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无乳支原体和牛支原体实验性诱导山羊肺部病变的免疫组织化学特征

Immunohistochemical characterization of lung lesions induced experimentally by Mycoplasma agalactiae and Mycoplasma bovis in goats.

作者信息

Rodríguez F, Sarradell J, Poveda J B, Ball H J, Fernández A

机构信息

Department of Comparative Pathology, University of Las Palmas de Gran Canaria, Trasmontaña, 35416 Arucas, Gran Canaria, Spain.

出版信息

J Comp Pathol. 2000 Nov;123(4):285-93. doi: 10.1053/jcpa.2000.0418.

DOI:10.1053/jcpa.2000.0418
PMID:11041998
Abstract

Goats aged 3 months were inoculated with a recent isolate of Mycoplasma agalactiae (five animals) or Mycoplasma bovis (five animals) by a combined (intratracheal+intranasal) route. Two control goats were inoculated by the same route with sterile mycoplasma broth. Animals were killed 14 or 21 days after infection. At necropsy, tracheal and lung tissue was taken for pathological and immunohistochemical examination to determine changes in the lymphocyte subpopulations in the bronchus-associated lymphoid tissue (BALT). Consolidation of the lungs was not observed in any animal. M. agalactiae or M. bovis was recovered from the respiratory tract and lung of all but two infected animals. Both Mycoplasma spp. induced a moderate bronchointerstitial pneumonia, characterized by lymphoid hyperplasia of the BALT and infiltration of mononuclear cells into the alveolar walls. The predominant phagocytic cell in the pulmonary parenchyma and the airways was the macrophage. The main cellular type in the BALT was the CD3(+)T lymphocyte, and the ratio of CD4(+): CD8(+)cells was >1. It is likely that cellular immune mechanisms, through the activation of CD4(+)T lymphocytes, plays a prominent role in the acute and subacute phase of these infections.

摘要

对3月龄山羊通过气管内+鼻内联合途径接种无乳支原体近期分离株(5只动物)或牛支原体(5只动物)。两只对照山羊通过相同途径接种无菌支原体肉汤。感染后14天或21天处死动物。尸检时,采集气管和肺组织进行病理和免疫组织化学检查,以确定支气管相关淋巴组织(BALT)中淋巴细胞亚群的变化。所有动物均未观察到肺部实变。除两只感染动物外,所有感染动物的呼吸道和肺中均分离到无乳支原体或牛支原体。两种支原体均引起中度支气管间质性肺炎,其特征为BALT淋巴样增生和单核细胞浸润至肺泡壁。肺实质和气道中主要的吞噬细胞是巨噬细胞。BALT中的主要细胞类型是CD3(+)T淋巴细胞,CD4(+):CD8(+)细胞的比例>1。细胞免疫机制可能通过CD4(+)T淋巴细胞的激活,在这些感染的急性期和亚急性期发挥重要作用。

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