Engel S, Wehner H D, Meyermann R
Institute of Brain Research, University of Tübingen, Federal Republic of Germany.
Acta Neurochir Suppl. 1996;66:89-95.
The loss of neurons after severe closed head injury is not only a consequence of the primary impact but also of secondary damage mechanisms. Among the cell population of the central nervous system microglia is surely a candidate to influence secondary damage mechanisms by releasing cytotoxic cytokines [1]. About microglial reaction in closed traumatic brain injury (TBI), however, no data are available. In contrast to experiments using stab wound injury the covering of the CNS in closed TBI are still intact. We have examined 17 patients who died because of TBI after various times post injury. We studied the expression of antigens which are either permanently present on microglial cells or those which are only facultatively found on activated microglia. Low numbers of microglial cells were shown to express MHC-class II antigens immediately after TBI which is also true for CD 68 and leukocyte common antigen (LCA). Surprisingly, however, antigens such as HAM 56 were expressed not earlier than 72 hours after TBI as well as the lectin ricinus communis agglutinin-1 (RCA-1). The results indicate a delayed activation of microglia in traumatic brain injury.
严重闭合性颅脑损伤后神经元的丢失不仅是原发性撞击的结果，也是继发性损伤机制所致。在中枢神经系统的细胞群体中，小胶质细胞无疑是通过释放细胞毒性细胞因子来影响继发性损伤机制的一个候选因素[1]。然而，关于闭合性创伤性脑损伤（TBI）中的小胶质细胞反应，尚无相关数据。与使用刺伤损伤的实验不同，闭合性TBI中中枢神经系统的被膜仍然完整。我们检查了17例因TBI在受伤后不同时间死亡的患者。我们研究了那些要么永久存在于小胶质细胞上，要么仅在活化小胶质细胞上偶然发现的抗原的表达情况。结果显示，TBI后立即有少量小胶质细胞表达MHC-II类抗原，CD 68和白细胞共同抗原（LCA）也是如此。然而，令人惊讶的是，诸如HAM 56等抗原以及凝集素蓖麻凝集素-1（RCA-1）直到TBI后72小时才开始表达。这些结果表明创伤性脑损伤中小胶质细胞的激活存在延迟。
