Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model.
Helicobacter pylori infects the human gastric mucosa and elicits an aggressive inflammatory response. Despite the severity of the inflammatory response, the bacterium is able to persist and cause a chronic infection. It is believed that antioxidant defence mechanisms enable this organism to persist. Wild-type H. pylori strain SS1, and KatA- and KapA-deficient mutants, were used to infect C57/BL6 mice to test this hypothesis. Neither KatA nor KapA was essential for the initial colonization of H. pylori SS1 in the murine model of infection. The wild-type SS1 colonized the gastric mucosa at significantly higher levels than both mutants throughout the 24-week experiment. Neither KatA- nor KapA-deficient mutants were able to maintain consistent ongoing colonization for the 24-week period, indicating the necessity of both KapA and KatA in sustaining a long-term infection. At 24 weeks, 5/10 mice inoculated with the KatA mutant and 2/10 mice inoculated with the KapA mutant were colonized, compared with 10/10 of the mice inoculated with the wild-type SS1. An increase in the severity of inflammation in the wild-type-inoculated mice appeared to correlate with the decline in colonization of animals inoculated with the mutants, suggesting that increased oxidative stress militated against continued infection by the mutants. These data indicate that KapA may be of equal or greater importance than KatA in terms of sustained infection on inflamed gastric mucosae.
Harris
Andrew G
AG
Centre for Biomedical Research, Faculty of Sciences, University of Southern Queensland, Toowoomba, Australia 4350.|School of Microbiology and Immunology, University of New South Wales, Sydney, Australia 2052.
Wilson
John E
JE
School of Microbiology and Immunology, University of New South Wales, Sydney, Australia 2052.
Danon
Stephen J
SJ
CSIRO Molecular Science, North Ryde, NSW, Australia 1670.|School of Microbiology and Immunology, University of New South Wales, Sydney, Australia 2052.
Dixon
Michael F
MF
Department of Histopathology, The General Infirmary at Leeds, Leeds LS1 3EX, UK.
Donegan
Kevin
K
School of Quantitative Methods and Mathematical Sciences, University of Western Sydney, Campbelltown, NSW, Australia 2560.
Hazell
Stuart L
SL
Centre for Biomedical Research, Faculty of Sciences, University of Southern Queensland, Toowoomba, Australia 4350.
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D002374:Catalase / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000201:enzymology / Q000472:pathogenicity*; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D018384:Oxidative Stress; D013047:Specific Pathogen-Free Organisms
D001426:Bacterial Proteins; D006861:Hydrogen Peroxide; D002374:Catalase