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Influence of gastric acid on susceptibility to infection with ingested bacterial pathogens.

Authors
  • Tennant, Sharon M
  • Hartland, Elizabeth L
  • Phumoonna, Tongted
  • Lyras, Dena
  • Rood, Julian I
  • Robins-Browne, Roy M
  • van Driel, Ian R
Type
Published Article
Journal
Infection and Immunity
Publisher
American Society for Microbiology
Publication Date
Feb 01, 2008
Volume
76
Issue
2
Pages
639–645
Identifiers
PMID: 18025100
Source
Medline
License
Unknown

Abstract

Despite the widely held belief that gastric acid serves as a barrier to bacterial pathogens, there are almost no experimental data to support this hypothesis. We have developed a mouse model to quantify the effectiveness of gastric acid in mediating resistance to infection with ingested bacteria. Mice that were constitutively hypochlorhydric due to a mutation in a gastric H(+)/K(+)-ATPase (proton pump) gene were infected with Yersinia enterocolitica, Salmonella enterica serovar Typhimurium, Citrobacter rodentium, or Clostridium perfringens cells or spores. Significantly greater numbers of Yersinia, Salmonella, and Citrobacter cells (P < OR = 0.006) and Clostridium spores (P = 0.02) survived in hypochlorhydric mice, resulting in reduced median infectious doses. Experiments involving intraperitoneal infection or infection of mice treated with antacids indicated that the increased sensitivity of hypochlorhydric mice to infection was entirely due to the absence of stomach acid. Apart from establishing the role of gastric acid in nonspecific immunity to ingested bacterial pathogens, our model provides an excellent system with which to investigate the effects of hypochlorhydria on susceptibility to infection and to evaluate the in vivo susceptibility to gastric acid of orally administered therapies, such as vaccines and probiotics.

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