Castro-Faria-Neto H C, Penido C M, Larangeira A P, Silva A R, Bozza P T
Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz, Rio de Janeiro, Brasil.
Mem Inst Oswaldo Cruz. 1997;92 Suppl 2:197-200. doi: 10.1590/s0074-02761997000800026.
In the present work we review the existing evidence for a LPS-induced cytokine-mediated eosinophil accumulation in a model of acute inflammation. Intrathoracic administration of LPS into rodents (mice, rats or guinea pigs) induces a significant increase in the number of eosinophils recovered from the pleural fluid 24 hr later. This phenomenon is preceded by a neutrophil influx and accompanied by lymphocyte and monocyte accumulation. The eosinophil accumulation induced by LPs is not affected by inhibitors of cyclo or lipoxygenase nor by PAF antagonists but can be blocked by dexamethasone or the protein synthesis inhibitor cycloheximide. Transfer of cell-free pleural wash from LPS injected rats (LPS-PW) to naive recipient animals induces a selective eosinophil accumulation within 24 hr. The eosinophilotactic activity present on the LPS-PW has a molecular weight ranging between 10 and 50 kDa and its effect is abolished by trypsin digestion of the pleural wash indicating the proteic nature of this activity. The production of the eosinophilotactic activity depends on the interaction between macrophages and T-lymphocytes and its effect can not be blocked by anti-IL-5 monoclonal antibodies. Accumulated evidence suggest that the eosinophil accumulation induced by LPS is a consequence of a eosinophilotactic cytokine produced through macrophage and T-cell interactions in the site of a LPS-induced inflammatory reaction.
在本研究中，我们回顾了脂多糖（LPS）诱导的细胞因子介导的嗜酸性粒细胞在急性炎症模型中积聚的现有证据。向啮齿动物（小鼠、大鼠或豚鼠）胸腔内注射LPS会导致24小时后从胸腔积液中回收的嗜酸性粒细胞数量显著增加。这种现象之前会有中性粒细胞流入，并伴有淋巴细胞和单核细胞积聚。LPS诱导的嗜酸性粒细胞积聚不受环氧化酶或脂氧化酶抑制剂以及血小板活化因子（PAF）拮抗剂的影响，但可被地塞米松或蛋白质合成抑制剂环己酰亚胺阻断。将来自注射LPS的大鼠的无细胞胸腔灌洗液（LPS-PW）转移到未处理的受体动物中，会在24小时内诱导选择性嗜酸性粒细胞积聚。LPS-PW上存在的嗜酸性粒细胞趋化活性的分子量在10至50 kDa之间，并且通过对胸腔灌洗液进行胰蛋白酶消化可消除其作用，这表明该活性具有蛋白质性质。嗜酸性粒细胞趋化活性的产生取决于巨噬细胞与T淋巴细胞之间的相互作用，并且其作用不能被抗白细胞介素-5单克隆抗体阻断。越来越多的证据表明，LPS诱导的嗜酸性粒细胞积聚是LPS诱导的炎症反应部位通过巨噬细胞和T细胞相互作用产生的嗜酸性粒细胞趋化细胞因子的结果。
