Eden E, Turino G M
Immunopharmacology. 1986 Oct;12(2):81-8. doi: 10.1016/0162-3109(86)90033-0.
Human alveolar macrophages obtained from 7 normal volunteers and 7 patients with lung disease were stimulated with endotoxin (lipolysaccharide) to induce interleukin 1/leucocytic pyrogen (IL1/LP) secretion. Using the thymocyte assay we quantitated IL1/LP activity in macrophage supernatants obtained after 24 h. 10 micrograms/ml lipopolysaccharide stimulated alveolar macrophages to secrete significantly more IL1/LP activity than did 1 micrograms/ml. Apart from one patient with sarcoidosis, the presence of indomethacin did not significantly inhibit the quantity of IL1/LP secreted in response to LPS. We also demonstrated that the presence of indomethacin did not affect the response of thymocytes to IL1/LP. We conclude that the secretion of IL1/LP by human alveolar macrophages in response to endotoxin is not significantly reduced by the cyclooxygenase inhibitor indomethacin.
从7名正常志愿者和7名肺部疾病患者获取的人肺泡巨噬细胞，用内毒素（脂多糖）刺激以诱导白细胞介素1/白细胞热原（IL1/LP）分泌。我们使用胸腺细胞检测法对24小时后获得的巨噬细胞上清液中的IL1/LP活性进行定量。10微克/毫升脂多糖刺激肺泡巨噬细胞分泌的IL1/LP活性明显高于1微克/毫升。除一名结节病患者外，吲哚美辛的存在并未显著抑制对脂多糖反应所分泌的IL1/LP量。我们还证明，吲哚美辛的存在并不影响胸腺细胞对IL1/LP的反应。我们得出结论，环氧合酶抑制剂吲哚美辛不会显著降低人肺泡巨噬细胞对内毒素反应时IL1/LP的分泌。
