Department of Medicine, Division of Infectious Disease, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Department of Medicine, Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Can J Cardiol. 2021 Aug;37(8):1175-1180. doi: 10.1016/j.cjca.2021.05.006. Epub 2021 May 21.
It is unclear how oxidative stress triggered by smoking and vaping may alter specific immune cell subsets. In this study, we showed that tobacco cigarette smoking, but not electronic-cigarette vaping, is associated with increased expression of major proteins in the toll-like receptor 4 (TLR4) inflammasome-interleukin (IL)-6 signalling axis in monocyte subtypes and T cells. TLR4 senses oxidative stress in immune cells caspase-1 is a key protein of inflammasome activation, and IL-6R-α is the receptor for IL-6 that drives proatherogenic IL-6 signalling. These findings implicate the non-nicotine, pro-oxidant toxicants in tobacco cigarette smoke as instigators of increased expression of key proteins in the TLR4-inflammasome-IL-6 axis that contribute to atherogenesis.
目前尚不清楚吸烟和蒸气烟引起的氧化应激如何改变特定的免疫细胞亚群。在这项研究中，我们表明，香烟吸烟，但不是电子烟蒸气烟，与单核细胞亚型和 T 细胞中 TLR4（Toll 样受体 4）炎性小体-白细胞介素（IL）-6 信号轴中的主要蛋白表达增加有关。TLR4 感知免疫细胞中的氧化应激，caspase-1 是炎性小体激活的关键蛋白，而 IL-6R-α 是驱动致动脉粥样硬化的 IL-6 信号的 IL-6 受体。这些发现表明，烟草烟雾中的非尼古丁、促氧化剂毒素是 TLR4 炎性小体-白细胞介素 6 轴中关键蛋白表达增加的引发因素，这些蛋白参与动脉粥样硬化的形成。
