Das A M, Flower R J, Perretti M
Department of Biochemical Pharmacology, William Harvey Research Institute, London, United Kingdom.
J Leukoc Biol. 1998 Aug;64(2):156-62. doi: 10.1002/jlb.64.2.156.
Eotaxin administration intraperitoneally, but not into dorsal air-pouches, of ovalbumin-sensitized mice exhibiting blood eosinophilia induced a threefold increase in eosinophil (E phi s) infiltration. Transfer of 1 x 10(6) mixed peritoneal cavity cells (PCC), containing 3.5 to 4.5 x 10(4) mast cells (MC), from donor mice to air-pouches of sensitized (but not unsensitized) recipient mice, established an E phi infiltration to eotaxin (vehicle, 0.86 +/- 0.27 x 10(6); eotaxin, 1.63 +/- 0.16 x 10(6) E phi s/air-pouch). Neutrophil numbers were also increased. When MC-depleted (-93%) PCC were injected into air-pouches of recipient animals, E phi infiltration was not supported (-52%). Injection of macrophage-depleted (-99%) PCC into air-pouches elicited a full E phi response to eotaxin but not neutrophil infiltration (-81%). Systemic dexamethasone treatment of recipient mice reduced E phi accumulation; treatment of donor mice only reduced neutrophil accumulation. Our study points to a crucial role for MC in E phi recruitment by eotaxin.
对表现出血液嗜酸性粒细胞增多的卵清蛋白致敏小鼠腹腔注射嗜酸性粒细胞趋化因子（而非注入背部气袋），可使嗜酸性粒细胞浸润增加三倍。将来自供体小鼠的1×10⁶个混合腹腔细胞（PCC）（其中含有3.5至4.5×10⁴个肥大细胞（MC））转移至致敏（而非未致敏）受体小鼠的气袋中，可使嗜酸性粒细胞对嗜酸性粒细胞趋化因子产生浸润（溶媒组，0.86±0.27×10⁶个；嗜酸性粒细胞趋化因子组，1.63±0.16×10⁶个嗜酸性粒细胞/气袋）。中性粒细胞数量也增加。当将MC耗竭（-93%）的PCC注入受体动物的气袋中时，嗜酸性粒细胞浸润未得到支持（-52%）。将巨噬细胞耗竭（-99%）的PCC注入气袋可引发嗜酸性粒细胞对嗜酸性粒细胞趋化因子的完全反应，但不会引起中性粒细胞浸润（-81%）。对受体小鼠进行全身地塞米松治疗可减少嗜酸性粒细胞的积聚；仅对供体小鼠进行治疗则仅减少中性粒细胞的积聚。我们的研究表明肥大细胞在嗜酸性粒细胞趋化因子介导的嗜酸性粒细胞募集中起关键作用。
