Hermann G, Tovar C A, Beck F M, Sheridan J F
Department of Medical Microbiology and Immunology, College of Medicine, Ohio State University, Columbus 43210.
J Neuroimmunol. 1994 Jan;49(1-2):25-33. doi: 10.1016/0165-5728(94)90177-5.
The murine model of influenza viral infection was used to evaluate the effects of restraint stress on pathogenesis and survival in inbred strains of mice. We recently reported that restraint stress was associated with an enhanced probability of survival in one strain of inbred mouse, DBA/2, and not in another, C57BL/6. Those studies suggested that the protective mechanism(s) of stress on mortality in the DBA/2 mice might be attributable to elevated levels of circulating glucocorticoids. Therefore, daily levels of plasma glucocorticoids were measured during influenza viral infection in both these strains. The present studies demonstrated that influenza infection itself is perceived as a stressor in both C57BL/6 and DBA/2 mice as evidenced by elevated plasma glucocorticoid levels within 48 h of infection. However, augmentation of glucocorticoid levels was not seen in the DBA/2 mice that were also subjected to restraint stress during the course of infection. Thus, corticosterone levels alone did not account for the enhanced survival seen in this group of animals.
利用小鼠流感病毒感染模型来评估束缚应激对近交系小鼠发病机制和存活率的影响。我们最近报道，束缚应激与一种近交系小鼠DBA/2的存活率提高有关，而与另一种近交系小鼠C57BL/6无关。这些研究表明，应激对DBA/2小鼠死亡率的保护机制可能归因于循环糖皮质激素水平的升高。因此，在这两种品系小鼠感染流感病毒期间，对其血浆糖皮质激素的每日水平进行了测量。目前的研究表明，流感感染本身在C57BL/6和DBA/2小鼠中都被视为一种应激源，感染后48小时内血浆糖皮质激素水平升高即证明了这一点。然而，在感染过程中也受到束缚应激的DBA/2小鼠中，未观察到糖皮质激素水平的升高。因此，仅皮质酮水平并不能解释这组动物存活率的提高。
