Helicobacter pylori in peptic ulcer

Abstract

Helicobacter pylori is a gram-negative, curved, rod-shaped bacterium known to cause gastritis and to be an important factor in the pathogenesis of peptic ulcers. Serological testing has recently been proposed as an aid in diagnosis of H.pylori infections. Helicobacter pylori, like several other mucosal pathogens, probably uses recombination and slipped-strand mispairing within repeats as mechanisms for antigenic variation and adaptive evolution consistent with its restricted niche,

H. pylori has a few regulatory networks, and a limited metabolic repertoire and biosynthetic capacity. Its survival in acid conditions depends, in part, on its ability to establish a positive inside-membrane potential in low pH. We propose that these proteins may be retained on the outside surface of the cell membrane and contribute to the interaction between H. pylori and host cells. Studying the altered gene expression in the infected host cells can understand the regulatory mechanism that control pathological changes. H. pylori resides at the surface of gastric cells would lyse sometime after death, and the bacterial intracellular materials might also influence gastric cells. We speculate that this event is involved in the inflammantory response, which is an important factor of gastritis, ulcers and presumably, gastric cancer. At this moment, we can not make a conclusion whether or not those novels genes were specifically induced for H.pylori lysate, and we would not reject the assumption that yhose genes may be also highly induced by some other pathogenic bacteria.