Differential alterations of tissue T-cell subsets after sepsis

被引:57
作者
Sharma, Archna [1 ]
Yang, Weng-Lang [1 ,2 ]
Matsuo, Shingo [2 ]
Wang, Ping [1 ,2 ]
机构
[1] Feinstein Inst Med Res, Ctr Translat Res, Manhasset, NY 11030 USA
[2] Hofstra North Shore LIJ Sch Med, Dept Surg, Manhasset, NY 11030 USA
基金
美国国家卫生研究院;
关键词
Sepsis; T-lymphocytes; Natural killer T cells; Profiling; Tissue-specificity; NKT CELLS; IMPROVES SURVIVAL; INDUCED APOPTOSIS; HOST RESPONSE; SEPTIC SHOCK; CD8(+) T; MORTALITY; LYMPHOCYTES; INJURY; IMMUNOSUPPRESSION;
D O I
10.1016/j.imlet.2015.09.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Among immune cells in responding to sepsis, macrophages and neutrophils have been extensively studied, while the contribution of T lymphocytes and natural killer T (NKT) cells is less well characterized. Here we monitored tissue specific changes of T cell subsets in male C57BL/6 mice subjected to sham operation or cecal ligation and puncture (CLP) to induce polymicrobial sepsis. Thymus, spleen, liver, lungs and blood were processed and analyzed 20 h later. Total lymphocyte count showed a significant reduction in septic thymus, spleen and blood but not in lungs and liver. The septic thymi were hypocellular with severe reduction in cell numbers of immature CDT4(+)CD8(+) subset. CD4(+) T and CD8(+) T lymphocyte numbers in septic spleens were also significantly reduced, but the frequency of CD4(+)CD25(+) Tregs was significantly increased. In addition, naive and Tcm CD4(+) T cell numbers were significantly reduced in the septic spleens. By contrast, in septic liver the CD8(+)T cell numbers were significantly increased, whereas NKT cell numbers were reduced, but more activated with increased CD69 and CD25 expression. In the septic lungs, the CD4(+) T and CD8(+) T cell numbers showed no significant change, whereas they were severely reduced in the septic blood. Overall, this study provides important information on the alterations of different T-cell subsets in various tissues after sepsis. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:41 / 50
页数:10
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