Department of Biotechnology, Faculty of Engineering, Kyoto Sangyo University, Kyoto 603-8555, Japan.
Inhal Toxicol. 2009 Dec;21(14):1229-35. doi: 10.3109/08958370903176727.
Exposure to cigarette smoke impairs the pulmonary immune system, including alveolar macrophage function, although the mechanisms by which this occurs are not fully elucidated. This study investigates the effect of cigarette smoke exposure on the antigen-presenting activity of alveolar macrophages, which is required for antigen-specific response to T cells. C57BL/6 mice were exposed to cigarette smoke for 10 days using a Hamburg II smoking machine, and alveolar macrophages were obtained by bronchoalveolar lavage. The antigen-presenting activity of alveolar macrophages was significantly inhibited in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. Major histocompatibility complex class II cell surface molecule-positive cells, B7-1 molecule-positive cells, and interleukin-1beta messenger RNA gene expression in alveolar macrophages were significantly decreased in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. In contrast, DNA damage and generation of superoxide and hydrogen peroxide in alveolar macrophages were significantly increased by cigarette smoke exposure. These results suggest that inhibition of the antigen-presenting activity of alveolar macrophages may result from decreased expression of major histocompatibility complex class II and B7-1 molecules and interleukin-1beta messenger RNA gene expression following cigarette smoke exposure. Furthermore, inhibition of antigen presentation in alveolar macrophage may result from DNA damage induced by excessive amounts of reactive oxygen species being generated by alveolar macrophages following cigarette smoke exposure. These findings suggest that cigarette smoke impairs the immunological function of alveolar macrophages and, as a result, increases the risk for pulmonary infection.
香烟烟雾暴露会损害肺部免疫系统，包括肺泡巨噬细胞的功能，尽管其发生机制尚未完全阐明。本研究调查了香烟烟雾暴露对肺泡巨噬细胞呈递抗原活性的影响，这是 T 细胞对抗原特异性反应所必需的。C57BL/6 小鼠使用汉堡 II 吸烟机进行 10 天香烟烟雾暴露，通过支气管肺泡灌洗获得肺泡巨噬细胞。与未暴露于香烟烟雾的小鼠相比，暴露于香烟烟雾的小鼠的肺泡巨噬细胞的呈递抗原活性显著受到抑制。与未暴露于香烟烟雾的小鼠相比，暴露于香烟烟雾的小鼠的肺泡巨噬细胞表面主要组织相容性复合体 II 类分子阳性细胞、B7-1 分子阳性细胞和白细胞介素-1β信使 RNA 基因表达显著降低。相反，香烟烟雾暴露显著增加了肺泡巨噬细胞中的 DNA 损伤以及超氧阴离子和过氧化氢的生成。这些结果表明，肺泡巨噬细胞呈递抗原活性的抑制可能是由于香烟烟雾暴露后主要组织相容性复合体 II 和 B7-1 分子以及白细胞介素-1β信使 RNA 基因表达的减少所致。此外，肺泡巨噬细胞中抗原呈递的抑制可能是由于香烟烟雾暴露后肺泡巨噬细胞产生的大量活性氧引起的 DNA 损伤所致。这些发现表明，香烟烟雾会损害肺泡巨噬细胞的免疫功能，从而增加肺部感染的风险。
