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Abstract 379Developmental Pharmacology: Drug Effects on Neonatal Angiogenesis and Vascular Function Platform, Monday, 5/3
Group B Streptococci (GBS) is a leading cause of neonatal sepsis and meningitis with case fatality of 5-10%. Ibuprofen (IBU) and other non-steroidal anti-inflammatory drugs (NSAID) may slow down the progression of inflammatory response in neonatal meningitis. We have shown that in addition to Cyclooxygenase (COX) inhibition, IBU also decreases the inducible Nitric Oxide Synthase (iNOS) activity. The aim of our study is to determine the molecular mechanism of ibuprofen in GBS-induced inflammation of neonatal brain microvascular endothelial cells (CMVL). We tested the hypothesis that ibuprofen will prevent iNOS gene expression by blocking the activation of Nuclear Factor kappa B (NF-kB). Using RT-PCR, Northern and Western analysis the iNOS and COX-2 levels were analyzed in CMVL exposed to GBS (106 cfu/ml)(n=3) and /or IBU(100 ug/ml) (n=3) for 48 hrs. Our data show significant suppression of mRNA and protein 24 hrs post treatment of cells GBS + IBU compared to GBS alone (table).
Clinical Pharmacology, Children's Hospital of Michigan-Wayne State University, Detroit, Michigan, Perinatal Research, Lady Davis Institute-McGill University, Montreal, Quebec, Canada
Maria Glibetic, Jackie Parker, Kay D Beharry & J V Aranda
Glibetic, M., Parker, J., Beharry, K. et al. Molecular Action of Ibuprofen in Neonatal Meningitis.
Pediatr Res45, 66 (1999). https://doi.org/10.1203/00006450-199904020-00396
