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固定应激对急性小鼠弓形虫病发病机制的影响。

Effects of immobilization stress on the pathogenesis of acute murine toxoplasmosis.

作者信息

Chao C C, Peterson P K, Filice G A, Pomeroy C, Sharp B M

机构信息

Department of Medicine, Hennepin County Medical Center, Minneapolis, Minnesota.

出版信息

Brain Behav Immun. 1990 Jun;4(2):162-9. doi: 10.1016/0889-1591(90)90018-l.

DOI:10.1016/0889-1591(90)90018-l
PMID:2393725
Abstract

Stress modulates a variety of immune responses. We investigated the effects of immobilization stress on the pathogenesis of acute murine toxoplasmosis, an infection in which cell-mediated immunity is of major importance in host defense. Repetitive overnight immobilization beginning 3 days prior to infection enhanced (p less than 0.05) the mortality of mice infected with a virulent strain (C56) of Toxoplasma gondii (77% vs 15% mortality in restrained and control mice, respectively). Daily immobilization for 14 days prior to infection abrogated (p less than 0.05) the lethal effect of immobilization, suggesting an adaptive mechanism. To explore the effect of immobilization with a less virulent strain, the Me49 strain of T. gondii was studied. Acute infection with T. gondii Me49 resulted in anorexia and weight loss, while spleen size and respiratory burst activity of peritoneal exudate cells were enhanced (p less than 0.01). Immobilization (twice daily for 2 h) did not significantly alter survival or other clinical features of acute T. gondii infection. In addition, immobilization suppressed (p less than 0.05) phorbol myristate acetate-stimulated release of superoxide anion by peritoneal exudate cells in healthy naive mice, but not in infected mice. These findings indicate that immobilization stress can alter the pathogenesis of acute T. gondii infection in healthy mice, but the effect of this stress paradigm will be influenced, in part, by the timing of the immobilization and the virulence of the strain of T. gondii.

摘要

应激可调节多种免疫反应。我们研究了束缚应激对急性小鼠弓形虫病发病机制的影响,在这种感染中,细胞介导的免疫在宿主防御中至关重要。在感染前3天开始的重复性过夜束缚增加了(p<0.05)感染强毒株(C56)弓形虫的小鼠的死亡率(束缚组和对照组小鼠的死亡率分别为77%和15%)。在感染前每天束缚14天消除了(p<0.05)束缚的致死效应,提示存在一种适应性机制。为了探究束缚对毒力较低毒株的影响,研究了弓形虫Me49株。急性感染弓形虫Me49株导致厌食和体重减轻,而脾脏大小和腹腔渗出细胞的呼吸爆发活性增强(p<0.01)。束缚(每天两次,每次2小时)并未显著改变急性弓形虫感染的存活率或其他临床特征。此外,束缚抑制了(p<0.05)健康未感染小鼠腹腔渗出细胞中佛波酯肉豆蔻酸酯刺激的超氧阴离子释放,但对感染小鼠没有影响。这些发现表明,束缚应激可改变健康小鼠急性弓形虫感染的发病机制,但这种应激模式的影响将部分受到束缚时间和弓形虫毒株毒力的影响。

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