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. 2013 Jan 23;8(1):e54344. doi: 10.1371/journal.pone.0054344

Figure 2. H. pylori-induced KLF5 upregulation is independent of the cag pathogenicity island, VacA, or LPS.

Figure 2

AGS human gastric epithelial cells were co-cultured with wild-type cag+ H. pylori strain 60190, or its isogenic cagE−, cagA−, slt−, or vacA− mutants at an MOI of 100∶1 for 2 hours. (A) Quantitative real-time RT-PCR was used to assess KLF5 mRNA expression relative to GAPDH mRNA expression. (B) Western blot analysis was used to assess KLF5 protein expression relative to GAPDH protein expression. (C) Western blot analysis replicates were quantified using densitometry. (D) Gastric epithelial cells were co-cultured with the wild-type cag+ H. pylori strain 60190, heat-killed (HK) H. pylori strain 60190, or with strain 60190 in a transwell (TW) system for 2 hours and quantitative real-time RT-PCR was used to assess KLF5 mRNA expression relative to GAPDH mRNA expression. (E) Gastric epithelial cells were treated with H. pylori LPS (10 ng/ml or 100 ng/ml) for 2 hours and quantitative real-time RT-PCR was used to assess KLF5 mRNA expression relative to GAPDH mRNA expression. Data are represented as fold over uninfected (UI) control. Error bars indicate standard error of the mean from experiments performed on at least three independent occasions, and Mann-Whitney tests were used to determine statistical significance between groups.