Marini M, Soloperto M, Zheng Y, Mezzetti M, Mattoli S
Sezione di Biologia Cellulare e Molecolare Polmonare, Università di Milano, Italy.
Pulm Pharmacol. 1992;5(1):61-5. doi: 10.1016/0952-0600(92)90019-d.
Cultured human bronchial epithelial cells constitutively produce granulocyte-macrophage colony-stimulating factor (GM-CSF). The synthesis and release of GM-CSF is upregulated in bronchial epithelium of patients with symptomatic asthma and this may contribute to the local activation of inflammatory cells in their bronchial mucosa. The cause of this upregulation of GM-CSF expression is unknown, but an increased release of interleukin-1 (IL1) from other airway resident cells might be involved, as an increase in GM-CSF production can be induced in vitro in normal bronchial epithelial cells by IL1 and the airway secretions of asthmatics contain high amounts of this cytokine. In the present study, we have evaluated the effect of the anti-inflammatory and antiasthmatic drug, nedocromil sodium, on the spontaneous and IL1-induced expression of GM-CSF in cultured bronchial epithelial cells. This compound, at the concentration of 10(-5) M, reduced the IL1-induced increase in GM-CSF release from epithelial cells by more than 40%, but it did not affect the constitutive production of GM-CSF.
培养的人支气管上皮细胞可组成性地产生粒细胞巨噬细胞集落刺激因子（GM-CSF）。有症状哮喘患者支气管上皮中GM-CSF的合成与释放上调，这可能促成其支气管黏膜中炎症细胞的局部活化。GM-CSF表达上调的原因尚不清楚，但可能涉及其他气道驻留细胞白细胞介素-1（IL-1）释放增加，因为IL-1可在体外诱导正常支气管上皮细胞产生GM-CSF增加，且哮喘患者气道分泌物中含有大量这种细胞因子。在本研究中，我们评估了抗炎抗哮喘药物奈多罗米钠对培养的支气管上皮细胞中GM-CSF自发表达及IL-1诱导表达的影响。该化合物在浓度为10^(-5) M时，可使上皮细胞中IL-1诱导的GM-CSF释放增加减少40%以上，但不影响GM-CSF的组成性产生。
