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Damian N Meli, Stephan Christen, Stephen L Leib, Matrix Metalloproteinase-9 in Pneumococcal Meningitis: Activation via an Oxidative Pathway, The Journal of Infectious Diseases, Volume 187, Issue 9, 1 May 2003, Pages 1411–1415, https://doi.org/10.1086/374644
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Abstract
In experimental bacterial meningitis, matrix metalloproteinases (MMPs) and reactive oxygen species (ROS) contribute to brain damage. MMP-9 increases in cerebrospinal fluid (CSF) during bacterial meningitis and is associated with the brain damage that is a consequence of the disease. This study assesses the origin of MMP-9 in bacterial meningitis and how ROS modulate its activity. Rat brain-slice cultures and rat polymorphonuclear cells (PMNs) that had been challenged with capsule-deficient heat-inactivated Streptococcus pneumoniae R6 (hiR6) released MMP-9. Coincubation with either catalase, with the myeloperoxidase inhibitor azide, or with the hypochlorous acid scavenger methionine almost completely prevented activation, but not the release, of MMP-9, in supernatants of human PMNs stimulated with hiR6. Thus, in bacterial meningitis, both brain-resident cells and invading PMNs may act as sources of MMP-9, and stimulated PMNs may activate MMP-9 via an ROS-dependent pathway. MMP-9 activation by ROS may represent a target for therapeutic intervention in bacterial meningitis
- methionine
- bacterial meningitis
- azides
- traumatic brain injuries
- catalase
- gelatinase b
- heat (physical force)
- hypochlorous acid
- internship and residency
- matrix metalloproteinases
- pneumococcal meningitis
- neutrophils
- peroxidase
- reactive oxygen species
- streptococcus pneumoniae
- brain
- cerebrospinal fluid
- rats
- medical residencies