肺泡巨噬细胞对豚鼠气道平滑肌张力的调控

MODULATION OF ALVEOLAR MACROPHAGES ON TENSION OF AIRWAY SMOOTH MUSCLE OF GUINEA PIG

经调理酵母多糖(OPZ)刺激的大鼠肺泡巨噬细胞培养上清液可松弛豚鼠离体气管肌条,上清液中PGE_1增加,表明PGE_1是肺泡巨噬细胞松弛气管肌条的介质之一。经OPZ激活的肺泡巨噬细胞培养上清液与豚鼠血小板作用后,其松弛效应被逆转为收缩效应,提示可能由于肺泡巨噬细胞分泌血小板活化因子激活血小板,使释放收缩介质所致。肺泡巨噬细胞借助所分泌的介质经常性地调节气道阻力,对肺通气具有保护意义。

Alveolar macrophages (AM) harvested from Wistar rats by lung lavage were incubated with opsonized zymosan (OPZ) and the supernatant was collected. It was found that the supernatant decreased the tension of spirally cut trachea of guinea pigs in comparison with the control (p<0.01,n = 7). In addition, the radioimmunoassay (RIA) of the supernatant showed a higher content of prostaglandin E1(PGE1) than in the control (p<0.02). It is therefore considered that PGE1 probably is one of relaxant mediators by which AM relaxed the tracheal smooth muscle (TSM). However, after the supernatant had been cultured with guinea pig platelets, it induced a significant increase in the tension of TSM. Relaxation and platelet-dependent spasm of TSM induced by the supernatant of activated AM are very similar to the effect of platelet-activating factor (PAF) on TSM. PAF is also one of mediators produced by AM in vitro. This study suggests that AM can modulate airway resistance by producing some mediators, such as PGE15 PAF, etc. For example, AM secrets these relaxant mediators to keep the airway open in normal condition. When pulmonary inflammation or trauma occurs, the cellular components including platelet infiltrate and AM-derived PAF may induce a platelet-dependent bronchoconstriction for reducing airflow to the diseased area, and redistributing the airflow in lung to improve the efficiency of ventilation.