Fig. 5.
Fig. 5. Influence of pertussis toxin on the eosinophil functions. / Cells were incubated without or with 1 μg/mL pertussis toxin for 2 hours at 37°C and thereafter stimulated without or with 1 mmol/L ATP. (A) Lucigenin-dependent chemiluminescence in eosinophils was followed for 1 hour, and the integral counts were calculated. Data are means ± SEM (n = 5). (B) Actin polymerization after stimulation for 25 seconds was analyzed. Data are means ± SEM (n = 8). (C) Expression of CD11b was analyzed by flow cytometry after stimulation for 30 minutes. Data are means ± SEM (n = 6). (D) Ca++ transients were analyzed, and the ratio after stimulation for 10 seconds is given. Data are means ± SEM (n = 5). Global differences between groups: P ≤ .0001 (ANOVA); P ≤ .0001 (***) compared with pertussis toxin–pretreated cells (Tukey multiple comparison test);P ≤ .001 (**) compared with pertussis toxin–pretreated cells (Tukey test); P ≤ .01 (*) compared with pertussis toxin–pretreated cells (Tukey test).

Influence of pertussis toxin on the eosinophil functions.

Cells were incubated without or with 1 μg/mL pertussis toxin for 2 hours at 37°C and thereafter stimulated without or with 1 mmol/L ATP. (A) Lucigenin-dependent chemiluminescence in eosinophils was followed for 1 hour, and the integral counts were calculated. Data are means ± SEM (n = 5). (B) Actin polymerization after stimulation for 25 seconds was analyzed. Data are means ± SEM (n = 8). (C) Expression of CD11b was analyzed by flow cytometry after stimulation for 30 minutes. Data are means ± SEM (n = 6). (D) Ca++ transients were analyzed, and the ratio after stimulation for 10 seconds is given. Data are means ± SEM (n = 5). Global differences between groups: P ≤ .0001 (ANOVA); P ≤ .0001 (***) compared with pertussis toxin–pretreated cells (Tukey multiple comparison test);P ≤ .001 (**) compared with pertussis toxin–pretreated cells (Tukey test); P ≤ .01 (*) compared with pertussis toxin–pretreated cells (Tukey test).

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