Welsh C Jane, Steelman Andrew J, Mi Wentao, Young Colin R, Storts Ralph, Welsh Thomas H, Meagher Mary W
Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas 77843-4458, USA.
Ann N Y Acad Sci. 2009 Feb;1153:209-19. doi: 10.1111/j.1749-6632.2008.03984.x.
Psychological stress has been implicated in both the onset and exacerbation of multiple sclerosis (MS). Our research has focused on the role of stress at the onset of MS, using the mouse model Theiler's murine encephalomyelitis virus-induced demyelination. Theiler's virus is a natural pathogen of mice that causes a persistent infection of the central nervous system (CNS) and inflammatory immune-mediated demyelination that is very similar to MS. Our research has shown that restraint stress sufficiently increases corticosterone secretion to cause immunosuppression. Stressed mice develop decreased innate and adaptive immune responses, including decreased chemokine and cytokine responses, to virus, which leads to increased viral replication within the CNS. Higher levels of virus then cause increased later demyelinating disease. These findings may have important implications in our understanding of the interactions between stress and the development of autoimmune diseases induced by infectious agents.
心理压力与多发性硬化症（MS）的发病和病情加重均有关联。我们的研究聚焦于压力在MS发病时所起的作用，采用了小鼠模型——泰勒氏鼠脑脊髓炎病毒诱导的脱髓鞘模型。泰勒氏病毒是小鼠的一种天然病原体，会导致中枢神经系统（CNS）的持续性感染以及炎症免疫介导的脱髓鞘，这与MS非常相似。我们的研究表明，束缚应激会充分增加皮质酮分泌，从而导致免疫抑制。应激小鼠对病毒的先天性和适应性免疫反应均减弱，包括趋化因子和细胞因子反应降低，这导致中枢神经系统内病毒复制增加。更高水平的病毒进而导致后期脱髓鞘疾病加重。这些发现可能对我们理解压力与感染因子诱发的自身免疫性疾病发展之间的相互作用具有重要意义。
