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American Journal of Pathology, Vol 141, 53-60, Copyright © 1992 by American Society for Investigative Pathology

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Experimental pneumococcal meningitis causes central nervous system pathology without inducing the 72-kd heat shock protein

MG Tauber, SL Kennedy, JH Tureen and DH Lowenstein
Microbial Pathogenesis Unit, University of California, San Francisco 94143.

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.

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