Gene expression in vivo shows that Helicobacter pylori colonizes an acidic niche on the gastric surface

Abstract

Helicobacter pylori is a gastric-dwelling pathogen responsible, with acid secretion, for peptic ulcer and a 20-fold increase in the risk of gastric cancer. Several transcriptomes have been described after short-term exposure to acidity in vitro, but there are no data identifying the effects of chronic gastric exposure on bacterial gene expression. Comparison of the in vivo to the in vitro transcriptome at pH 7.4 identified several groups of genes of known function that increased expression >2-fold, and three of these respond both to acidity in vitro and to gastric infection. Almost all known acid acclimation genes are highly up-regulated. These include ureA, ureB, and rocF and the pH-gated urea channel, ureI. There is also up-regulation of two groups of motility and chemotaxis genes and for pathogenicity island genes, especially cagA, a predictor for pathogenicity. Most of these genes interact with HP0166, the response element of the pH-sensing two-component histidine kinase, HP0165/HP0166, ArsRS. Based on the pH profile of survival of ureI deletion mutants in vitro and their inability to survive in gastric acidity, the habitat of the organism at the gastric surface is acidic with a pH < 4.0. Hence, the pH of the habitat of H. pylori on the surface of the stomach largely determines the regulation of these specific groups of genes.acid acclimation ͉ gastric pH ͉ global transcriptome ͉ microarray

Iron deficiency accelerates Helicobacter pylori–induced carcinogenesis in rodents and humans

“…Plates tamine synthetase. Urease is required for colonization of the acidic gastric niche (42), while GroEL has been shown to be expressed in conjunction with other known virulence constituents, including FlaA, UreB, VacA, and CagA (43). Further, heat shock proteins, such as GroEL, are associated with the presence of gastric cancer (44).…”

Gastric Acid-Dependent Diseases: A Twentieth-Century Revolution

“…17). The transcriptome of Hp recovered from the gerbil stomach is consistent with a \pH 4.0 habitat [55].…”

A Recombination Puzzle Solved: Role for New DNA Repair Systems in Helicobacter pylori Diversity/Persistence

“…In addition, the H. pylori recN mutant is much more sensitive to low pH than the wild type strain, suggesting that RecN is also involved in repair of acid-induced DNA damage [83]. This could be relevant to its physiological condition, as H. pylori appears to colonize an acidic niche on the gastric surface [41]. As mentioned in the sections above, loss of H. pylori RecA, RuvB or RuvC functions results in a great decrease of DNA recombination frequency.…”