Pathogenic properties of Helicobacter pylori

Helicobacter pylori possesses factors that allow it to colonize the gastrointestinal mucosa and persist at that site. Here it produces adverse pathological changes, and thereby causes disease. Colonization factors: animal models have shown that motility and the production of urease are essential for colonization by H. pylori. The ability of an organism to adhere to host structures is often considered pivotal in colonization. A number of adhesins associated with H. pylori have been described, which may imply that adherence is a multistep process and that different adhesins mediate adherence to different sites in the gastric tissue. Persistence factors: H. pylori lipopolysaccharide (LPS) possess low immunological activity, thereby minimizing the local inflammatory response and contributing to the persistence of the infection. There is also evidence that the LPS affects the qualitative nature of gastric mucin and stimulates pepsinogen secretion. Whether survival during exposure to antimicrobial agents is aided by the development of coccoid forms with intact membranes and polyphosphate energy reserves is not yet known. Putative disease-inducing factors: these include the vacuolating cytotoxin that is capable of inducing gastric ulceration in mice, ammonia products that induce vacuolation, and phospholipases that may affect the hydrophobicity of the mucosa. Mimicry of Lewis blood group antigens on the surface of H. pylori may also contribute to pathogenesis. Characteristics of certain strains, such as the expression of a cytotoxin-associated gene (cagA) and the ability to induce rapid chemiluminescence in neutrophils, are associated with the induction of peptic ulceration.