Experimental pneumococcal meningitis causes central nervous system pathology without inducing the 72-kd heat shock protein.
Experimental pneumococcal meningitis causes central nervous system pathology without inducing the 72-kd heat shock protein.
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发表时间：
1992-07
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通讯作者：
M. Tauber;S. Kennedy;J. Tureen;Daniel H. Lowensteinl
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作者：
M. Tauber;S. Kennedy;J. Tureen;Daniel H. Lowensteinl
我们检查了实验性肺炎球菌脑膜炎是否诱导 72-kd 热休克蛋白 (HSP72)，这是其他中枢神经系统 (CNS) 损伤模型中神经元应激的敏感标志物。脑损伤的特征是受感染动物的皮层出现血管炎、脑炎和脓肿形成。这些变化的程度与接种量（P小于0.003）和疾病严重程度的病理生理参数相关，即脑脊液（CSF）乳酸（r = 0.61，P小于0.0001）和CSF葡萄糖浓度（r = -0.55，P小于0.0001）。尽管存在许多具有损伤形态学证据的皮质区域，但在大多数动物中未检测到 HSP72。当存在时，只有罕见的神经元呈 HSP72 阳性。大脑样本的蛋白质印迹分析证实了 HSP72 诱导的缺乏。该模型中神经元 HSP72 表达的缺乏表明，与与 HSP72 诱导相关的 CNS 疾病相比，至少一些导致脑膜炎神经元损伤的事件是独特的。
We examined whether experimental pneumococcal meningitis induced the 72-kd heat shock protein (HSP72), a sensitive marker of neuronal stress in other models of central nervous system (CNS) injury. Brain injury was characterized by vasculitis, cerebritis, and abscess formation in the cortex of infected animals. The extent of these changes correlated with the size of the inoculum (P less than 0.003) and with pathophysiologic parameters of disease severity, i.e., cerebrospinal fluid (CSF) lactate (r = 0.61, P less than 0.0001) and CSF glucose concentrations (r = -0.55, P less than 0.0001). Despite the presence of numerous cortical regions having morphologic evidence of injury, HSP72 was not detected in most animals. When present, only rare neurons were HSP72 positive. Western blot analysis of brain samples confirmed the paucity of HSP72 induction. The lack of neuronal HSP72 expression in this model suggests that at least some of the events leading to neuronal injury in meningitis are unique, when compared with CNS diseases associated with HSP72 induction.