Immunopathology of Experimental Bronchiectasis

支气管扩张 免疫系统 发病机制 单核细胞浸润 病理 外周血单个核细胞 薄壁组织 免疫学 渗透(HVAC) 医学 支气管 生物 呼吸道疾病 内科学 物理 热力学 体外 生物化学
作者
José Roberto Lapa e Silva,Diamantino Guerreiro,Bernice Noble,L W Poulter,Peter Cole
出处
期刊:American Journal of Respiratory Cell and Molecular Biology [American Thoracic Society]
卷期号:1 (4): 297-304 被引量:58
标识
DOI:10.1165/ajrcmb/1.4.297
摘要

In human bronchiectasis, the bronchial wall is the seat of abnormal mononuclear cell infiltration, which suggests the presence of a cell-mediated immune reaction. The histopathology of a recently devised animal model of experimental bronchiectasis resembles that of the human disease. We have investigated its immunohistology to validate the similarity to that of human bronchiectasis in order to provide a model for the study of cellular immune aspects of the pathogenesis of bronchiectasis. The immunohistology of the bronchial wall mononuclear cell population in experimental rat bronchiectasis was compared with that in control and normal rats. The control rats did not develop bronchiectasis, and the composition and distribution of mononuclear cells in the bronchial wall were similar to those of normal animals. In the rats developing bronchiectasis, there was infiltration of T lymphocytes, macrophages, and dendritic cells (as defined by monoclonal antibodies) in all compartments of the lung, particularly in the bronchial wall and around vessels. The bronchus-associated lymphoid tissue was disrupted by heavy infiltration of T cells, and follicular aggregates of T lymphocytes were seen deeper in the lung parenchyma. Expression of Ia antigen increased in the bronchial epithelium and in large numbers of mononuclear cells throughout the lung. These findings suggest that a cell-mediated immune response appears during the development of experimental bronchiectasis in this rat model. This cellular immune response is similar to that described in human bronchiectasis and may enable this animal model to be used in defining the role of cellular immunity in the pathogenesis of bronchiectasis.
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