Genetic Evolution of a Helicobacter pylori Acid-Sensing Histidine Kinase and Gastric Disease.

Krishna U, Romero-Gallo J, Suarez G, Azah A, Krezel AM, Varga MG, Forsyth MH, Peek RM
J Infect Dis. 2016 214 (4): 644-8

PMID: 27190191 · PMCID: PMC4957439 · DOI:10.1093/infdis/jiw189

Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma, which develops within a hypochlorhydric environment. We sequentially isolated H. pylori (strain J99) from a patient who developed corpus-predominant gastritis and hypochlorhydia over a 6-year interval. Archival J99 survived significantly better under acidic conditions than recent J99 strains. H. pylori arsRS encodes a 2-component system critical for stress responses; recent J99 isolates harbored 2 nonsynonymous arsS mutations, and arsS inactivation abolished acid survival. In vivo, acid-resistant archival, but not recent J99, successfully colonized high-acid-secreting rodents. Thus, genetic evolution of arsS may influence progression to hypochlorhydia and gastric cancer.

© The Author 2016. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail

MeSH Terms (15)

Achlorhydria Acids Animals Bacterial Proteins Evolution, Molecular Gastritis Gerbillinae Helicobacter Infections Helicobacter pylori Histidine Kinase Humans Male Mice, Inbred C57BL Microbial Viability Mutation, Missense

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