Eotaxin-induced eosinophil migration in the peritoneal cavity of ovalbumin-sensitized mice: mechanism of action.
Eotaxin-induced eosinophil migration in the peritoneal cavity of ovalbumin-sensitized mice: mechanism of action.
复制标题
嗜酸性粒细胞在卵清蛋白致敏小鼠腹腔内诱导嗜酸性粒细胞迁移：作用机制。
DOI：
10.4049/jimmunol.159.3.1466
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发表时间：
1997
影响因子：
4.4
通讯作者：
M. Perretti
中科院分区：
文献类型：
--
作者：
A. Das;R. Flower;M. Perretti
在体内研究了响应于腹膜内施用C-C趋化因子（eotaxin）的细胞积累。OVA致敏小鼠表现出血液嗜酸性粒细胞增多，在6 h时对500 ng嗜酸性粒细胞趋化因子的反应中，嗜酸性粒细胞（ESTs）的蓄积（注射溶媒，3.0 +/- 0.5 x 10（5）;注射嗜酸性粒细胞趋化因子，8.6 +/- 1.0 x 10（5））大于未致敏的注射嗜酸性粒细胞趋化因子的小鼠（2.5 +/- 0.4 x 10（5））。在溶媒和嗜酸性粒细胞活化趋化因子注射腔中均观察到非特异性中性粒细胞迁移。注射嗜酸性粒细胞活化趋化因子后，腹腔灌洗液中完整肥大细胞的数量显著低于注射溶剂的动物（分别为0.8 +/-0.3 x 104 vs 2.8 +/-0.6 x 104）。当在施用嗜酸细胞活化趋化因子之前用化合物48/80耗尽内源性腹膜肥大细胞时，埃托啡积累减少51%。这表明内源性肥大细胞在介导嗜酸性粒细胞趋化因子的作用中具有重要作用。还研究了肥大细胞介质在嗜酸性粒细胞趋化因子作用中的潜在作用。用组胺-H1或5-羟色胺拮抗剂预处理可使对嗜酸性粒细胞趋化因子的反应性Eclampin迁移减少50 - 65%。此外，用特异性抗TNF-α的mAb预处理后，仅非特异性中性粒细胞流入减弱。使用中和单克隆抗体，发现Eclamping迁移依赖于粘附分子P-和E-选择素和CD 11b。雌二醇蓄积对地塞米松也敏感，剂量低至0.2 mg/kg可诱导100%抑制。这项研究提供了有益的洞察eotaxin的作用机制。
Cell accumulation in response to i.p. administration of the C-C chemokine, eotaxin, was studied in vivo. OVA-sensitized mice, exhibiting blood eosinophilia, had greater eosinophil (Eø) accumulation in response to 500 ng of eotaxin at 6 h (vehicle-injected, 3.0 +/- 0.5 x 10(5); eotaxin-injected, 8.6 +/- 1.0 x 10(5)) than nonsensitized, eotaxin-injected mice (2.5 +/- 0.4 x 10(5)). A nonspecific neutrophil migration was observed in both vehicle- and eotaxin-injected cavities. The number of intact mast cells in the peritoneal lavages after eotaxin injection was significantly lower than that in vehicle-injected animals (0.8 +/- 0.3 x 10(4) vs 2.8 +/-0.6 x 10(4), respectively). When endogenous peritoneal mast cells were depleted with compound 48/80 before eotaxin administration, there was a 51% reduction in Eø accumulation. This suggests an important role for endogenous mast cells in mediating the actions of eotaxin. The potential role of mast cell mediators in the actions of eotaxin was also investigated. Pretreatment with histamine-H1 or serotonin antagonists reduced Eø migration in response to eotaxin by 50 to 65%. Further, following pretreatment with a specific mAb against TNF-alpha, only nonspecific neutrophil influx was attenuated. Using neutralizing mAbs, Eø migration was found to be dependent on the adhesion molecules P- and E-selectin and CD11b. Eø accumulation was also sensitive to dexamethasone, with doses as low as 0.2 mg/kg inducing 100% inhibition. This study provides useful insight into the mechanisms of action of eotaxin.