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Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are important mediators of host-induced tissue destruction and are implicated in the pathogenesis of neuroinflammatory diseases.1 MMPs are secreted by all cell types in the CNS and degrade constituents of the blood–brain barrier (BBB) basement membrane, such as type IV collagen, laminin, aggrin, and fibronectin.1 Models of CNS infections have shown infiltrating leukocytes use MMPs to traverse the glia limitans. Mmp knockout mice showed less immune pathology, BBB breakdown, and cellular infiltration,2 and MMP inhibitors gave better outcomes in experimental pneumococcal meningitis.3 However, the role of MMPs/TIMPs in the pathogenesis of CNS infection in humans is not well-defined.
Methods.
We measured pretreatment CSF MMP-1 to -10 and TIMP-1, -2, and -4 concentrations by ELISA (R&D, Abingdon, UK) in 96 HIV-negative, randomly chosen Vietnamese adults admitted to the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam, with bacterial (n = 31), tuberculous (n = 11), fungal (n = 13), parasitic (n = 11), or viral (n = 10) meningitis. Ten patients with cerebral malaria and 10 patients without infections served as controls. All were recruited between November 2006 and November 2008. We followed a predefined plan to explore relationships between CSF MMP/TIMP expression and prospectively recorded clinical features and outcome.
Standard protocol approvals, registrations, and patient consent.
The study was approved by the hospital's ethical and scientific committees and written informed consent was obtained from patients or relatives.
Results.
The baseline clinical and laboratory features of the patients are …
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