Publication | Open Access
Macrophages release arachidonic acid, prostaglandin E2, and thromboxane in response to late complement components.
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1984
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Arachidonic Acid MetabolismImmunologyImmune SystemCellular PhysiologyInflammationCell SignalingMacrophage BiologyLate Complement ComponentsMolecular PhysiologyArachidonic AcidChronic InflammationVascular BiologyImmune-mediated Inflammatory DiseasesPharmacologyInflammatory DiseasePhagocyteCytokineComplement SystemProstaglandin E2Signal TransductionAnti-inflammatoryPhysiologyMedicineNormal Rabbit
Rat peritoneal macrophages released arachidonic acid, prostaglandin E2, and thromboxane B2 when treated with normal rabbit or C6-deficient rabbit complement in vitro. Normal rabbit complement, however, was more efficient, which indicates that late complement components, in addition to the known effects of C3a and C3b, were responsible for an enhanced arachidonic acid turnover. Indeed, in the absence of the C3 cleavage products, the purified late complement components C5b6, C7, C8, and C9 stimulated the arachidonic acid, as well as the prostaglandin E2 and thromboxane B2 release. Incubation of C5b6, C7, C8, and C9 for 1 hr at 37 degrees C before addition to the macrophages abolished the stimulatory activity, being in complete agreement with the fact that a fluid phase-formed complex of C5-9 loses its membrane-binding capacity. Although the mechanism by which C5b-9-membrane interaction affects the arachidonic acid metabolism remains unclear, the data describe a new function of the late complement components.