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J Infect Dis. 2016 Aug 15;214(4):644-8. doi: 10.1093/infdis/jiw189. Epub 2016 May 10.

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

Author information

  • 1Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition.
  • 2Meharry Medical College School of Medicine, Nashville, Tennessee.
  • 3Department of Biochemistry and Molecular Biophysics, Washington University in St Louis, Missouri.
  • 4Department of Cancer Biology, Vanderbilt University School of Medicine.
  • 5Department of Biology, The College of William and Mary, Williamsburg, Virginia.
  • 6Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition Department of Cancer Biology, Vanderbilt University School of Medicine.

Abstract

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.

KEYWORDS:

H. pylori; acid resistance; hypochlorhydia

PMID:
27190191
PMCID:
PMC4957439
[Available on 2017-08-15]
DOI:
10.1093/infdis/jiw189
[PubMed - in process]
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