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Increased serum concentrations of tissue plasminogen activator correlate with an adverse clinical outcome in patients with bacterial meningitis

Bacterial meningitis is the most common serious infection of the central nervous system. It is still characterised by high mortality and morbidity in adults. In this disease extensive perpetuated inflammation with leucocyte invasion into the central nervous system (CNS) results in breakdown of the blood–brain barrier and promotes neuronal damage.1

Tissue type plasminogen activator (tPA) has been shown to have various biological effects that could have an impact on the pathophysiological changes observed in bacterial meningitis. In the CNS, endothelial cells, microglia, astrocytes, and neurones can produce the 70 kDa protein tPA, which normally does not cross the blood–brain barrier.2 Raised tPA levels in the cerebrospinal fluid (CSF) have previously been reported for certain CNS diseases such as multiple sclerosis, leukaemia, and encephalitis,3 and raised serum tPA levels for patients with sepsis.4

tPA converts plasminogen into plasmin, a rate limiting step in the proteolysis of fibrin, but also in the degradation of extracellular matrix, matrix metalloproteinase activation, and the processing of growth factors and cytokines.2 Further, tPA has been shown to increase neuronal cell death during excitotoxicity and cerebral ischaemia.2 Thus tPA may promote blood–brain barrier disruption, proinflammatory signalling, and neuronal damage, and so be involved in the pathophysiology of bacterial …