Stress-induced facilitation of host response to bacterial challenge in F344 rats is dependent on extracellular heat shock protein 72 and independent of alpha beta T cells
Stress-induced facilitation of host response to bacterial challenge in F344 rats is dependent on extracellular heat shock protein 72 and independent of alpha beta T cells
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DOI：
10.3109/10253890.2011.653596
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发表时间：
2012-11-01
影响因子：
2.3
通讯作者：
Fleshner, Monika
中科院分区：
文献类型：
--
作者：
Campisi, Jay;Sharkey, Craig;Fleshner, Monika
体内应激反应的激活可以促进抗菌宿主防御。这种效应的一个可能机制是应激诱导的热休克蛋白72（Hsp 72）释放到细胞外环境中。Hsp 72是一种普遍存在的细胞蛋白，其响应于细胞应激而上调，并且当在细胞外环境中发现时调节免疫功能的各个方面，包括巨噬细胞炎症/杀菌反应和T细胞功能。目前的研究测试了这样一种假设，即炎症部位的体内细胞外Hsp 72（eHsp 72）有助于应激诱导的细菌限制性发育，并促进从细菌诱导的炎症中恢复，并且这种作用不依赖于α β（α β）T细胞。将雄性F344大鼠暴露于不可避免的电尾电击或无应激，并皮下注射大肠杆菌（ATCC 15746）。eHsp 72的作用通过在炎症部位的Hsp 72-免疫中和来研究。通过检测缺乏成熟α β T细胞的雄性无胸腺（rnu/rnu）裸大鼠和杂合胸腺完整对照（rnu/+）大鼠，检查T细胞的潜在贡献。结果是，应激暴露增加了血浆中eHsp 72的浓度，并促进了细菌性炎症的恢复。eHsp 72在炎症部位的免疫中和减弱了这种作用。应激暴露在无胸腺和完整对照大鼠中同样影响细菌炎症和eHsp 72。这些结果支持炎症部位的eHsp 72而不是α β T细胞有助于应激源暴露对皮下细菌炎症的影响的假设。
Activation of the in vivo stress response can facilitate antibacterial host defenses. One possible mechanism for this effect is stress-induced release of heat shock protein 72 (Hsp72) into the extracellular environment. Hsp72 is a ubiquitous cellular protein that is up-regulated in response to cellular stress, and modulates various aspects of immune function including macrophage inflammatory/bactericidal responses and T-cell function when found in the extracellular environment. The current study tested the hypothesis that in vivo extracellular Hsp72 (eHsp72) at the site of inflammation contributes to stress-induced restricted development of bacteria, and facilitated recovery from bacteria-induced inflammation, and that this effect is independent of alpha beta (alpha beta) T cells. Male F344 rats were exposed to either inescapable electrical tail-shocks or no stress, and subcutaneously injected with Escherichia coli (ATCC 15746). The role of eHsp72 was investigated by Hsp72-immunoneutralization at the inflammatory site. The potential contribution of T cells was examined by testing male athymic (rnu/rnu) nude rats lacking mature alpha beta T cells and heterozygous thymic intact control (rnu/+) rats. The results were that stressor exposure increased plasma concentrations of eHsp72 and facilitated recovery from bacterial inflammation. Immunoneutralization of eHsp72 at the inflammatory site attenuated this effect. Stressor exposure impacted bacterial inflammation and eHsp72 equally in both athymic and intact control rats. These results support the hypothesis that eHsp72 at the site of inflammation, and not alpha beta T cells, contributes to the effect of stressor exposure on subcutaneous bacterial inflammation.