Sumi Y, Nagura H, Takeuchi M, Miyakawa M
Laboratory of Germfree Life, Nagoya University School of Medicine, Japan.
Virchows Arch. 1994;424(6):661-8. doi: 10.1007/BF00195782.
The health hazards associated with grain dust exposure have been recognized as a cause of lung diseases. In the present study, we used germ-free rats exposed to Aspergillus versicolor to elucidate the mechanism for the lung damage induced by grain dust exposure. One month after exposure to the mold, remarkable proliferation of bronchus-associated lymphoid tissues with germinal centres was induced by aspiration of mold spores. After 1 month, alveolar macrophages increased, becoming foamy macrophages by ingestion and digestion of mold spores. They expressed interleukin (IL)-1, Ia antigens and intercellular adhesion molecule-1 intensely and occasionally bound lymphocytes. Numerous lymphocytes infiltrated the granulomatous lesions which consisted of accumulated foamy macrophages and some T lymphocytes which carried IL-2 receptor. Granulomatous lesions were identified in the entire lung, especially around bronchioles. They extended from alveolar ducts to alveolar spaces for 6 months after exposure to the mold. The macrophage appears to be a key effector cell in granulomatous reactions to inhaled molds.
与接触谷物粉尘相关的健康危害已被确认为肺部疾病的一个病因。在本研究中,我们使用无菌大鼠暴露于杂色曲霉,以阐明谷物粉尘暴露所致肺损伤的机制。暴露于该霉菌1个月后,通过吸入霉菌孢子诱导了具有生发中心的支气管相关淋巴组织显著增生。1个月后,肺泡巨噬细胞增多,通过摄取和消化霉菌孢子变成泡沫状巨噬细胞。它们强烈表达白细胞介素(IL)-1、Ia抗原和细胞间黏附分子-1,偶尔还结合淋巴细胞。大量淋巴细胞浸润由聚集的泡沫状巨噬细胞和一些携带IL-2受体的T淋巴细胞组成的肉芽肿性病变。在整个肺中都发现了肉芽肿性病变,尤其是在细支气管周围。暴露于霉菌后6个月,它们从肺泡管延伸至肺泡腔。巨噬细胞似乎是对吸入霉菌的肉芽肿反应中的关键效应细胞。