Release of prostaglandin E and thromboxane from macrophages by stimulation with factor H.
Recently novel actions of factor H of complement other than regulation of alternative pathway activation have been described. We examined the influence of H on the arachidonic acid (AA) metabolism of macrophages. Guinea-pig peritoneal macrophages cultured for up to 18 h under serum free conditions were supplied with homologous factor H. H, tested over a concentration range of 12.5-100 micrograms/ml, promoted an indomethacin sensitive release of prostaglandin E and thromboxane B2 in a dose-dependent manner. Stimulation of AA conversion to prostanoids in response to H was shown to be specific as evidenced by immunoabsorption experiments. This novel effect attests to the potential of H to act not only as regulatory protein of the complement pathway but also as an inducer of cellular release reactions. Moreover, these findings emphasize the close functional links that exist between the three main constituents of the inflammatory process: macrophages, the complement system and the AA cascade.
D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D002478:Cells, Cultured; D003180:Complement C3b Inactivator Proteins / Q000494:pharmacology*; D017242:Complement Factor H; D004305:Dose-Response Relationship, Drug; D006168:Guinea Pigs; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis*; D013929:Thromboxane B2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*; D013997:Time Factors
D003180:Complement C3b Inactivator Proteins; D011458:Prostaglandins E; D013931:Thromboxanes; D013929:Thromboxane B2; D017242:Complement Factor H