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Nitric Oxide-Dependent Regulation of Pro-inflammatory Cytokines in Group B Streptococcal Inflammation of Rat Lung

Address correspondence to John P. Ofenstein, Ph.D., Clinical Pharmacology and Toxicology Laboratory, Children’s Hospital of Michigan/Wayne State University School of Medicine, 3901 Beaubien Boulevard, Detroit, MI 48201, USA; tel 313 745 5873; fax 313 745 5441; e-mail john.ofenstein{at}wayne.edu.

Group B Streptococcus (GBS) infection leading to sepsis and lung injury is a major cause of neonatal morbidity and mortality. Lung injury may result from overproduction of pro-inflammatory mediators (cytokines), caused by nitric oxide (NO). Our objective was to characterize the molecular signaling events involving the pro-inflammatory mediators interleukin-6 (IL-6) and macrophage inflammatory protein (MIP-2) in the presence of aminoguanidine (AG), an inducible nitric oxide synthase (iNOS) specific inhibitor, in lung tissue from GBS-treated young rats. Changes in iNOS mRNA, lactic acid, and rectal temperature were determined as markers of the inflammatory response. Expression and regulation of IL-6 and MIP-2 mRNA in lung tissue were studied by RT-PCR with densitometry analysis. GBS treatment of young rats induced the expression of pro-inflammatory mediators IL-6 (6-fold) and MIP-2 (3-fold) in lung tissue compared to controls. AG decreased IL-6 and MIP-2 expression. Addition of L-arginine (L-arg) reversed the AG effect on IL-6 and MIP-2 expression. These data suggest a role for the nitric oxide pathway in the overproduction of pro-inflammatory mediators IL-6 and MIP-2 during GBS-induced lung inflammation. This pathway may be responsible for the initiation of lung injury.

Keywords: Group B streptococcus, neonatal sepsis, lung injury, aminoguanidine, arginine, interleukin-6, macrophage inflammatory protein

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