在泰勒氏病毒早期感染期间的慢性束缚应激会加剧SJL小鼠随后的脱髓鞘疾病。
Chronic restraint stress during early Theiler's virus infection exacerbates the subsequent demyelinating disease in SJL mice.
作者信息
Sieve Amy N, Steelman Andrew J, Young Colin R, Storts Ralph, Welsh Thomas H, Welsh C Jane R, Meagher Mary W
机构信息
Department of Psychology, Behavioral and Cellular Neuroscience Program, College of Liberal Arts, Texas A&M University, College Station, TX 77843-4235, USA.
出版信息
J Neuroimmunol. 2004 Oct;155(1-2):103-18. doi: 10.1016/j.jneuroim.2004.06.006.
Chronic restraint stress, administered during early infection with Theiler's virus, was found to exacerbate the acute central nervous system (CNS) viral infection and the subsequent demyelinating phase of disease (an animal model of Multiple Sclerosis (MS)) in SJL male and female mice. During early infection, stressed mice displayed decreased body weights and spontaneous activity; while increased behavioral signs of illness and plasma corticosterone (CORT) levels. During the subsequent chronic demyelinating phase of disease, previously stressed mice had greater behavioral signs of the chronic phase, worsened rotarod performance, and increased inflammatory lesions of the spinal cord. In addition, mice developed autoantibodies to myelin basic protein (MBP), proteolipid protein peptide (PLP139-151), and myelin oligodendrocyte glycoprotein peptide (MOG33-55).
研究发现，在感染泰勒氏病毒的早期对SJL雄性和雌性小鼠施加慢性束缚应激，会加剧急性中枢神经系统（CNS）病毒感染以及随后疾病的脱髓鞘阶段（多发性硬化症（MS）的动物模型）。在早期感染期间，受应激的小鼠体重下降且自发活动减少；而疾病行为体征和血浆皮质酮（CORT）水平升高。在随后的疾病慢性脱髓鞘阶段，先前受应激的小鼠具有更明显的慢性期行为体征、转棒试验表现恶化，且脊髓炎症性病变增加。此外，小鼠产生了针对髓鞘碱性蛋白（MBP）、蛋白脂蛋白肽（PLP139 - 151）和髓鞘少突胶质细胞糖蛋白肽（MOG33 - 55）的自身抗体。
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