文摘
嗜酸性粒细胞聚集和激活机制在支气管粘膜哮喘的发病机制的关键。专门的成纤维细胞的位置,myofibroblasts,支气管基底膜下和他们接近浸润嗜酸性粒细胞可能使myofibroblasts调节嗜酸性粒细胞哮喘的生存和功能。本研究的目的是调查的影响支气管myofibroblasts嗜曙红细胞体外生存。从人类外周血中嗜酸性粒细胞暴露在细胞培养和支气管myofibroblasts myofibroblast-conditioned媒体。嗜酸性粒细胞可行性评估和粒细胞/巨噬细胞集落刺激因子(gm - csf)在培养上清液和生产检查信使核糖核酸(mRNA) myofibroblasts。嗜酸性粒细胞生存显著增加,嗜酸性粒细胞凋亡的抑制是通过与myofibroblasts培养。条件培养基从肿瘤坏死因子-α(tnf)刺激myofibroblasts也长期嗜曙红细胞生存。这种效应可能被gm - csf抗体。gm - csf mRNA和myofibroblasts分泌物培养和增加了eosinophil-conditioned媒介。tnf抗体和interleukin-1α(il - 1α)培养导致显著减少嗜酸性粒细胞生存和gm - csf水平。 Blocking of fibronectin in the co-cultures did not affect the eosinophil survival enhancing activity. Prednisolone inhibited the eosinophil survival enhancing activity of the co-cultures by suppression of GM-CSF production. Soluble eosinophil-derived cytokines are involved in the interaction of eosinophils with myofibroblasts, which results in a tumour necrosis factor-alpha/interleukin-1 alpha mediated release of granulocyte/macrophage colony-stimulating factor from myofibroblasts. Bronchial myofibroblasts can, thereby, contribute to allergic inflammation by granulocyte/macrophage colony-stimulating factor-mediated inhibition of eosinophil apoptosis.