Sheridan J F, Feng N G, Bonneau R H, Allen C M, Huneycutt B S, Glaser R
Section of Oral Biology, Ohio State University College of Dentistry, Columbus 43210.
J Neuroimmunol. 1991 Mar;31(3):245-55. doi: 10.1016/0165-5728(91)90046-a.
Physical restraint administered to C57BL/6 mice significantly altered the inflammatory response to influenza virus infection and depressed anti-viral cellular immunity. Restraint-stressed animals showed a pattern of reduced mononuclear cell infiltration and lung consolidation which coincided with elevated plasma corticosterone levels. Furthermore, cellular immunity to virus was significantly depressed; interleukin-2 secretion was reduced by 96% and 59% in the mediastinal lymph nodes and spleens, respectively, as compared to a non-restrained group. However, the magnitude of the humoral immune response to influenza virus was unaffected by restraint stress. Anti-viral IgG antibody levels in restrained/infected mice did not differ when compared to a non-restrained/infected control group 14 days post-infection.
对C57BL/6小鼠实施身体束缚显著改变了其对流感病毒感染的炎症反应，并抑制了抗病毒细胞免疫。受到束缚应激的动物表现出单核细胞浸润减少和肺实变的模式，这与血浆皮质酮水平升高相一致。此外，对病毒的细胞免疫显著受到抑制；与未受束缚的组相比，纵隔淋巴结和脾脏中的白细胞介素-2分泌分别减少了96%和59%。然而，对流感病毒的体液免疫反应强度不受束缚应激的影响。感染后14天，与未受束缚/感染的对照组相比，受束缚/感染小鼠的抗病毒IgG抗体水平没有差异。
