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. 2003 Feb;71(2):830–837. doi: 10.1128/IAI.71.2.830-837.2003

FIG. 1.

FIG. 1.

H. pylori-induced ERK1/2 and p38 MAPK activation. AGS gastric epithelial cells were stimulated by H. pylori at a cell-to-bacterium ratio of 1:100. (A) Cell lysates were prepared at the designated time points after H. pylori strain 99 (cagA+, cytotoxin positive) infection. Western blot analysis was performed for phosphorylated ERK1/2 (P-ERK1/2), total ERK1/2, phosphorylated p38 (P-p38), and total p38. (B) AGS gastric epithelial cells were stimulated with H. pylori cagA mutants (strains 28 and 45) and cagA+ strains (strains 92 and 99) with or without pretreatment by MEK1/2 inhibitor PD98050 (20 μM) for 1 h. Cell lysates were prepared at 90 min after H. pylori infection. Western blot analysis was performed for phosphorylated ERK1/2 (upper panel) and total ERK1/2 (lower panel). (C) AGS gastric epithelial cells were stimulated with H. pylori cagA mutants (strains 28 and 45) and cagA+ strains (strains 92 and 99) with or without pretreatment by p38 inhibitor SB203580 (10 μM) for 1 h. Western blot analysis was performed for phosphorylated p38 (upper panel) and total p38 (lower panel). Representative data of three independent experiments are shown.