Konstantinos A P, Sheridan J F
Department of Oral Biology, The Ohio State University Health Sciences Center, 305 W. 12th Avenue, PO Box 182357, Columbus, OH 43218-2357, USA.
Respir Physiol. 2001 Oct;128(1):71-7. doi: 10.1016/s0034-5687(01)00266-3.
Viral infection of the respiratory tract induces a complex series of cellular and molecular events leading to immunological responses designed to terminate viral replication. Anti-viral immunity involves natural resistance mechanisms that overlap and modulate the development of the subsequent adaptive immune responses. An experimental murine infection with influenza A/PR8 virus was used to examine the effects of stress-induced activation of the nervous and endocrine systems on components of innate immunity. Proinflammatory cytokine responses (IL-1alpha, IL-6 and TNFalpha) were measured in the lungs during an influenza A/PR8 viral infection. For activation of the nervous and endocrine systems, restraint stress (RST) was applied prior to and during infection. Following infection, IL-1alpha increased transiently, while elevated IL-6 persisted; TNFalpha was not detected. RST suppressed virally-induced IL-1alpha, while IL-6 was unaffected. These data demonstrate differential regulation of proinflammatory cytokines by stress. The mechanism underlying suppression of the lung IL-1alpha in stressed mice is currently unknown; its downregulation may contribute to increased viral pathogenesis in stressed individuals.
呼吸道的病毒感染会引发一系列复杂的细胞和分子事件，从而导致旨在终止病毒复制的免疫反应。抗病毒免疫涉及自然抵抗机制，这些机制与随后适应性免疫反应的发展相互重叠并对其进行调节。利用甲型流感病毒A/PR8对小鼠进行实验性感染，以研究应激诱导的神经和内分泌系统激活对先天免疫成分的影响。在甲型流感病毒A/PR8感染期间，检测了肺部促炎细胞因子反应（IL-1α、IL-6和TNFα）。为了激活神经和内分泌系统，在感染前及感染期间施加束缚应激（RST）。感染后，IL-1α短暂增加，而升高的IL-6持续存在；未检测到TNFα。RST抑制了病毒诱导的IL-1α，而IL-6未受影响。这些数据表明应激对促炎细胞因子有不同的调节作用。目前尚不清楚应激小鼠肺部IL-1α受抑制的潜在机制；其下调可能导致应激个体的病毒致病性增加。
