Host cell wounding and repair modulates T. cruzi invasion. (A) HeLa cells were exposed to trypomastigotes in the absence (white column) or presence (black columns) of increasing concentrations of SLO for 20 min, fixed, and processed for quantification of intracellular parasites. The data correspond to the mean of triplicates ± SD. *, P = 0.0149, Student’s t test comparing control and 38 ng/ml SLO-treated cells; ***, P < 0.0001, Student’s t test comparing control and 50 ng/ml SLO-treated cells. (B) Cells were pretreated for 20 min with increasing concentrations of SLO, washed, further incubated for 20 min, and exposed to trypomastigotes for 20 min followed by fixation and quantification of intracellular parasites. The data correspond to the mean of triplicates ± SD. *, P = 0.0182, Student’s t test comparing control and 25 ng/ml SLO-treated cells; ***, P < 0.0006, Student’s t test comparing control and 38 ng/ml or 50 ng/ml SLO-treated cells. (C) HeLa cells were treated with the indicated concentrations of the ASM inhibitor desipramine for 1 h, washed and exposed to trypomastigotes for 30 min, fixed, and processed for determination of the number of intracellular parasites. The data correspond to the mean of triplicates ± SD. *, P = 0.0125, Student’s t test; **, P = 0.0016, Student’s t test comparing control (white bars) and treated (black bars) bars. (D) Cells preincubated with 30 µM desipramine for 1 h were exposed to trypomastigotes for the indicated periods of time, washed, and processed for quantification of intracellular parasites. The data correspond to the mean of triplicates ± SD. **, P < 0.0014, Student’s t test; ***, P < 0.0001, Student’s t test comparing control (white bars) and treated (black bars) cells. These results are representative of four independent experiments.