Takanaski S, Nonaka R, Xing Z, O'Byrne P, Dolovich J, Jordana M
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
J Exp Med. 1994 Aug 1;180(2):711-5. doi: 10.1084/jem.180.2.711.
In this study we have investigated the effects of interleukin 10 (IL-10) on human peripheral blood eosinophils stimulated with granulocyte/macrophage colony stimulating factor (GM-CSF) and lipopolysaccharide (LPS). We show that LPS was able to enhance eosinophil survival in a dose-dependent manner, as well as release of the cytokines GM-CSF, tumor necrosis factor alpha, and IL-8. LPS-induced eosinophil survival was largely inhibited by an anti-GM-CSF neutralizing antibody and completely blocked by polymyxin B, suggesting GM-CSF involvement in the survival enhancing mechanism and LPS specificity, respectively. IL-10 significantly inhibited survival of, and cytokine production from, eosinophils induced by LPS, but did not inhibit the survival induced by GM-CSF. These observations suggest a novel activation mechanism of eosinophils and, also, that IL-10 may participate in the regulation of diseases characterized by eosinophil infiltration.
在本研究中，我们调查了白细胞介素10（IL-10）对粒细胞/巨噬细胞集落刺激因子（GM-CSF）和脂多糖（LPS）刺激的人外周血嗜酸性粒细胞的影响。我们发现，LPS能够以剂量依赖的方式提高嗜酸性粒细胞的存活率，以及细胞因子GM-CSF、肿瘤坏死因子α和IL-8的释放。抗GM-CSF中和抗体在很大程度上抑制了LPS诱导的嗜酸性粒细胞存活，而多粘菌素B则完全阻断了该过程，这分别表明GM-CSF参与了存活增强机制以及LPS的特异性作用。IL-10显著抑制了LPS诱导的嗜酸性粒细胞存活及其细胞因子产生，但不抑制GM-CSF诱导的存活。这些观察结果提示了嗜酸性粒细胞一种新的激活机制，并且IL-10可能参与以嗜酸性粒细胞浸润为特征的疾病的调节。
