Tennenberg S D, Solomkin J S
J Surg Res. 1987 Aug;43(2):143-8. doi: 10.1016/0022-4804(87)90157-0.
Complement-mediated neutrophil activation (CMNA) is an important host defense mechanism that is essential for effective neutrophil (PMN) proinflammatory activity. It has also been implicated as a pathogenic mechanism contributing toward the development of adult respiratory distress syndrome. Utilizing zymosan-activated serum pretreatment as an in vitro model for CMNA, we characterized the effects of CMNA on PMN superoxide (SO) production and N-formyl-methionyl-leucyl-phenylalanine (FMLP) receptor status. CMNA was associated with a 132 +/- 38% increase in FMLP-induced SO generation and a 110 +/- 30% increase in FMLP receptor expression. Methylprednisolone pretreatment prevented both the FMLP receptor mobilization and the SO priming effects of CMNA. These data support a concept that FMLP receptor mobilization is an important element in the PMN activation process. In addition, blocking this phenomenon may have clinical significance in attempts to modulate the potential damaging effects of the increased PMN oxidative metabolism associated with CMNA.
补体介导的中性粒细胞激活(CMNA)是一种重要的宿主防御机制,对于中性粒细胞(PMN)有效的促炎活性至关重要。它也被认为是导致成人呼吸窘迫综合征发生的一种致病机制。利用酵母聚糖激活血清预处理作为CMNA的体外模型,我们研究了CMNA对PMN超氧化物(SO)产生和N-甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)受体状态的影响。CMNA与FMLP诱导的SO生成增加132±38%以及FMLP受体表达增加110±30%相关。甲基强的松龙预处理可防止FMLP受体的动员以及CMNA的SO启动效应。这些数据支持了这样一个概念,即FMLP受体的动员是PMN激活过程中的一个重要因素。此外,在试图调节与CMNA相关的PMN氧化代谢增加的潜在破坏作用时,阻断这一现象可能具有临床意义。