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IBD_21489_sm_suppfig1.eps941KSupplemental figure 1. Schemata of H. pylori and S. typhimurium infection. In two independent experiments, female C57/BL6 mice were infected with H. pylori with an oral gavage of 108 cfu/ml of live organisms three times over 1 week. Control animals received HBSS by oral gavage. 34 days after the H. pylori infection, half of the H. pylori animals (St+Hp) received 20 mg streptomycin (strep) by oral gavage to disrupt the cecal flora followed by infection with 3x106 cfu S. typhimurium δaroA in 100 μl 0.1M HEPES buffer (pH = 8.0). The other half of the H. pylori-infected cohort (Hp) was not infected with S. typhimurium but received streptomycin and HBSS on the same schedule. As H. pylori is streptomycin resistant, streptomycin treatment does not affect H. pylori colonization. Of the animals uninfected with H. pylori, half received streptomycin and subsequent S. typhimurium infection (St). Negative control (no Tx) animals were not infected with S. typhimurium but received streptomycin and HBSS. Mice were euthanized 21 days post S. typhimurium infection. Boxes represent the four experimental groups.
IBD_21489_sm_suppfig2.eps810KSupplemental figure 2. H. pylori infects the stomach but not the cecum. A. H. pylori colonizes the stomach as determined by QPCR of H. pylori urease A in stomach of uninfected (no Tx) compared to H. pylori (Hp), S. typhimurium (St) and H. pylori/S. typhimurium (St+Hp) infected mice. Diamonds represent individual mice (n = 5 per experimental group), horizontal bar represents the average for each group. Dashed line represents assay limit of detection. B. H. pylori does not colonize the cecum as determined by QPCR of H. pylori urease A of uninfected (no Tx) compared to H. pylori (Hp), S. typhimurium (St) and H. pylori/S. typhimurium (St+Hp) infected mice. Diamonds represent individual mice (n = 5 per experimental group), horizontal bar represents the average for each group. Dashed line represents assay limit of detection. (** P<0.01, ***P <0.001)

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