Rosen M S, Baker D G, Schumacher H R, Cherian P V
Arthritis Rheum. 1986 Dec;29(12):1473-9. doi: 10.1002/art.1780291208.
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.
尿酸单钠（MSU）晶体诱导多形核细胞（PMN）产生超氧阴离子（O2-）可能在急性痛风的发病机制中起重要作用。在将MSU晶体暴露于PMN之前用IgG包被，可显著增强O2-的产生。这种增强作用被来自超声处理的PMN或在37℃下暴露于MSU晶体5小时的PMN的上清液（称为细胞裂解物）所抑制。当在MSU晶体暴露于IgG之前、期间或之后与MSU晶体一起孵育时，裂解物可有效抑制O2-的产生。从同时暴露于裂解物和IgG的晶体中无法洗脱IgG。免疫电子显微镜显示，晶体与裂解物和IgG孵育后，晶体表面几乎没有IgG。这些数据表明，PMN损伤产物可调节PMN对MSU晶体的进一步反应。这种现象提供了一个负反馈回路，是急性痛风发作自我限制的一种可能机制。
