Exogenous hydrogen sulfide induces functional inhibition and cell death of cytotoxic lymphocytes subsets
Exogenous hydrogen sulfide induces functional inhibition and cell death of cytotoxic lymphocytes subsets
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DOI：
10.1002/jcp.21151
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发表时间：
2007-12-01
影响因子：
5.6
通讯作者：
Vitale, Marco
中科院分区：
文献类型：
--
作者：
Mirandola, Prisco;Gobbi, Giuliana;Vitale, Marco
本文详细研究了外源性硫化氢对人外周血淋巴细胞的毒性作用。硫化氢现在被认为是一种气体递质，在不同的细胞类型中具有特定的功能作用，如神经元和血管平滑肌。在这里，我们表明，外源性硫化氢诱导依赖于其细胞内谷胱甘肽水平的外周血淋巴细胞的半胱天冬酶非依赖性细胞死亡，与生理相关的子集特异性CD8（+）T细胞和NK细胞。虽然淋巴细胞活化并不改变他们的敏感性HS-，暴露于硫化氢24小时后，存活的淋巴细胞亚群显示出显着降低的增殖反应的有丝分裂原和减少IL-2的生产。总体而言，我们的数据表明，HS（-）降低外周血淋巴细胞的细胞毒性反应以及它们的IL-2的产生，因此使局部炎症反应的主要参与者失活，为临床上众所周知的硫化合物的抗炎作用增加了新的基础知识。
The toxic effects of exogenous hydrogen sulfide on peripheral blood lymphocytes have been investigated in detail. Hydrogen sulfide is now considered as a gasotransmitter with specific functional roles in different cell types, like neurons and vascular smooth muscle. Here we show that exogenous hydrogen sulfide induces a caspase-independent cell death of peripheral blood lymphocytes that depends on their intracellular glutathion levels, with a physiologically relevant subset specificity for CD8(+) T cells and NK cells. Although lymphocyte activation does not modify their sensitivity to HS-, after 24 h exposure to hydrogen sulfide surviving lymphocyte subsets show a dramatically decreased proliferation in response to mitogens and a reduced IL-2 production. Overall, our data demonstrate that HS(-)reduces the cellular cytotoxic response of peripheral blood lymphocytes as well as their production of IL-2, therefore de-activating the major players of local inflammatory responses, adding new basic knowledge to the clinically well known anti-inflammatory effects of sulfur compounds.