Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model

Article


Harris, Andrew G., Wilson, John E., Danon, Stephen J., Dixon, Michael F., Donegan, Kevin and Hazell, Stuart L.. 2003. "Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model." Microbiology. 149 (3), pp. 665-672. https://doi.org/10.1099/mic.0.26012-0
Article Title

Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model

ERA Journal ID2499
Article CategoryArticle
AuthorsHarris, Andrew G. (Author), Wilson, John E. (Author), Danon, Stephen J. (Author), Dixon, Michael F. (Author), Donegan, Kevin (Author) and Hazell, Stuart L. (Author)
Journal TitleMicrobiology
Journal Citation149 (3), pp. 665-672
Number of Pages8
Year2003
Place of PublicationUnited Kingdom
ISSN1350-0872
1465-2080
Digital Object Identifier (DOI)https://doi.org/10.1099/mic.0.26012-0
Abstract

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.

Keywordsanimal model; animal tissue; article; bacterial colonization; bacterial strain; bacterium mutant; controlled study; disease severity; Helicobacter infection; Helicobacter pylori; hypothesis; inflammation; inoculation; mouse strain; nonhuman; oxidative stress; protein deficiency; stomach mucosa
ANZSRC Field of Research 2020310701. Bacteriology
310702. Infectious agents
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Byline AffiliationsUniversity of New South Wales
General Infirmary at Leeds, United Kingdom
University of Western Sydney
Faculty of Sciences
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