Castranova V, Ma J Y, Yang H M, Antonini J M, Butterworth L, Barger M W, Roberts J, Ma J K
National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA.
Environ Health Perspect. 2001 Aug;109 Suppl 4(Suppl 4):609-12. doi: 10.1289/ehp.01109s4609.
There are at least three mechanisms by which alveolar macrophages play a critical role in protecting the lung from bacterial or viral infections: production of inflammatory cytokines that recruit and activate lung phagocytes, production of antimicrobial reactive oxidant species, and production of interferon (an antiviral agent). In this article we summarize data concerning the effect of exposure to diesel exhaust particles on these alveolar macrophage functions and the role of adsorbed organic chemicals compared to the carbonaceous core in the toxicity of diesel particles. In vitro exposure of rat alveolar macrophages to diesel exhaust particles decreased the ability of lipopolysaccharide (LPS), a bacterial product] to stimulate the production of inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha). Methanol extract exhibited this potential but methanol-washed diesel particles did not. Exposure of rats to diesel exhaust particles by intratracheal instillation also decreased LPS-induced TNF-alpha and IL-1 production from alveolar macrophages. In contrast, carbon black did not exhibit this inhibitory effect. Exposure of rats to diesel exhaust particles by inhalation decreased the ability of alveolar macrophages to produce antimicrobial reactive oxidant species in response to zymosan (a fungal component). In contrast, exposure to coal dust increased zymosan-stimulated oxidant production. In vivo exposure to diesel exhaust particles but not to carbon black decreased the ability of the lungs to clear bacteria. Inhalation exposure of mice to diesel exhaust particles but not to coal dust depressed the ability of the lung to produce the antiviral agent interferon and increased viral multiplication in the lung. These results support the hypothesis that exposure to diesel exhaust particles increases the susceptibility of the lung to infection by depressing the antimicrobial potential of alveolar macrophages. This inhibitory effect appears to be due to adsorbed organic chemicals rather than the carbonaceous core of the diesel particles.
产生招募和激活肺部吞噬细胞的炎性细胞因子、产生抗微生物活性氧物种以及产生干扰素（一种抗病毒剂）。在本文中，我们总结了有关接触柴油废气颗粒对这些肺泡巨噬细胞功能的影响以及与碳质核心相比吸附有机化学物质在柴油颗粒毒性中的作用的数据。大鼠肺泡巨噬细胞体外接触柴油废气颗粒降低了脂多糖（一种细菌产物）刺激炎性细胞因子白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNF-α）产生的能力。甲醇提取物具有这种潜力，但用甲醇洗涤过的柴油颗粒则没有。通过气管内滴注使大鼠接触柴油废气颗粒也降低了肺泡巨噬细胞中脂多糖诱导的TNF-α和IL-1的产生。相比之下，炭黑没有表现出这种抑制作用。通过吸入使大鼠接触柴油废气颗粒降低了肺泡巨噬细胞响应酵母聚糖（一种真菌成分）产生抗微生物活性氧物种的能力。相比之下，接触煤尘增加了酵母聚糖刺激的氧化剂产生。体内接触柴油废气颗粒而非炭黑降低了肺部清除细菌的能力。小鼠吸入接触柴油废气颗粒而非煤尘抑制了肺部产生抗病毒剂干扰素的能力，并增加了肺部的病毒增殖。这些结果支持以下假设：接触柴油废气颗粒会通过降低肺泡巨噬细胞的抗菌潜力而增加肺部对感染的易感性。这种抑制作用似乎是由于吸附的有机化学物质而非柴油颗粒的碳质核心。
