In superfusion experiments, the complement peptide C5a-desArg and the leukotriene B4 (LTB4) enhanced adhesion of guinea pig polymorphonuclear leukocytes to autologous aortic strips (threshold at about 10––8M, maximal effects at 10––7M). C5a-desArg acted primarily by stimulation of the leukocytes: pretreatment of them with the peptide abolished their response by deactivation, whereas pretreatment of the endothelium did not affect adhesion. However, the endothelium obviously cooperated in the response: enhanced adhesion was obtained only when the leukocytes were exposed to C5a-desArg while in contact with the endothelium. The cooperation is most probably due to release of arachidonic acid from endothelium and formation of lip-oxygenase products (LTB4?) therefrom by the stimulated leukocytes. Incubation of leukocytes with nordihydroguaiaretic acid or with relatively high concentrations of indomethacin – both known to inhibit lipoxygenases -lowered the effect of C5a-desArg, but not that of LTB4 nor the spontaneous adhesion. On the other hand, the stable prostacyclin analogue ZK 36 374 decreased C5a-desArg-induced adhesion, while pretreatment of the aortic strips with indomethacin increased it. These results suggest that endogenous prostacyclin may also play a role in this system by reducing adhesion.

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© 1985 S. Karger AG, Basel
1985
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