SUPPRESSION AND RECOVERY OF THE ALVEOLAR MACROPHAGE PHAGOCYTIC SYSTEM DURING CONTINUOUS EXPOSURE TO 0.5 PPM OZONE
SUPPRESSION AND RECOVERY OF THE ALVEOLAR MACROPHAGE PHAGOCYTIC SYSTEM DURING CONTINUOUS EXPOSURE TO 0.5 PPM OZONE
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DOI：
10.3109/01902149109062864
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发表时间：
1991-01-01
影响因子：
1.7
通讯作者：
JAKAB, GJ
中科院分区：
文献类型：
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作者：
GILMOUR, MI;HMIELESKI, RR;JAKAB, GJ
已知短期暴露于臭氧（O3）会以剂量相关的方式损害肺部抗菌防御和肺泡巨噬细胞（AM）吞噬作用。 为了确定长期暴露于O3的影响，瑞士小鼠连续暴露于0.5 ppm O3。 在1，3，7，和14天，肺内杀伤进行了评估，通过吸入挑战与金黄色葡萄球菌或奇异变形杆菌，并通过比较在4小时之间的O3暴露和对照动物的肺中剩余的活菌数。 为了评估O3对AM功能能力的影响，评估了Fc受体介导的吞噬作用。 臭氧暴露对肺内S.金黄色葡萄球菌在1和3天;然而，随着延长暴露，肺的杀菌能力恢复正常。 这种最初抑制随后恢复的趋势反映在AM的吞噬能力中。 与S.金黄色葡萄球菌，当奇异变形杆菌被用作挑战生物体时，O3暴露对肺杀菌活性没有抑制作用，这与肺中吞噬细胞群体的增加相关。 灌洗的巨噬细胞的形态学检查表明，在1天的O3暴露后，AM更泡沫，并含有显着更多的空泡。 在第3天，双核细胞也显著增加。 这些研究表明，连续暴露于O3调节AM依赖性肺防御，并指出挑战生物和暴露方案在确定O3的不良反应中的重要性。
Short-term exposures to ozone (O3) are known to impair pulmonary antibacterial defenses and alveolar macrophage (AM) phagocytosis in a dose-related manner. To determine the effect of prolonged O3 exposure, Swiss mice were exposed continuously to 0.5 ppm O3. At 1, 3, 7, and 14 days, intrapulmonary killing was assessed by inhalation challenge with Straphylococcus aureus or Proteus mirabilis and by comparing the number of viable bacteria remaining in the lungs at 4 h between O3-exposed and control animals. To evaluate the effects of O3 on the functional capacity of the AMs, Fc-receptor mediated phagocytosis was assessed. Ozone exposure impaired the intrapulmonary killing of S. aureus at 1 and 3 days; however, with prolonged exposure, the bactericidal capacity of the lungs returned to normal. This trend of an initial suppression followed by recovery was reflected in the phagocytic capacity of the AMs. In contrast to S. aureus, when P. mirabilis was used as the challenge organism, O3 exposure had no suppressive effect on pulmonary bactericidal activity, which correlated with an increase in the phagocytic cell population in the lungs. Morphologic examination of the lavaged macrophages showed that after 1 day of O3 exposure, the AMs were more foamy, and contained significantly more vacuoles. There was also a significant increase in binucleated cells at 3 days. These studies demonstrate that continuous exposure to O3 modulates AM-dependent lung defenses and points to the importance of the challenge organism and exposure protocol in establishing the adverse effect of O3.