MODULATION OF HUMAN ALVEOLAR MACROPHAGE PROPERTIES BY OZONE EXPOSURE INVITRO
MODULATION OF HUMAN ALVEOLAR MACROPHAGE PROPERTIES BY OZONE EXPOSURE INVITRO
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DOI：
10.1016/0041-008x(91)90042-d
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发表时间：
1991-09-15
影响因子：
3.8
通讯作者：
KOREN, HS
中科院分区：
文献类型：
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作者：
BECKER, S;MADDEN, MC;KOREN, HS
我们研究了人肺泡巨噬细胞（HAM）功能在体外暴露于臭氧（O3）（0.1 - 1.0 ppm，2-4小时）后的变化。研究的功能反映了O3对支气管肺泡空间中宿主防御机制有害的担忧。HAM暴露于O3引起前列腺素E2（PGE 2）释放的浓度依赖性增加，前列腺素E2是炎症、吞噬作用和氧化爆发的重要调节剂。虽然颗粒免疫复合物的吞噬作用减少O3，我们发现没有变化的HAM表面上的Fc受体和补体受体的数量。超氧化物（O2-）的生产响应佛波酯后，HAM暴露于O3减少，而基础O2-释放响应塑料粘附不受影响。HAM对机会性酵母新生隐球菌的生长抑制作用不受O3暴露的影响。暴露于O3不会诱导炎症介质和免疫调节剂（如肿瘤坏死因子-α、白细胞介素1和白细胞介素6）的产生。然而，与对照组相比，O3暴露的HAM产生显着较低水平的这些细胞因子时，细菌脂多糖（LPS）刺激。二维凝胶电泳分析的蛋白质HAM后，在体外暴露于O3确定了11个蛋白质的合成率显着改变。因此，这些研究表明，暴露于O3改变了HAM的功能能力。虽然对蛋白质表达或合成的影响很小，但HAM对颗粒免疫复合物、细菌LPS和PMA的反应受损。花生四烯酸和PGE 2的释放表明O3的作用主要针对HAM细胞膜。这些变化可能最终导致O3暴露个体对吸入性感染因子的易感性增加。
We have investigated changes in human alveolar macrophage (HAM) function after exposure in vitro to ozone (O3) (0.1 – 1.0 ppm for 2–4 hr). The functions studied reflect concern that O3is detrimental to host defense mechanisms in the bronchoalveolar spaces. Exposure of HAM to O3caused a concentration-dependent increase in release of prostaglandin E2(PGE2), an important modulator of inflammation, phagocytosis, and oxidative burst. Although phagocytosis of particulate immune complexes was decreased by O3, we found no change in the quantity of Fc receptors and complement receptors on the HAM surface. Superoxide (O2−) production in response to phorbol ester was reduced after exposure of HAM to O3while the basal O2−release in response to plastic adherence was not affected. Growth inhibition of the opportunistic yeast Cryptococcus neoformans by HAM was not affected by O3exposure. The production of inflammatory mediators and immune modulators such as tumor necrosis factor-α, interleukin 1, and interleukin 6 were not induced by exposure to O3. However, compared to controls, O3-exposed HAM produced significantly lower levels of these cytokines when stimulated with bacterial lipopolysaccharide (LPS). Two-dimensional gel electrophoretic analysis of proteins made by HAM following in vitro exposure to O3identified 11 proteins whose rate of synthesis was significantly altered. Thus, these studies show that exposure to O3alters the functional competence of HAM. While there is a minimal effect on protein expression or synthesis, the responses of HAM to particulate immune complexes, to bacterial LPS, and to PMA are impaired. The release of arachidonic acid and PGE2suggest that the effect of O3is primarily targeted to the HAM cell membrane. These changes may ultimately result in increased susceptibility to inhaled infectious agents in the O3-exposed individual.