Nakamura Y, Azuma M, Okano Y, Sano T, Takahashi T, Ohmoto Y, Sone S
Third Department of Internal Medicine, University of Tokushima School of Medicine, Japan.
Am J Respir Cell Mol Biol. 1996 Nov;15(5):680-7. doi: 10.1165/ajrcmb.15.5.8918375.
Airway epithelial cells are known to produce a granulocyte/macrophage colony-stimulating factor (GM-CSF), which induces eosinophilic inflammation in bronchial asthma. Interleukin-4 (IL-4), IL-10, and IL-13 produced by Th2 cells are involved in the pathogenesis of bronchial asthma. To assess their contributions to airway inflammation, we examined their effects on GM-CSF production by bronchial epithelial cells. Human bronchial epithelial cells were obtained under bronchoscopy from 21 patients with various respiratory diseases and incubated with or without IL-4, IL-10, or IL-13. Then the GM-CSF concentrations in the cell-free supernatants were measured by enzyme-linked immunosorbent assay. Results showed that IL-4 and IL-13 stimulated GM-CSF production by the epithelial cells dose-dependently, whereas IL-10 did not. The eosinophil survival-stimulating activity in the culture supernatants was closely correlated with GM-CSF concentration and was neutralized by anti-GM-CSF antibody. Thus, IL-4 and IL-13 may contribute to airway inflammation by upregulating GM-CSF production by bronchial epithelial cells.
已知气道上皮细胞可产生粒细胞/巨噬细胞集落刺激因子(GM-CSF),该因子可诱发支气管哮喘中的嗜酸性粒细胞炎症。Th2细胞产生的白细胞介素-4(IL-4)、IL-10和IL-13参与支气管哮喘的发病机制。为评估它们对气道炎症的作用,我们检测了它们对支气管上皮细胞产生GM-CSF的影响。在支气管镜检查下从21例患有各种呼吸道疾病的患者获取人支气管上皮细胞,并在有或无IL-4、IL-10或IL-13的情况下进行培养。然后通过酶联免疫吸附测定法测量无细胞上清液中的GM-CSF浓度。结果显示,IL-4和IL-13可剂量依赖性地刺激上皮细胞产生GM-CSF,而IL-10则无此作用。培养上清液中的嗜酸性粒细胞存活刺激活性与GM-CSF浓度密切相关,并被抗GM-CSF抗体中和。因此,IL-4和IL-13可能通过上调支气管上皮细胞产生GM-CSF而导致气道炎症。