Digestive Diseases and Sciences

, Volume 48, Issue 5, pp 976–985

Decreased Gastric Bacterial Killing and Up-Regulation of Protective Genes in Small Intestine in Gastrin-Deficient Mouse

Authors

  • Francis J. Sun
    • Laboratory Animal Resources
  • Simran Kaur
    • Department of Anatomy & Cell BiologyUniversity of Kansas Medical Center
  • Donna Ziemer
    • Department of Anatomy & Cell BiologyUniversity of Kansas Medical Center
  • Snigdha Banerjee
    • Department of Anatomy & Cell BiologyUniversity of Kansas Medical Center
  • Linda C. Samuelson
  • Robert C. De Lisle
    • Department of Anatomy & Cell BiologyUniversity of Kansas Medical Center
Article

DOI: 10.1023/A:1023068116934

Cite this article as:
Sun, F.J., Kaur, S., Ziemer, D. et al. Dig Dis Sci (2003) 48: 976. doi:10.1023/A:1023068116934

Abstract

Gastrin regulates gastric acid secretion, believed to be primarily responsible for killing ingested microbes. We examined gastric killing of gavaged E. coli in gastrin-deficient mice, which have decreased gastric acid production. Additionally, the expression of intestinal genes involved in epithelial protection were analyzed: the mucus layer glycoprotein muclin, the polymeric Ig receptor, trefoil factor 3, and small proline-rich protein 2a (sprr2a). Gastric pH was 2.5 pH units greater in gastrin-deficient mice, and E. coli survival was increased greater than 20-fold at 10 min after gavage compared to control. Muclin and sprr2a gene expression were significantly increased (2.0- and 2.6-fold) in the intestine, and antibiotic treatment reversed these effects. In conclusion, reduced gastric acid secretion results in increased survival of ingested microorganisms in gastrin-deficient mice. Bacterial survival is associated with increased expression of muclin and sprr2a in the intestine, indicating that these genes play protective roles in the intestine.

gastrinintestinemuclinpolymeric Ig receptorsmall proline-rich protein 2atrefoil factor3

Copyright information

© Plenum Publishing Corporation 2003