Genetic evolution of a helicobacter pylori acid-sensing histidine kinase and gastric disease

Uma Krishna, Judith Romero-Gallo, Giovanni Suarez, Ayeetin Azah, Andrzej M. Krezel, Matthew G. Varga, Mark H. Forsyth, Richard M. Peek

Research output: Contribution to journalArticle

4 Scopus citations

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.

Original languageEnglish
Pages (from-to)644-648
Number of pages5
JournalJournal of Infectious Diseases
Volume214
Issue number4
DOIs
StatePublished - Aug 15 2016

Keywords

  • Acid resistance
  • H. pylori
  • Hypochlorhydia

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    Krishna, U., Romero-Gallo, J., Suarez, G., Azah, A., Krezel, A. M., Varga, M. G., Forsyth, M. H., & Peek, R. M. (2016). Genetic evolution of a helicobacter pylori acid-sensing histidine kinase and gastric disease. Journal of Infectious Diseases, 214(4), 644-648. https://doi.org/10.1093/infdis/jiw189