EPITHELIAL AND EXTRACELLULAR-MATRIX INJURY IN QUARTZ-INFLAMED LUNG - ROLE OF THE ALVEOLAR MACROPHAGE
EPITHELIAL AND EXTRACELLULAR-MATRIX INJURY IN QUARTZ-INFLAMED LUNG - ROLE OF THE ALVEOLAR MACROPHAGE
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DOI：
10.2307/3431357
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发表时间：
1992-07-01
影响因子：
10.4
通讯作者：
LI, XY
中科院分区：
文献类型：
--
作者：
DONALDSON, K;BROWN, GM;LI, XY
石英炎肺的肺泡白细胞密度梯度分为巨噬细胞和中性粒细胞浓集。在体外，中性粒细胞丰富的群体显示出对上皮细胞和纤维连接蛋白损伤的最大活性。染石英肺炎性巨噬细胞群具有引起纤维连接蛋白降解的能力，但不会对上皮细胞造成超过对照肺泡巨噬细胞的脱离损伤。体内纤维连接蛋白的损伤可能是导致肺结缔组织支架紊乱的一个重要因素，从而有利于纤维化。在体外，石英比惰性微粒二氧化钛更能刺激肺泡巨噬细胞产生细胞因子。细胞因子可能在体内上调肺细胞膜上的黏附分子；这一过程有助于白细胞/肺细胞的接触，使上皮损伤得以表达，也可能是导致病理变化的一个因素。
The bronchoalveolar leukocytes from quartz-inflamed lung were separated into macrophage-enriched and neutrophil-enriched populations on density gradients. Neutrophil-enriched populations showed the greatest activity in causing injury to epithelial cells and fibronectin in vitro. Inflammatory macrophage-enriched populations from quartz-exposed lung had the ability to cause fibronectin degradation but could not cause detachment injury to epithelial cells over and above that caused by control alveolar macrophages. Fibronectin damage in vivo could be an important factor in disordering the connective tissue scaffold of the lung, thereby favoring fibrosis. In vitro quartz stimulated more production of cytokines by alveolar macrophages than the inert particulate titanium dioxide. Cytokines could be important in upregulating adhesion molecules in the membranes of lung cells in vivo; this process could aid leukocyte/lung cell contact, allowing epithelial injury to be expressed, and could also be a factor leading to pathological change.