Antony V B, Repine J E, Harada R N, Good J T, Sahn S A
Acta Cytol. 1983 May-Jun;27(3):355-61.
A model of tuberculous pleurisy in New Zealand white rabbits was developed to describe the sequential cellular and biochemical changes in pleural fluid. Bacille Calmette-Guérin (BCG) in 4 X 10(7) colony-forming units was introduced into the right pleural space of rabbits previously sensitized by intradermal BCG. Pleural fluid was obtained via serial thoracenteses. A normal-pH, normal-glucose, exudative effusion was seen through 144 hours. Polymorphonuclear leukocytes were the first cells to respond to the introduction of tubercle bacilli in the pleural space; they remained the predominant cell for the first 24 hours and were followed by macrophages, which peaked at 96 hours, and then by lymphocytes. Numerous granulomata were observed on both the visceral and parietal pleura ten days following intrapleural instillation of BCG. We propose that the polymorphonuclear leukocyte influx is not a nonspecific response to pleural injury and that such a leukocyte response, either itself or through its interaction with the macrophage, plays a role in host defense mechanisms against the tubercle bacilli.
建立了新西兰白兔结核性胸膜炎模型，以描述胸腔积液中细胞和生化变化的顺序。将4×10⁷菌落形成单位的卡介苗（BCG）注入先前经皮内注射BCG致敏的兔子右胸腔。通过连续胸腔穿刺获取胸腔积液。在144小时内观察到pH值正常、葡萄糖正常的渗出性胸腔积液。多形核白细胞是最早对胸腔内引入结核杆菌作出反应的细胞；它们在最初24小时内一直是主要细胞，随后是巨噬细胞，在96小时达到峰值，然后是淋巴细胞。在胸腔内注入BCG十天后，在内脏和壁层胸膜上均观察到大量肉芽肿。我们认为多形核白细胞的流入不是对胸膜损伤的非特异性反应，并且这种白细胞反应本身或通过其与巨噬细胞的相互作用，在宿主抵抗结核杆菌的防御机制中发挥作用。
