Tamaoki Jun, Chiyotani Atsushi, Tagaya Etsuko, Araake Minako, Nagai Atsushi
First Department of Medicine8-1 Kawada-Cho, Shinjuku, Tokyo 162Japan.
Department of Microbiology, Tokyo Women's Medical College8-1 Kawada-Cho, Shinjuku, Tokyo 162Japan.
Microbiology (Reading). 1998 Sep;144 ( Pt 9):2481-2486. doi: 10.1099/00221287-144-9-2481.
To determine whether mycoplasma infection produces airway hyper-responsiveness to tachykinins and bradykinin and, if so, to elucidate the role of neutral endopeptidase (NEP), isolated hamster tracheal segments were studied under isometric conditions in vitro. Nasal inoculation with Mycoplasma pneumoniae potentiated contractile responses to neurokinin A and bradykinin, causing a leftward shift of the dose-response curves to a lower concentration by 1 log unit for each agonist, whereas there was no response with acetylcholine. Pretreatment of tissues with the NEP inhibitor phosphoramidon augmented neurokinin A- and bradykinin-induced contractions in saline-treated control tissues, but did not further potentiate the responsiveness in M. pneumoniae-infected tissues. NEP activity in the tracheal epithelium, but not in epithelium-denuded tissues, was decreased in infected animals. These results suggest that M. pneumoniae infection causes airway bronchoconstrictor hyper-responsiveness to neurokinin A and bradykinin and that this effect may be associated with an inhibition of epithelial NEP activity.
为了确定支原体感染是否会导致气道对速激肽和缓激肽产生高反应性，若如此，则阐明中性内肽酶（NEP）的作用，我们在体外等长条件下研究了分离的仓鼠气管节段。用肺炎支原体进行鼻腔接种可增强对神经激肽A和缓激肽的收缩反应，使每种激动剂的剂量反应曲线向左移动1个对数单位至更低浓度，而对乙酰胆碱则无反应。用NEP抑制剂磷酰胺素预处理组织可增强生理盐水处理的对照组织中神经激肽A和缓激肽诱导的收缩，但不会进一步增强肺炎支原体感染组织的反应性。感染动物气管上皮中的NEP活性降低，而在无上皮组织中未降低。这些结果表明，肺炎支原体感染会导致气道对神经激肽A和缓激肽产生支气管收缩高反应性，且这种效应可能与上皮NEP活性的抑制有关。
