Gastric Biology of Helicobacter pylori
George Sachs, Yi Wen and David R. Scott
from: Helicobacter pylori: Molecular Genetics and Cellular Biology (Edited by: Yoshio Yamaoka). Caister Academic Press, U.K. (2008)
Helicobacter pylori colonizes the highly acidic environment of the gastric mucosa. H. pylori, although a neutralophile, is able to flourish in its acidic gastric niche by buffering its periplasm to near neutrality using the mechanism of acid acclimation. This unique acid acclimation, in contrast to acid resistance or tolerance expressed by other neutralophiles, is dependent on urease activity, a proton gate urea channel, UreI, that enables rapid urea access to cytoplasmic urease, and a periplasmic membrane anchored α-carbonic anhydrase. The genes encoding these proteins increased transcription in acid in vitro and are members of the acid sensing ArsRS regulon that responds to a decline of periplasmic pH. Analysis of the in vivo transcriptome of H. pylori infecting the gerbil stomach also showed up-regulation of 11 of these 12 genes as well as 23 other genes in the ArsRS regulon indicating that the site of infection is indeed acidic, lowering periplasmic pH to < 6.2. Other genes increased transcription in vivo including some for chemotaxis, motility, transport, cell envelope, adhesion, bioenergetics and metabolism providing information as to other requirements for colonization. Therefore although acid acclimation is necessary it may not be sufficient for gastric colonization read more ...