Forschungsdatenbank PMU-SQQUID

PMU-Autor/inn/en

Abstract

Adverse outcome in bacterial meningitis is associated with the breakdown of the blood-brain barrier (BBB). Matrix-metalloproteinases (MMPs) facilitate this process by degradation of components of the BBB. This in turn results in acute complications of bacterial meningitis including edema formation, increased intracranial pressure and subsequent ischemia. We determined the parenchymal balance of MMP-9 and TIMP-1 (tissue inhibitor of MMP) and the structural integrity of the BBB in relation to cortical damage in an infant rat model of pneumococcal meningitis. The data demonstrate that the extent of cortical damage is significantly associated with parenchymal gelatinolytic activity and collagen type IV degradation. The increased gelatinolysis was found to be associated with a brain parenchymal imbalance of MMP-9/TIMP-1. These findings provide support to the concept that MMPs mediated disruption of the BBB contributes to the pathogenesis of bacterial meningitis and that protection of the vascular unit may have neuroprotective potential.

Useful keywords (using NLM MeSH Indexing)

Animals

Animals, Newborn

Blood-Brain Barrier/pathology

Blotting, Western

Cerebral Cortex/metabolism

Cerebral Cortex/microbiology

Cerebral Cortex/pathology*

Collagen Type IV/metabolism*

Disease Models, Animal

Immunohistochemistry

Matrix Metalloproteinase 2

Matrix Metalloproteinase 9/metabolism*

Meningitis, Pneumococcal/metabolism

Meningitis, Pneumococcal/pathology

Meningitis, Pneumococcal/physiopathology*

Rats

Rats, Sprague-Dawley

Tissue Inhibitor of Metalloproteinase-1/metabolism*

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