Complement as a mediator of inflammation in acute gouty arthritis. I. Studies on the reaction between human serum complement and sodium urate crystals.

Abstract

Abstract The acute inflammatory response in gouty arthritis is induced by sodium urate crystals (NUC), but the mechanism of this reaction has not been established. Experiments presented in this report indicate that complement (C) may be one of the systems which mediate the acute inflammatory response in gout. C activation was initiated by incubating NUC in human serum and activation was manifested by a consumptive depletion of C. The loss of C activity was related to the time and temperature of incubation and crystal concentration. C depletion was inhibited by raising the ionic strength and by the absence of Ca2 2+ and Mg 2+ . C activity was not diminished in serum incubated with either calcium pyrophosphate crystals or heated NUC 200 °C. for 2 hours; however, C activity was diminished in serum incubated with preparations of either sodium orotate or sodium hypoxanthinate crystals. The hemolytic activity of C1 was minimally decreased in serum incubated with NUC, but the hemolytic activities of C4, C2, C3, and C5 were markedly diminished. Properdin and Hageman factor were not required for the activation of C by NUC. A serum factor that could not be identified with either IgA, IgG, or IgM appeared to be necessary for the reaction between NUC and C.