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犊牛自然感染牛呼吸道合胞体病毒的发病机制:补体和肥大细胞介质参与的证据

Pathogenesis of naturally acquired bovine respiratory syncytial virus infection in calves: evidence for the involvement of complement and mast cell mediators.

作者信息

Kimman T G, Terpstra G K, Daha M R, Westenbrink F

机构信息

Department of Herd Health and Pathology, Central Veterinary Institute, AB Lelystad, The Netherlands.

出版信息

Am J Vet Res. 1989 May;50(5):694-700.

PMID:2786355
Abstract

Indicators of immune-mediated disease were studied in calves with severe natural bovine respiratory syncytial virus infection. Although antigen and antibody were detected concurrently in most calves, immune complexes were not detected by use of immunofluorescence, ELISA, and binding of the 1q component of complement. Complement component C3, however, was observed by immunofluorescence in the cranioventral, virus-infected portion of the lungs of 19 of 25 calves. Reductions in the amount of histamine and in the numbers of mast cells and mast cell granules in the virus-positive cranioventral and virus-negative caudodorsal portions of the lungs, indicated activation of mast cells and liberation of their granule contents. On the basis of these and previous findings, a model for the pathogenesis of bovine respiratory syncytial virus-induced disease was proposed.

摘要

对患有严重自然感染牛呼吸道合胞病毒的犊牛的免疫介导疾病指标进行了研究。尽管在大多数犊牛中同时检测到了抗原和抗体,但通过免疫荧光、ELISA以及补体1q成分的结合均未检测到免疫复合物。然而,通过免疫荧光在25头犊牛中19头的肺脏颅腹侧、病毒感染部位观察到了补体成分C3。肺脏病毒阳性颅腹侧和病毒阴性尾背侧部位组胺量的减少以及肥大细胞和肥大细胞颗粒数量的减少,表明肥大细胞被激活并释放了其颗粒内容物。基于这些及之前的研究结果,提出了牛呼吸道合胞病毒诱导疾病发病机制的模型。

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