Borlace, G.Keep, S.Prodoehl, M.Jones, H.Butler, R.Brooks, D.2015-10-252015-10-252012American Journal of Physiology - Gastrointestinal and Liver Physiology, 2012; 303(2):G169-G1790193-18571522-1547http://hdl.handle.net/2440/95649The 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.enCopyright © 2012 the American Physiological Societychronic inflammation; gastric cancer; macrophage; phagocytic killing; ulcerJournal article003003663910.1152/ajpgi.00320.20110003064160000032-s2.0-84863897704199124Brooks, D. [0000-0001-9098-3626]