Title

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

Authors

Uma Krishna, Vanderbilt Univ, Sch Med, Dept Med, Div Gastroenterol Hepatol & Nutr, 2215 Garland Ave,1030C Med Res Bldg 4, Nashville, TN 37232 USA;
Judith Romero-Gallo, Vanderbilt Univ, Sch Med, Dept Med, Div Gastroenterol Hepatol & Nutr, 2215 Garland Ave,1030C Med Res Bldg 4, Nashville, TN 37232 USA;
Giovanni Suarez, Vanderbilt Univ, Sch Med, Dept Med, Div Gastroenterol Hepatol & Nutr, 2215 Garland Ave,1030C Med Res Bldg 4, Nashville, TN 37232 USA;
Mark H. Forsyth, Coll William & Mary, Dept Biol, Williamsburg, VA 23185 USA

Document Type

Article

Department/Program

Biology

Journal Title

Journal of Infectious Diseases

Pub Date

2016

Volume

4

Issue

214

First Page

644

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.

Recommended Citation

Krishna, U., Romero-Gallo, J., Suarez, G., Azah, A., Krezel, A. M., Varga, M. G., ... & Peek Jr, R. M. (2016). Genetic evolution of a Helicobacter pylori acid-sensing histidine kinase and gastric disease. The Journal of infectious diseases, 214(4), 644-648.

DOI

10.1093/infdis/jiw189