Stanley S. Scott Cancer Center, Louisiana State University-Health Sciences Center, New Orleans, LA 70112, USA.
Cell Immunol. 2013 Mar;282(1):38-43. doi: 10.1016/j.cellimm.2013.04.005. Epub 2013 Apr 22.
Tobacco smoking predisposes the development of diseases characterized by chronic inflammation and T cell dysfunction. In this study, we aimed to determine the direct effects of cigarette smoke on primary T cells and to identify the corresponding molecular mediators. Activated T cells cultured in the presence of cigarette smoke extract (CSE) displayed a dose-dependent decrease in cell proliferation, which associated with the induction of cellular apoptosis. T cell apoptosis by CSE was independent of caspases and mediated through reactive oxygen and nitrogen species endogenously contained within CSE. Additional results showed that exposure of T cells to CSE induced phosphorylation of the stress mediator eukaryotic-translation-initiation-factor 2 alpha (eIF2α). Inhibition of the phosphorylation of eIF2α in T cells prevented the cellular apoptosis induced by CSE. Altogether, the results show the direct effects of CSE on T cells, which advance in the understanding of how cigarette smoking promotes chronic inflammation and immune dysfunction.
吸烟使慢性炎症和 T 细胞功能障碍为特征的疾病易于发生。在这项研究中，我们旨在确定香烟烟雾对原代 T 细胞的直接影响，并确定相应的分子介质。在香烟烟雾提取物（CSE）存在下培养的激活 T 细胞表现出细胞增殖的剂量依赖性下降，这与细胞凋亡的诱导有关。CSE 通过细胞内 CSE 中包含的活性氧和氮物种诱导的 T 细胞凋亡与半胱天冬酶无关。其他结果表明，CSE 暴露于 T 细胞诱导应激调节剂真核翻译起始因子 2α（eIF2α）的磷酸化。在 T 细胞中抑制 eIF2α 的磷酸化可防止 CSE 诱导的细胞凋亡。总之，这些结果表明 CSE 对 T 细胞的直接影响，有助于理解吸烟如何促进慢性炎症和免疫功能障碍。
