Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Penetration of basement membrane is believed to be an essential step in the pathogenesis of bacterial meningitis. Consequently Streptococcus pneumoniae strains were tested for their ability to adhere to reconstituted basement membrane (Matrigel) and in a proceeding step penetrate this membrane by the use of surface activated plasmin. A majority of S. pneumoniae strains tested were found to adhere to reconstituted basement membrane as well as to the purified laminin component. Three out of seventeen strains also adhered to the collagen IV component. All the investigated strains also demonstrated a capacity to bind plasminogen with up to 42,000 plasminogen binding sites per bacterium as estimated by Scatchard analysis. Two strains selected for optimal adhesion and plasminogen binding were further tested for basement membrane penetration using a dual chamber model. Our data show that penetration was achieved within 3-4 h in the presence of plasminogen whereas without plasminogen no strain was able to penetrate during a 21 h incubation. The results suggest a potential role of surface associated plasminogen in bacterial penetration of basement membranes and extracellular matrix.
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PMID:Surface bound plasmin promotes migration of Streptococcus pneumoniae through reconstituted basement membranes. 1008 58

All forms of cerebral inflammation as found in bacterial meningitis, cerebral malaria, brain injury, and subarachnoid haemorrhage have been associated with vasospasm of cerebral arteries and arterioles. Vasospasm has been associated with permanent neurological deficits and death in subarachnoid haemorrhage and bacterial meningitis. Increased levels of interleukin-1 may be involved in vasospasm through calcium dependent and independent activation of the myosin light chain kinase and release of the vasoconstrictor endothelin-1. Another key factor in the pathogenesis of cerebral arterial vasospasm may be the reduced bioavailability of the vasodilator nitric oxide. Therapeutic trials in vasospasm related to inflammation in subarachnoid haemorrhage in humans showed a reduction of vasospasm through calcium antagonists, endothelin receptor antagonists, statins, and plasminogen activators. Combination of therapeutic modalities addressing calcium dependent and independent vasospasm, the underlying inflammation, and depletion of nitric oxide simultaneously merit further study in all conditions with cerebral inflammation in double blind randomised placebo controlled trials. Auxiliary treatment with these agents may be able to reduce ischemic brain injury associated with neurological deficits and increased mortality.
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PMID:Vasospasm in cerebral inflammation. 2561 Jul 3