Fig. 2. (A ) N-formylmethionine-leucyl-phenylalanine (fMLP)- and platelet-activating factor (PAF)-induced human polymorphonuclear neutrophil (hPMN) activation. fMLP (black bar) induces superoxide anion production, whereas PAF has virtually no activating properties (gray bars). Untreated: baseline superoxide anion production by untreated hPMNs (white bar). (B ) Superoxide anion production by hPMNs activated by fMLP (left bar, data from fig. 2A) or after priming for 5 min with PAF. (C ) Preincubation of hPMNs with petussis toxin (PTX; grey bar) inhibits superoxide anion production of PAF-primed–fMLP-activated hPMNs. *Significant difference compared with PAF-primed–fMLP-activated control response. (D ) PAF increases superoxide anion production in hPMNs induced by 1 nm phorbol myristate acetate (PMA). (E ) PTX (1 μg/ml) has no significant effect on PAF-primed–PMA-activated superoxide anion production (gray bar) compared with PAF-primed–PMA-activated control hPMNs (black bar). (F ) PAF increases superoxide anion production in hPMNs induced by 1 nm PMA (data from fig. 2D). U-73122, a phospholipase C antagonist, completely abolishes the priming effect of PAF (gray bar). See text for details.