Neurotoxicity of glia activated by gram-positive bacterial products depends on nitric oxide production

Kim, YS; Täuber, MG (1996). Neurotoxicity of glia activated by gram-positive bacterial products depends on nitric oxide production. Infection and immunity, 64(8), pp. 3148-53. New York, N.Y.: American Society for Microbiology

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The present study examined the mechanism by which bacterial cell walls from two gram-positive meningeal pathogens, Streptococcus pneumoniae and the group B streptococcus, induced neuronal injury in primary cultures of rat brain cells. Cell walls from both organisms produced cellular injury to similar degrees in pure astrocyte cultures but not in pure neuronal cultures. Cell walls also induced nitric oxide production in cultures of astrocytes or microglia. When neurons were cultured together with astrocytes or microglia, the cell walls of both organisms became toxic to neurons. L-NAME, a nitric oxide synthase inhibitor, protected neurons from cell wall-induced toxicity in mixed cultures with glia, as did dexamethasone. In contrast, an excitatory amino acid antagonist (MK801) had no effect. Low concentrations of cell walls from either gram-positive pathogen added together with the excitatory amino acid glutamate resulted in synergistic neurotoxicity that was inhibited by L-NAME. The induction of nitric oxide production and neurotoxicity by cell walls was independent of the presence of serum, whereas endotoxin exhibited these effects only in the presence of serum. We conclude that gram-positive cell walls can cause toxicity in neurons by inducing the production of nitric oxide in astrocytes and microglia.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases

UniBE Contributor:

Täuber, Martin G.






American Society for Microbiology




Factscience Import

Date Deposited:

04 Oct 2013 15:00

Last Modified:

04 May 2014 23:17

PubMed ID:


Web of Science ID:


URI: (FactScience: 60915)

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