Title of article
Effects of cigarette smoke extract on primary activated T cells
Author/Authors
Hernandez، نويسنده , , Claudia P. and Morrow، نويسنده , , Kevin and Velasco، نويسنده , , Cruz and Wyczechowska، نويسنده , , Dorota D. and Naura، نويسنده , , Amarjit S. and Rodriguez، نويسنده , , Paulo C.، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2013
Pages
6
From page
38
To page
43
Abstract
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.
Keywords
Reactive oxygen species , Peroxynitites , Phospho-eIF2? , apoptosis , cigarette smoke , T cells
Journal title
Cellular Immunology
Serial Year
2013
Journal title
Cellular Immunology
Record number
1862471
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