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Pathogenesis of helicobacter pylori infection involves interaction between host and bacteria
Helicobacter pylori is the most ubiquitous bacterial infection worldwide infecting at least 50% of the world‘s population. Scientific evidence abound on the age long cohabitation of H. pylori and humans. However, following infection, development of disease depends upon three main factors namely: the virulence of the infecting H. pylori strain; the type and extent of the host immune response to infection, and modulating cofactors such as smoking and diet. It is now clear that both bacterial virulence factors and host susceptibility play key roles in disease pathogenesis. The nature and levels of these interactions between these major factors has been found to determine the spectrum of clinical outcomes of the infection with this important bacterium. Virulence factors include the cag pathogenicity island, which induces pro-inflammatory, pro-proliferative epithelial cell signaling; the cytotoxinVacA, which causes epithelial damage; and an adhesin, BabA. Host genetic polymorphisms that lead to high-level pro-inflammatory cytokine release in response to infection increase cancer risk. Pathogenesis is also dependent upon inflammation, mainly through a Th-1 acquired immune response.