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Am J Physiol Lung Cell Mol Physiol 280: L400-L408, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 3, L400-L408, March 2001

L-Arginine attenuates lipopolysaccharide-induced lung chemokine production

Casey M. Calkins1, Denis D. Bensard1,2, Julie K. Heimbach1, Xianzhong Meng1, Brian D. Shames1, Edward J. Pulido1, and Robert C. McIntyre Jr.1

1 Department of Surgery, University of Colorado Health Sciences Center and The Veterans Affairs Hospital, Denver 80262; and 2 Department of Pediatric Surgery, The Children's Hospital, Denver, Colorado 80218

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-kappa B (NF-kappa B), an inducible transcription factor under the control of inhibitory factor kappa B-alpha (Ikappa B-alpha ). We have previously demonstrated that L-arginine (L-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized that L-Arg would attenuate the production of lung chemokines by stabilizing Ikappa B-alpha and preventing NF-kappa B DNA binding. We examined the effect of L-Arg on chemokine production, Ikappa B-alpha degradation, and NF-kappa B DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was given before L-Arg. LPS induced the production of chemokine protein and mRNA. L-Arg attenuated the production of chemokine protein and mRNA, prevented the decrease in Ikappa B-alpha levels, and inhibited NF-kappa B DNA binding. NO synthase inhibition abolished the effects of L-Arg on all measured parameters. Our results suggest that L-Arg abrogates chemokine protein and mRNA production in rat lung after LPS. This effect is dependent on NO and is mediated by stabilization of Ikappa B-alpha levels and inhibition of NF-kappa B DNA binding.

nitric oxide; nitric oxide synthase; cytokine-induced neutrophil chemoattractant-1; macrophage inflammatory protein-2; acute lung injury; nuclear factor-kappa B; inhibitory factor kappa B


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