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首页> 外文期刊>American Journal of Physiology >Secretory phospholipases A2 stimulate mucus secretion, induce airway inflammation, and produce secretory hyperresponsiveness to neutrophil elastase in ferret trachea.
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Secretory phospholipases A2 stimulate mucus secretion, induce airway inflammation, and produce secretory hyperresponsiveness to neutrophil elastase in ferret trachea.

机译：分泌型磷脂酶A2刺激粘液分泌，诱发气道炎症，并对雪貂气管中的中性粒细胞弹性蛋白酶产生分泌性高反应性。

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摘要

Secretory phospholipases A(2) (sPLA(2)) are increased in the bronchoalveolar lavage fluid of patients with asthma and acute respiratory distress syndrome. Intratracheal sPLA(2) instillation induces acute lung injury in the rat and guinea pig. We hypothesized that sPLA(2) would stimulate mucus secretion in vitro and that intratracheal sPLA(2) exposure would induce mucus hypersecretion and airway inflammation in the ferret trachea in vivo. In vitro, porcine pancreatic sPLA(2) at a concentration of 0.5 or 5 U/ml significantly increased mucous glycoconjugate (MG) secretion from the excised ferret trachea. P-bromophenacylbromide (a sPLA(2) inhibitor), quercetin (a lipoxygenase inhibitor), or MK-886 (a 5-lipoxygenase inhibitor), each at 10(-4) M, significantly reduced sPLA(2)-induced MG secretion. sPLA(2)-stimulated MG secretion was decreased in Ca(2+)-free medium. In vivo, ferrets were intubated for 30 min once per day for 3 days using an ETT coated with 20 units of porcine pancreatic sPLA(2) mixed in water-soluble jelly. Constitutive MG secretion increased 1 day after sPLA(2) exposure and returned to control 5 days later. Human neutrophil elastase (HNE) at 10(-8) M increased MG secretion in the sPLA(2)-exposed trachea compared with that in the control trachea, but methacholine at 10(-7) M did not. sPLA(2)-induced secretory hyperresponsiveness continued for at least 5 days after sPLA(2) exposure ended. sPLA(2) increased tracheal inflammation, MG secretion, and secretory hyperresponsiveness to HNE probably through enzymatic action rather than by activation of its receptor.
机译：哮喘和急性呼吸窘迫综合征患者的支气管肺泡灌洗液中分泌性磷脂酶A（2）（sPLA（2））增加。气管内sPLA（2）滴注在大鼠和豚鼠中引起急性肺损伤。我们假设sPLA（2）会刺激体外黏液分泌，而气管内sPLA（2）暴露会在体内雪貂气管中引起黏液分泌过多和气道炎症。在体外，浓度为0.5或5 U / ml的猪胰腺sPLA（2）显着增加了从切除的雪貂气管分泌粘液糖结合物（MG）的能力。 P-溴苯乙酰胺（一种sPLA（2）抑制剂），槲皮素（一种脂氧合酶抑制剂）或MK-886（一种5-脂氧合酶抑制剂）各自在10（-4）M时显着降低sPLA（2）诱导的MG分泌。 sPLA（2）刺激MG分泌减少无Ca（2+）的培养基。在体内，使用涂有20单位猪胰sPLA（2）的ETT包被的雪貂，将其每天一次插管30分钟，共3天，并混合在水溶性果冻中。 sPLA（2）暴露后1天，组成性MG分泌增加，5天后恢复正常。与对照气管相比，在暴露于sPLA（2）的气管中，人中性粒细胞弹性蛋白酶（HNE）在10（-8）M时增加了MG的分泌，但在10（-7）M时，乙酰甲胆碱却没有。 sPLA（2）暴露结束后，sPLA（2）诱导的分泌性高反应性持续至少5天。 sPLA（2）可能通过酶促作用而不是通过激活其受体来增加气管炎症，MG分泌和对HNE的分泌性高反应性。

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