Influence of lysophospholipids and PAF on the oxidative burst of PMNL

Abstract

Lysophosphatidylcholine (LC), platelet activating factor (PAF) and its precursor lysophosphatidalcholine (LP) enhance O-2-release by polymorphonuclear leucocytes (PMNL) triggered by PMA whereas lysophospholipids with other polar headgroups fail to do so. The generation of these lysophosphatidylcholine-like molecules appears to represent an essential step in the activation of the oxidative burst of the PMNL triggered by PMA since inhibition of phospholipase A2 (PLA2) by p-bromophenacylbromide (BB) or mepacrine results in an inhibition of the O-2 release. This inhibition seems to be due to the reduced generation of the phospholipids studied as it could be reversed by LP. In addition, stimulation of the oxidative burst of the PMNL by the chemotactic stimuli, N-formyl-methionyl-leucylphenylalanine (FMLP), and the complement fragment C5a could also be significantly enhanced by LP as shown by chemiluminescence. However, the response to the phagocytic stimulus, opsonized zymosan (Zx), is not affected by LP. These data provide evidence for the participation of phospholipid metabolism in the initiation of the oxidative burst of PMNL induced by the soluble monomeric stimuli PMA, FMLP and C5a.