THE TOXICOLOGIC INTERACTIONS RESULTING FROM INHALATION OF CARBON-BLACK AND ACROLEIN ON PULMONARY ANTIBACTERIAL AND ANTIVIRAL DEFENSES
THE TOXICOLOGIC INTERACTIONS RESULTING FROM INHALATION OF CARBON-BLACK AND ACROLEIN ON PULMONARY ANTIBACTERIAL AND ANTIVIRAL DEFENSES
复制标题
DOI：
10.1006/taap.1993.1142
复制
发表时间：
1993-08-01
影响因子：
3.8
通讯作者：
JAKAB, GJ
中科院分区：
文献类型：
--
作者：
JAKAB, GJ
本研究的目的是调查是否共同暴露于炭黑和丙烯醛的毒理学相互作用对肺防御感染病原体的影响。这一目标是通过体内研究实现的，该研究利用感染性病原体的吸入挑战来探测包括肺的综合防御的多组分系统的功能完整性。金黄色葡萄球菌用于肺泡巨噬细胞（AM）监视吞噬系统，奇异变形杆菌用于由AM和炎性多形核白细胞（PMN）组成的双重吞噬系统，单核细胞增生李斯特菌用于获得性细胞免疫应答的淋巴因子介导的臂，甲型流感病毒用于细胞毒性T细胞介导的细胞免疫效应机制。将瑞士小鼠暴露于目标浓度为10 mg/m3的炭黑和2.5 ppm丙烯醛，持续4小时/天，持续4天，在暴露后第一天抑制了金黄色葡萄球菌的肺内杀灭，并在第7天恢复至对照水平。与此相反，共同暴露增强了肺内杀死奇异变形杆菌，这与从肺中回收的辅助吞噬性PMN的显著增加相关。同时接触炭黑和丙烯醛也会导致L.单核细胞增多症和甲型流感病毒。无论是单独接触炭黑还是单独接触丙烯醛，对肺防御四种感染因子的功能完整性都没有任何影响。这些数据证明了同时暴露于惰性颗粒和丙烯醛的毒理学相互作用对肺部先天和后天防御的影响。增强生物学效应的机制可能是炭黑颗粒作为丙烯醛的载体机制到达肺深部。
The goal of this study was to investigate whether coexposures to carbon black and acrolein result in a toxicologic interaction having effects on lung defenses against infectious agents. This aim was accomplished through in vivo studies with inhalation challenges of infectious agents that probe the functional integrity of the multicomponent system that comprises the integrated defenses of the lungs. Staphylococcus aureus was used for the alveolar macrophage (AM) surveillance phagocytic system, Proteus mirabilis for the dual phagocytic system composed of AMs and inflammatory polymorphonuclear leukocytes (PMNs), Listeria monocytogenes for the lymphokine-mediated arm of the acquired cellular immune response, and influenza A virus for the cytotoxic T-cell-mediated effector mechanism of cellular immunity. Exposures of Swiss mice to target concentrations of 10 mg/m3of carbon black and 2.5 ppm acrolein for 4 hr/day for 4 days suppressed the intrapulmonary killing of S.aureus a day after exposure with a return to control levels by Day 7. In contrast, the coexposure enhanced the intrapulmonary killing of P. mirabilis which correlated with a significant increase in accessory phagocytic PMNs recovered from the lungs. Combined exposure to carbon black and acrolein also resulted in impaired elimination of L. monocytogenes and influenza A virus from the lungs. Neither exposure to carbon black alone nor exposure to acrolein alone had any effect on the functional integrity of lung defenses against the four infectious agents. These data demonstrate the effects of the toxicologic interaction of coexposures to an inert particle and acrolein on innate and acquired defenses of the lungs. The mechanism for the enhanced biologic effect may be that the carbon black particle acts as a carrier mechanism for acrolein to the deep lung.