Frevert C W, Farone A, Danaee H, Paulauskis J D, Kobzik L
Physiology Program, Harvard School of Public Health, Boston, Massachusetts.
Inflammation. 1995 Feb;19(1):133-42. doi: 10.1007/BF01534386.
Expression of mRNA for the C-X-C chemokine, macrophage inflammatory protein-2 (MIP-2), is induced during acute inflammation in rat models of disease. We have characterized the phlogistic potential of rat recombinant MIP-2 (rMIP-2) protein in vitro and in vivo. Recombinant MIP-2 caused marked PMN chemotaxis in vitro, with peak chemotactic activity at 10 nM. Incubation of whole blood with rMIP-2 caused a significant loss of L-selectin and a significant increase in Mac-1 expression on the PMN surface. Under similar conditions rMIP-2 also caused a modest respiratory burst in PMNs. The intratracheal instillation of 10 and 50 micrograms of rMIP-2 caused a significant influx of PMNs into the airspace of the lungs. Rat MIP-2 is a potent neutrophil chemotactic factor capable of causing neutrophil activation and is likely to function in PMN recruitment during acute inflammation in rat disease models.
在大鼠疾病模型的急性炎症过程中,C-X-C趋化因子巨噬细胞炎性蛋白-2(MIP-2)的mRNA表达被诱导。我们已在体外和体内对大鼠重组MIP-2(rMIP-2)蛋白的促炎潜力进行了表征。重组MIP-2在体外引起显著的PMN趋化作用,在10 nM时趋化活性达到峰值。用rMIP-2孵育全血导致PMN表面L-选择素显著丢失,Mac-1表达显著增加。在相似条件下,rMIP-2也引起PMN适度的呼吸爆发。气管内滴注10微克和50微克的rMIP-2导致大量PMN流入肺脏气腔。大鼠MIP-2是一种能够引起中性粒细胞活化的强效中性粒细胞趋化因子,并且可能在大鼠疾病模型的急性炎症期间的PMN募集过程中发挥作用。