Cordier G, Cozon G, Greenland T, Rocher F, Guiguen F, Guerret S, Brune J, Mornex J F
INSERM U 80, CNRS URA 1177, Université Claude Bernard, Hôpital Edouard Herriot, Lyon, France.
Clin Immunol Immunopathol. 1990 Jun;55(3):355-67. doi: 10.1016/0090-1229(90)90124-9.
Sheep infected by visna-maedi virus, a lentivirus related to the human immunodeficiency virus, develop a chronic interstitial lung disease. Since monocyte/macrophages are known to be specifically infected by visna-maedi virus, we investigated the role of macrophages in the appearance of pulmonary lesions in animals with naturally occurring disease. Alveolitis in maedi leads to a doubling in bronchoalveolar lavage total cell counts and of macrophages as compared to normal sheep. A significant increase in the relative percentage of neutrophils was also observed, accompanied by an increased spontaneous release of neutrophil chemotactic activity by alveolar macrophages of diseased animals, suggesting that they may be activated. Macrophage activation is also demonstrated by the observation of a significant (x3) increase of spontaneous fibronectin release by alveolar macrophages from maedi lungs, and furthermore by the high level expression of major histocompatibility complex class II antigens on most of these cells. Thus viral infection, although restricted to a small population of macrophages, is able to modulate extensive activation of macrophages in the lung. Activated macrophages release mediators likely to play a role in the development of the alveolitis and the parenchymal desorganization. These findings may be relevant to our understanding of the mechanisms by which human immunodeficiency virus infection leads to pulmonary disease other than that caused by opportunistic infections.
感染了维斯纳-梅迪病毒（一种与人类免疫缺陷病毒相关的慢病毒）的绵羊会患上慢性间质性肺病。由于已知单核细胞/巨噬细胞会被维斯纳-梅迪病毒特异性感染，我们研究了巨噬细胞在自然发病动物肺部病变出现过程中的作用。与正常绵羊相比，梅迪病中的肺泡炎导致支气管肺泡灌洗总细胞数和巨噬细胞数量增加一倍。还观察到中性粒细胞的相对百分比显著增加，同时患病动物的肺泡巨噬细胞自发释放中性粒细胞趋化活性增加，这表明它们可能被激活。梅迪病肺部的肺泡巨噬细胞自发释放纤连蛋白显著增加（增至3倍），并且这些细胞中的大多数主要组织相容性复合体II类抗原高表达，这也证明了巨噬细胞的激活。因此，病毒感染虽然局限于一小部分巨噬细胞，但能够调节肺部巨噬细胞的广泛激活。活化的巨噬细胞释放的介质可能在肺泡炎和实质结构破坏的发展中起作用。这些发现可能有助于我们理解人类免疫缺陷病毒感染导致除机会性感染引起的肺部疾病之外的其他肺部疾病的机制。
