Expression of microglial markers in the human CNS after closed head injury.

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.