Pathogenesis of Helicobacter Pylori Infection: Colonization, Virulence Factors of the Bacterium and Immune and Non-immune Host Response

Abstract

Helicobacter pylori (Hp), a gram-negative, spiral-shaped bacterium is one of the most widely spread pathogens in humans, as it concerns half of the world population. Mechanisms that allow Hp to cause a life-long infection involve modulation of the immune response and host cellular processes which include activation of the innate immune response, resistance to phagocytosis, modulation of dendritic cell activity and regulatory T cells, and production of proinflammatory cytokines. This is accomplished via virulence factors such as colonization factors (a variety of adhesins), factors that allow it to evade host defence (flagella and motility, urease system, induction of hypochlorhydria) and factors that are responsible for tissue injury (heat shock proteins A and B, vacuolating cytotoxin A, neutrophil activating protein of Hp, and cytotoxin-associated gene A). The interaction between bacterial effectors, environmental factors (genetic susceptibility to infection) and factors that modulate the host's response, such as polymorphisms in genes encoding cytokines or cytokine receptors, have been shown to influence the clinical outcome of Hp infection either towards peptic ulcer and/or cancer. Future studies, directed toward understanding interactions between Hp and immune cells in vivo, may lead to the development of novel therapeutic approaches for eradication of Hp.