Effects of cigarette smoke extract on primary activated T cells

被引:42
作者
Hernandez, Claudia P. [1 ]
Morrow, Kevin [1 ]
Velasco, Cruz [1 ]
Wyczechowska, Dorota D. [1 ]
Naura, Arnarjit S. [1 ]
Rodriguez, Paulo C. [1 ,2 ]
机构
[1] Louisiana State Univ, Stanley S Scott Canc Ctr, Hlth Sci Ctr, New Orleans, LA 70112 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Dept Microbiol Immunol & Parasitol, New Orleans, LA 70112 USA
关键词
T cells; Cigarette smoke; Reactive oxygen species; Peroxynitites; Phospho-eIF2; alpha; Apoptosis; ENDOPLASMIC-RETICULUM STRESS; PROTEIN-HOMOLOGOUS PROTEIN; PEGYLATED ARGINASE I; APOPTOSIS; LUNG; MECHANISMS; INDUCTION; EXPOSURE; CANCER; VIRUS;
D O I
10.1016/j.cellimm.2013.04.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 (eIF2 alpha.). Inhibition of the phosphorylation of eIF2 alpha 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. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:38 / 43
页数:6
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