Products of polymorphonuclear cell injury inhibit IgG enhancement of monosodium urate-induced superoxide production.
The generation of polymorphonuclear cell (PMN) superoxide ion (O2-) by monosodium urate (MSU) crystals may be important in the pathogenesis of acute gout. Coating MSU crystals with IgG prior to exposure to PMN markedly augmented O2- generation. This augmentation was inhibited by supernates, termed cell lysate, derived from sonicated PMN or PMN exposed to MSU crystals for 5 hours at 37 degrees C. Lysate was effective in inhibiting O2- production when incubated with MSU crystals prior to, during, or after MSU crystals were exposed to IgG. No IgG could be eluted from crystals exposed to both lysate and IgG. Immunoelectron microscopy showed virtually no IgG on crystal surfaces after incubation of crystals with lysate and IgG. These data suggest that products of PMN injury can modulate further PMN responses to MSU crystals. This phenomenon provides a negative feedback loop and is one possible mechanism for the self-limitation of acute gouty attacks.
D000818:Animals; D003460:Crystallization; D006073:Gout / Q000209:etiology; D006801:Humans; D007074:Immunoglobulin G / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D008854:Microscopy, Electron; D009504:Neutrophils / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D011817:Rabbits; D013481:Superoxides / Q000096:biosynthesis*; D014527:Uric Acid / Q000494:pharmacology*
D007074:Immunoglobulin G; D011506:Proteins; D013481:Superoxides; D014527:Uric Acid