한 숙주의 방어시스템
서울대학교 약학대학 발암기전 및 분자암예방 국가지정연구실, 아주대학교 의과대학 소화기내과학교실 및 간 및 소화기질환 유전체연구센터
Even though Helicobacter pylori infection is generally acknowledged as etiologic microbe for several gastric diseases including gastric cancer, still unsolved question is that why the most of the infected persons remain asymptomatic, while others suffered from complicating peptic ulcer diseases and chronic atrophic gastritis. Neither host genetic polymorphism nor bacterial virulence factors explain the discrepancies. As far as damaging factors are engaged, chronic persistent, uncontrolled gastric inflammations by H. pylori are possible basis for ensuing gastric carcinogenesis, for which COX-2 or nitric oxide had been implicated as playing a crucial role in the progress of H. pylori-associated gastric inflammation and carcinogenesis and their expressions are primarily controlled by the transcriptional regulation. Both genes have nuclear factor-kappaB (NF-κB)-binding sites in their promoter regions, and H. pylori is known to stimulate activation of NF-κB. Another oxidant-sensitive transcription factor, activator protein-1 (AP-1) mediates the H. pylori-induced COX-2, iNOS, and IL-8 gene transcription. Only scant information was reported about the adaptive cellular responses to H. pylori-induced proinflammatory and prooxidative injury. A wide array of phase II detoxifying or antioxidant enzymes constitute a fundamental cellular defense system against oxidative and proinflammatory insults. One of the major cellular antioxidant/ detoxifying enzymes is heme oxygenase-1 (HO-1). The H. pylori treatment enhanced antioxidant response element (ARE) binding and nuclear translocation of Nrf2, a redox-sensitive transcription factor responsible for regulating expression of many antioxidant and detoxifying genes, including HO-1. Based on these facts, we hypothesized that the balance between damaging factors and defenseive factors after H. pylori infection can determine the outcomes of H. pylori infection. In this review article, we describe that H. pylori infection can trigger the proinflammatory response through up-regulation of COX-2, which provokes adaptive/defensive response by Nrf2-mediated up- regulation of antioxidant enzymes, such as HO-1, thereby, protecting cells and tissues against subsequent prooxidative and proinflammatory insults. (The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2006;6:1-10)
Key Words: Helicobacter pylori, Inflammation response, Cyclooxgenase-2, Defense mechanism, Nrf2, ARE

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