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经典猪瘟期间脾脏中的淋巴细胞凋亡与血小板减少:巨噬细胞和细胞因子的作用

Lymphocyte apoptosis and thrombocytopenia in spleen during classical swine fever: role of macrophages and cytokines.

作者信息

Sánchez-Cordón P J, Núñez A, Salguero F J, Pedrera M, Fernández de Marco M, Gómez-Villamandos J C

机构信息

Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Córdoba. Edificio de Sanidad Animal, Campus de Rabanales, 14014, Córdoba, Spain.

出版信息

Vet Pathol. 2005 Jul;42(4):477-88. doi: 10.1354/vp.42-4-477.

DOI:10.1354/vp.42-4-477
PMID:16006607
Abstract

Thirty-two Large White x Landrace pigs, 4 months old, were inoculated with the classical swine fever (CSF) or hog cholera virus strain "Alfort" in order to identify the mechanism responsible for the lymphopenia and thrombocytopenia observed in the spleen during the experimental induction of disease, by immunohistochemical and ultrastructural techniques. Results showed a progressive depletion of splenic lymphoid structures and evidence of platelet aggregation processes. Lymphoid depletion was due to lymphocyte apoptosis, which could not be ascribed to the direct action of the virus on these cells; direct virus action could play only a secondary role in the death of these cells. Absence of severe tissue and endothelial damage, together with moderate procoagulant cytokine levels in the serum, suggest that these pathologies can be ruled out as the cause of platelet aggregation and thrombocytopenia in CSF. Monocyte/macrophages were the main target cells for the CSF virus, and they exhibited phagocytic and secretory activation leading to the synthesis and release of tumor necrosis factor alpha, which proved to be the chief mediator, followed by IL-6, IL-1alpha, and C1q complement component. In view of their characteristics, TNF-alpha and, to a lesser extent, IL-1alpha and IL-6 appear to be the major cytokines involved in the pathogenesis of lymphocytopenia and thrombocytopenia; a clear spatial and temporal relationship was observed between these two phenomena.

摘要

为了通过免疫组织化学和超微结构技术确定在实验性疾病诱导过程中脾脏中观察到的淋巴细胞减少和血小板减少的机制,对32头4月龄的大白猪×长白猪进行了经典猪瘟(CSF)或猪霍乱病毒株“阿尔福特”的接种。结果显示脾脏淋巴结构逐渐耗竭,并有血小板聚集过程的证据。淋巴耗竭是由于淋巴细胞凋亡,这不能归因于病毒对这些细胞的直接作用;病毒的直接作用在这些细胞的死亡中仅起次要作用。缺乏严重的组织和内皮损伤,以及血清中适度的促凝细胞因子水平,表明这些病理状况可被排除为CSF中血小板聚集和血小板减少的原因。单核细胞/巨噬细胞是CSF病毒的主要靶细胞,它们表现出吞噬和分泌激活,导致肿瘤坏死因子α的合成和释放,事实证明肿瘤坏死因子α是主要介质,其次是IL-6、IL-1α和C1q补体成分。鉴于它们的特性,TNF-α以及在较小程度上的IL-1α和IL-6似乎是参与淋巴细胞减少和血小板减少发病机制的主要细胞因子;在这两种现象之间观察到了明确的时空关系。

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