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仙台病毒感染改变了大鼠细支气管上皮细胞中克拉拉胰蛋白酶的亚细胞定位。

Sendai virus infection changes the subcellular localization of tryptase Clara in rat bronchiolar epithelial cells.

作者信息

Sakai K, Kohri T, Tashiro M, Kishino Y, Kido H

机构信息

Dept of Nutrition, School of Medicine, University of Tokushima, Japan.

出版信息

Eur Respir J. 1994 Apr;7(4):686-92. doi: 10.1183/09031936.94.07040686.

Abstract

Tryptase Clara activates the infectivity of Sendai and influenza viruses proteolytically. In this study, we investigated changes in the subcellular localization of tryptase Clara in rat bronchioles with progression of Sendai virus infection. Tryptase Clara and Sendai virus F2 antigen were localized by light and electron immunohistochemical studies. In the uninfected rat lung, tryptase Clara was specifically localized in the secretory granules of respiratory bronchiolar epithelial nonciliated cells, but not in bronchiolar ciliated, or alveolar cells. In the initial stage of Sendai virus infection with slight pathological changes, however, anti-tryptase Clara was highly reactive in luminal peripheral membranes of both nonciliated and ciliated epithelial cells of the bronchioles together with some Sendai virus envelope glycoprotein, F2 antigen. In the progressed stage, tryptase Clara was hard to detect, with heavy accumulation of F2 antigen in the epithelial cells. These immunohistochemical results support our previous findings that in the bronchial lavage fluid tryptase Clara is significantly increased both in amount and activity after viral infection. These results suggest that Sendai virus stimulates the secretion of tryptase Clara from nonciliated bronchiolar epithelial cells to the airway lumen. Accumulation of tryptase Clara on the luminal surface of the bronchiolar epithelial cells and/or in the airway lumen may produce favourable conditions for proteolytic viral activation and multiplication.

摘要

克拉拉组织蛋白酶通过蛋白水解作用激活仙台病毒和流感病毒的感染性。在本研究中,我们调查了随着仙台病毒感染的进展,大鼠细支气管中克拉拉组织蛋白酶亚细胞定位的变化。通过光镜和电镜免疫组织化学研究对克拉拉组织蛋白酶和仙台病毒F2抗原进行定位。在未感染的大鼠肺中,克拉拉组织蛋白酶特异性定位于呼吸性细支气管上皮无纤毛细胞的分泌颗粒中,而不是细支气管纤毛细胞或肺泡细胞中。然而,在仙台病毒感染的初始阶段,病理变化轻微,抗克拉拉组织蛋白酶在细支气管无纤毛和纤毛上皮细胞的管腔外周膜中与一些仙台病毒包膜糖蛋白F2抗原一起具有高反应性。在进展阶段,很难检测到克拉拉组织蛋白酶,F2抗原在上皮细胞中大量积累。这些免疫组织化学结果支持了我们之前的发现,即病毒感染后支气管灌洗液中克拉拉组织蛋白酶的量和活性均显著增加。这些结果表明,仙台病毒刺激克拉拉组织蛋白酶从无纤毛细支气管上皮细胞分泌到气道腔中。克拉拉组织蛋白酶在细支气管上皮细胞腔表面和/或气道腔中的积累可能为病毒的蛋白水解激活和增殖创造有利条件。

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