A role for altered phagosome maturation in the long-term persistence of Helicobacter pylori infection

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dc.contributor.authorBorlace, G.
dc.contributor.authorKeep, S.
dc.contributor.authorProdoehl, M.
dc.contributor.authorJones, H.
dc.contributor.authorButler, R.
dc.contributor.authorBrooks, D.
dc.date.issued2012
dc.description.abstractThe vigorous host immune response that is mounted against Helicobacter pylori is unable to eliminate this pathogenic bacterium from its niche in the human gastric mucosa. This results in chronic inflammation, which can develop into gastric or duodenal ulcers in 10% of infected individuals and gastric cancer in 1% of infections. The determinants for these more severe pathologies include host (e.g., high IL-1β expression polymorphisms), bacterial [e.g., cytotoxicity-associated gene (cag) pathogenicity island], and environmental (e.g., dietary nitrites) factors. However, it is the failure of host immune effector cells to eliminate H. pylori that underlies its persistence and the subsequent H. pylori-associated disease. Here we discuss the mechanisms used by H. pylori to survive the host immune response and, in particular, the role played by altered phagosome maturation.
dc.description.statementofresponsibilityGlenn N. Borlace, Stacey J. Keep, Mark J. R. Prodoehl, Hilary F. Jones, Ross N. Butler, and Doug A. Brooks
dc.identifier.citationAmerican Journal of Physiology - Gastrointestinal and Liver Physiology, 2012; 303(2):G169-G179
dc.identifier.doi10.1152/ajpgi.00320.2011
dc.identifier.issn0193-1857
dc.identifier.issn1522-1547
dc.identifier.orcidBrooks, D. [0000-0001-9098-3626]
dc.identifier.urihttp://hdl.handle.net/2440/95649
dc.language.isoen
dc.publisherAmerican Physiological Society
dc.rightsCopyright © 2012 the American Physiological Society
dc.source.urihttps://doi.org/10.1152/ajpgi.00320.2011
dc.subjectchronic inflammation; gastric cancer; macrophage; phagocytic killing; ulcer
dc.titleA role for altered phagosome maturation in the long-term persistence of Helicobacter pylori infection
dc.typeJournal article
pubs.publication-statusPublished

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