Peão M N, Aguas A P, Grande N R
Department of Anatomy, Abel Salazar Institute for the Biomedical Sciences, University of Porto, Portugal.
Exp Lung Res. 1992 Nov-Dec;18(6):863-76. doi: 10.3109/01902149209031712.
CD-1 mice were used to study the cellular kinetics of the inflammatory response of the pleural space to the injection of 250 micrograms of silica or of tungsten microparticles. The pleural exudates were collected by lavage of the serous cavity of mice that were sacrificed at 30 min and up to 7 days after the intrapleural instillation of the particles. The samples were studied by light and electron microscopy (transmission and scanning modes); the quantitative cellular kinetics of the inflammation was determined by leukocyte counting in exudates using cytocentrifuge preparations. The normal resident population of cells of CD-1 mice was made up of (2.47 +/- 0.37) x 10(6) cells. It consisted mostly of macrophage-like cells ((2.03 +/- 0.26) x 10(6) cells, 82% of total cells), some lymphocytes ((0.37 +/- 0.07) x 10(6) cells, 15% of total cells), a few mast cells and eosinophilic granulocytes (1-2% of total cells). The initial inflammatory reaction (30-60 min after injection) was characterized by a decrease in the number of cells harvested from the pleural space. This was followed by an intense recruitment of granulocytes and monocytes that resulted in a peak of intrapleural cells at 24 h ((16.8 +/- 4.0) x 10(6) cells induced by silica particles and (18.3 +/- 4.2) x 10(6) cells induced by tungsten particles). In tungsten-injected mice (but not in silica-treated animals) the enhancement in the number of intrapleural macrophages continued up to 72 h after particle injection. The highest percentage of macrophages with ingested tungsten (50% of total macrophages) was found early (6 h) and decreased thereafter; at day 7 it encompassed just 17% of the macrophages. Injection of any of the two particulates led to the disappearance of mast cells from the pleural space of mice. Silica particles attracted a high number of eosinophils to the pleural cavity of mice. Light and electron microscopy documented that pleural macrophages underwent striking morphological changes during the inflammatory response: the phagocytes showed marked increase in size and in number of surface processes, and their cytoplasm often contained large amounts of the injected particles and also of cellular debris. This study establishes the mouse as a reliable animal model to study the dynamics of the pleural space and it offers a precise definition of the cellular kinetics of inflammation in this serous cavity. The data indicate that the kinetics of experimental pleural inflammation induced by particulates may depend on the nature of the injected particles.
采用CD - 1小鼠研究胸膜腔对注射250微克二氧化硅或钨微粒的炎症反应的细胞动力学。在胸膜腔内注入微粒后30分钟至7天内处死小鼠,通过冲洗其浆膜腔收集胸膜渗出液。对样本进行光学显微镜和电子显微镜(透射和扫描模式)研究;使用细胞离心机制备渗出液中的白细胞计数来确定炎症的定量细胞动力学。CD - 1小鼠正常的常驻细胞群由(2.47±0.37)×10⁶个细胞组成。主要由巨噬细胞样细胞((2.03±0.26)×10⁶个细胞,占总细胞的82%)、一些淋巴细胞((0.37±0.07)×10⁶个细胞,占总细胞的15%)、少数肥大细胞和嗜酸性粒细胞(占总细胞的1 - 2%)组成。最初的炎症反应(注射后30 - 60分钟)的特征是从胸膜腔收获的细胞数量减少。随后粒细胞和单核细胞大量募集,导致胸膜腔内细胞在24小时达到峰值(二氧化硅颗粒诱导的为(16.8±4.0)×10⁶个细胞,钨颗粒诱导的为(18.3±4.2)×10⁶个细胞)。在注射钨的小鼠中(但在二氧化硅处理的动物中未出现),胸膜巨噬细胞数量的增加持续到颗粒注射后72小时。摄取钨的巨噬细胞的最高百分比(占总巨噬细胞的50%)在早期(6小时)出现,此后下降;在第7天仅占巨噬细胞的17%。注射这两种微粒中的任何一种都会导致小鼠胸膜腔中的肥大细胞消失。二氧化硅颗粒吸引大量嗜酸性粒细胞到小鼠胸膜腔。光学显微镜和电子显微镜记录显示,胸膜巨噬细胞在炎症反应过程中发生了显著的形态变化:吞噬细胞的大小和表面突起数量明显增加,其细胞质中常常含有大量注入的颗粒以及细胞碎片。本研究确立了小鼠作为研究胸膜腔动力学的可靠动物模型,并对该浆膜腔炎症的细胞动力学给出了精确的定义。数据表明,微粒诱导的实验性胸膜炎症的动力学可能取决于注入颗粒的性质。