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Thursday, Feb. 2, 2017, 12:00 PM
by Laura Daniel
The greatest risk factor for gastric cancer is chronic infection by the bacterium, Helicobacter pylori.
In a study in mice published by the Proceedings of the National Academy of Sciences, Dana Hardbower, Keith Wilson, M.D., and colleagues found that macrophage activation has a critical role in regulating H. pylori colonization and gastric inflammation.
Macrophages are an essential component of the innate immune system and can be activated within either the M1 or M2 paradigms. M1 macrophages are highly inflammatory and contribute to clearance of pathogens.
The Wilson lab previously found that H. pylori infection upregulates expression of ODC, a key enzyme regulator of polyamine metabolism within cells.
In the current study, deletion of the gene for ODC in macrophages significantly increased inflammation, enhanced M1 macrophage activation, and reduced H. pylori colonization. The group is hopeful that by targeting ODC, new treatments for chronic infections in humans will be possible.
The research was supported in part by National Institutes of Health grants DK053620, AT004821, CA190612, CA116087, CA028842, AT006896, GM008554, and DK010715.
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Health and Medicine, Reporter, Research Aliquots, gastric cancer, h. pylori, Helicobacter pylori, immune system, Keith Wilson, NCCIH, NCI, NIDDK, NIGMS, NIH, Proceedings of the National Academy of Sciences, Reporter Feb 3 2017
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