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. 2007 May 21;75(8):3868–3876. doi: 10.1128/IAI.00195-07

FIG. 5.

FIG. 5.

(A) Activation of p38 MAPK and ERK1/2 in response to the reorganization of the actin cytoskeleton. Cells were treated with TcdB (6 nM) and latrunculin B (Lat B; 2 μg/ml) for 1 h in the absence or presence of 3 μM bafilomycin A1. Immunoblot analysis shows the phosphorylation of p38 MAPK (p-p38) (upper panel) and ERK1/2 (p-ERK1/2) (middle panel). Beta-actin, shown in the lower panel, serves as a control for identical protein loads. (B) Effect of p38 MAPK inhibition by SB202190 (10 μM) on hexosaminidase release induced by TcdB (6 nM) or latrunculin B (2 μg/ml). In comparison to what occurred in control cells (100% ± 34%), the TcdB-induced (288% ± 8%) and the latrunculin B-induced (196% ± 23%) release of hexosaminidase was partially reduced by the p38 MAPK inhibitor SB202190 (TcdB, 236% ± 39%; latrunculin B, 133% ± 11%). Shown are mean values ± standard deviations from three separate experiments.