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首页> 美国卫生研究院文献>Environmental Health Perspectives >Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.
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Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.

机译：柴油机尾气颗粒（DEP）对单核细胞增生性李斯特菌的肺部免疫力的改变。 I. DEPs对早期肺反应的影响。

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It has been hypothesized that diesel exhaust particles (DEPs) aggravate pulmonary bacterial infection by both innate and cell-mediated immune mechanisms. To test this hypothesis, we investigated the effects of DEP exposure on the functions of alveolar macrophages (AMs) and lymphocytes from lung-draining lymph nodes using a rat Listeria monocytogenes infection model. In the present study, we focused on the effects of DEP exposure on AM functions, including phagocytic activity and secretion of proinflammatory cytokines. The Listeria infection model was characterized by an increase in neutrophil count, albumin content, and acellular lactate dehydrogenase activity in the bronchoalveolar lavage (BAL) fluid at 3 and 7 days postinfection. Short-term DEP inhalation (50 and 100 mg/m(3), 4 hr) resulted in a dose-dependent suppression of lung clearance of Listeria, with the highest bacteria count occurring at day 3. This aggravated bacterial infection was consistent with the inhibitory effect of DEPs on macrophage functions. DEPs suppressed phagocytosis and Listeria-induced basal secretion of interleukin-1ss (IL-1ss) and IL-12 by AMs in a dose-dependent manner. The amount of IL-1ss and IL-12 in the BAL fluid was also reduced by DEP exposure. In addition, DEPs decreased Listeria-induced lipopolysaccharide-stimulated secretion of tumor necrosis factor-alpha (TNF-alpha), IL-1ss, and IL-12 from AMs. These results suggest that DEPs retard bacterial clearance by inhibiting AM phagocytosis and weaken the innate immunity by inhibiting AM secretion of IL-1ss and TNF-alpha. DEPs may also suppress cell-mediated immunity by inhibiting AM secretion of IL-12, a key cytokine for the initiation of T helper type 1 cell development in Listeria infection.
机译：据推测，柴油机排气颗粒（DEP）通过先天和细胞介导的免疫机制加重了肺部细菌感染。为了验证该假设，我们使用大鼠单核细胞增生李斯特菌感染模型调查了DEP暴露对肺泡巨噬细胞（AMs）和肺引流淋巴结淋巴细胞功能的影响。在本研究中，我们集中于DEP暴露对AM功能的影响，包括吞噬活性和促炎细胞因子的分泌。李斯特菌感染模型的特征是感染后3天和7天时嗜中性粒细胞计数，白蛋白含量和支气管肺泡灌洗（BAL）液中无细胞乳酸脱氢酶活性增加。短期DEP吸入（50和100 mg / m（3），4 hr）导致剂量依赖性抑制李斯特菌的肺清除，在第3天细菌计数最高。这种严重的细菌感染与DEPs对巨噬细胞功能的抑制作用。 DEPs以剂量依赖性方式抑制AMs吞噬作用和李斯特菌诱导的白介素1ss（IL-1ss）和IL-12的基础分泌。通过DEP暴露，BAL液中的IL-1ss和IL-12的量也减少了。此外，DEPs减少了李斯特菌诱导的脂多糖刺激AMs分泌肿瘤坏死因子-α（TNF-alpha），IL-1ss和IL-12。这些结果表明，DEP通过抑制AM吞噬作用来延迟细菌清除，并通过抑制IL-1β和TNF-α的AM分泌来削弱先天免疫力。 DEPs还可以通过抑制IL-12的AM分泌来抑制细胞介导的免疫，IL-12是利斯特氏菌感染中引发T辅助1型细胞发展的关键细胞因子。

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