Receptor cross talk from the PAFR induces reactivation of FPR1_des.

<p>Human neutrophils (10⁵) were desensitized with the FPR1 agonist fMIFL (0.1 nM) as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0060169#pone-0060169-g001" target="_blank">Figure 1</a>. (<b>A</b>) The FPR1_des neutrophils were activated with PAF (100 nM, added at time indicated by arrow; solid line). The involvment of FPR1 and PAFR in the PAF-induced response was examined by addition of cyclosporin H (1 µM, FPR1 antagonist, broken line) or WEB2086 (1 µM, PAFR antagonist, dotted line) at 3 min prior to PAF addition. For comparison, the oxidative response to PAF in naïve neutrophils is shown (inset). A representative experiment is shown, n>5. Abscissa, time of study (min); Ordinate, superoxide production (counts per minute×10⁶; Mcpm). (<b>B</b>) Inhibition of the PAF-induced response in FPR1_des cells by cyclosporin H (1 µM, FPR1 specific antagonist) or WEB2086 (1 µM, PAFR antagonist) shown as mean peak values ±SEM of the responses (Mcpm, n = 5 for WEB2086, n = 19 for control, cyclosporine H). The PAF induced response in naïve neutrophils is shown for comparison (n = 19). (<b>C</b>) Human neutrophils (10⁵) were activated/desensitized with different concentrations of the FPR1 agonist fMIFL (added at time indicated by arrow to the left). The neutrophils were then activated with PAF (100 nM final concentration, added at time indicated by arrow to the right). For comparison, a PAF-induced response in naïve neutrophils is shown (solid line). A representative experiment is shown, n>5. Abscissa, time of study (min); Ordinate, superoxide production (counts per minute×10⁶; Mcpm).