RELATIONSHIP OF INFLAMMATORY CELL CYTOKINES TO DISEASE SEVERITY IN INDIVIDUALS WITH OCCUPATIONAL INORGANIC DUST EXPOSURE
RELATIONSHIP OF INFLAMMATORY CELL CYTOKINES TO DISEASE SEVERITY IN INDIVIDUALS WITH OCCUPATIONAL INORGANIC DUST EXPOSURE
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DOI：
10.1002/ajim.4700190104
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发表时间：
1991-01-01
影响因子：
3.5
通讯作者：
ROM, WN
中科院分区：
文献类型：
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作者：
ROM, WN
因长期职业接触石棉、煤炭或二氧化硅而导致的尘肺病的特点是肺泡巨噬细胞主导的肺泡炎，伴有过度自发释放的介质：氧化剂、中性粒细胞趋化因子和成纤维细胞生长因子。对 66 名不吸烟、接触过无机粉尘且胸部 X 线检查≥ 1/0 的个体进行了支气管肺泡灌洗，并根据是否存在限制性呼吸障碍进行分层，以及 28 名未接触过无机粉尘的对照者。与正常人相比，根据是否存在损伤进行分层的灰尘暴露组中，通过灌洗回收的总细胞数量有所增加，而呼吸损伤组（n = 40）的中性粒细胞回收百分比和数量显着增加。同样，只有呼吸障碍患者的巨噬细胞会自发释放大量氧化剂超氧阴离子和过氧化氢。从对照组到灰尘暴露无损伤的巨噬细胞释放纤连蛋白的趋势显着，而对于有损伤的人则有显着的趋势。两个粉尘暴露组的肺泡巨噬细胞衍生的进展生长因子的释放也有所增加，但这明显低于特发性肺纤维化患者的巨噬细胞。由于有呼吸障碍和无呼吸障碍的无机粉尘暴露个体的职业暴露几乎相同，因此巨噬细胞介质释放的数量差异可能是由于宿主易感性因素造成的。
The pneumoconioses due to chronic occupational exposure to asbestos, coal, or silica are characterized by an alveolar macrophage‐dominated alveolitis with exaggerated spontaneous release of mediators: oxidants, chemotaxins for neutrophils, and fibroblast growth factors. Bronchoalveolar lavage was performed on 66 non‐smoking inorganic dust‐exposed individuals with a chest x‐ray ≥ 1/0 stratified by presence or absence of restrictive respiratory impairment, and 28 unexposed non‐smoking controls. Both dust‐exposed groups stratified by presence or not of impairment had increased numbers of total cells recovered by lavage compared to normals, and those with respiratory impairment (n = 40) had a significant increase in percent and number of neutrophils recovered. Similarly, only those with respiratory impairment had macrophages that spontaneously released significant amounts of the oxidants superoxide anion and hydrogen peroxide. There was a significant trend for the release of fibronectin by macrophages from controls to dust‐exposed without impairment to those with impairment. Both dust‐exposed groups also had increased release of alveolar macrophage‐derived progression growth factor, but this was significantly less than macrophages from patients with idiopathic pulmonary fibrosis. Since occupational exposure was virtually identical in inorganic dust‐exposed individuals with versus without respiratory impairment, the quantitative differences in the release of macrophage mediators may be due to factors in host susceptibility.