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084 EPIDERMAL GROWTH FACTOR ALTERS THE HOST INFLAMMATORY RESPONSE TO REDUCE GASTRIC COLONIZATION BY HELICOBACTER PYLORI JP Fedwick1,3, PL Beck2,3, AG Buret1,3 Helicobacter pylori is a spiral, gram-negative bacterium that chronically infects the human stomach. In some individuals, H. pylori-induced chronic gastritis may progress to gastroduodenal ulceration and gastric cancers. Currently, the host-microbial interactions that determine the clinical outcome of infection remain unknown. In response to ulceration, the gastric mucosa produces a number of peptides involved in host defence and repair. The epidermal growth factor (EGF) peptide has previously been shown to decrease the healing time and bacterial colonization of experimentally-induced gastric ulcers. This study investigated the effects of EGF on H. pylori. In this study, therapeutic oral administration of EGF decreased the number of H. pylori colonizing the stomach of C57BL/6 mice. In contrast, exposure of H. pylori to EGF in vitro had no effect on bacterial growth or metabolic activity. Administration of EGF caused a significant increase in myeloperoxidase activity, a marker of inflammation, in infected mice. In conclusion, therapeutic oral administration of EGF was found to decrease the colonization of gastric tissues by H. pylori, independent of a direct microbiocidal effect. The mechanism of reduced colonization may be mediated through modulation of the host inflammatory response.
1Departments of Biological Sciences, 2Medicine, 3Mucosal Inflammation Research Group, University of Calgary, Calgary, Alberta