The Ohio State University, College of Dentistry, Section of Oral Biology, Columbus, OH 43218-2357, USA.
J Neuroimmunol. 2012 Feb 29;243(1-2):34-42. doi: 10.1016/j.jneuroim.2011.12.011. Epub 2012 Jan 12.
Social disruption stress (SDR) prior to primary influenza A virus (IAV) infection augments memory to IAV re-challenge in a T cell-specific manner. However, the effect of SDR on the primary anti-viral immune response has not been elucidated. In this study, SDR-infected (INF) mice terminated viral gene expression earlier and mounted an enhanced pulmonary IAV-specific CD8(+)T cell response versus controls. Additionally, SDR-INF mice had a more pro-inflammatory lung profile prior to and during infection and an attenuated corticosterone response. These data demonstrate neuroendocrine modification of the lung microenvironment and increased antigen-specific T cell activation, clonal expansion and viral control in stress-exposed mice.
社会扰乱应激（SDR）在原发性甲型流感病毒（IAV）感染前增强了对 IAV 再挑战的记忆，具有 T 细胞特异性。然而，SDR 对原发性抗病毒免疫反应的影响尚未阐明。在这项研究中，与对照组相比，SDR 感染（INF）小鼠更早地终止了病毒基因表达，并引发了更强的肺 IAV 特异性 CD8+T 细胞反应。此外，SDR-INF 小鼠在感染前和感染期间具有更具炎症性的肺部特征，以及减弱的皮质酮反应。这些数据表明，应激暴露的小鼠中，肺微环境的神经内分泌发生了改变，抗原特异性 T 细胞的激活、克隆扩增和病毒控制得到了增强。
