L-Arginine attenuates lipopolysaccharide-induced lung chemokine production

Casey M. Calkins, Denis D. Bensard, Julie K. Heimbach, Xianzhong Meng, Brian D. Shames, Edward J. Pulido, Robert C. McIntyre

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-κB (NF-κB), an inducible transcription factor under the control of inhibitory factor κB-α (IκB-α). 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 IκB-α and preventing NF-κB DNA binding. We examined the effect of L-Arg on chemokine production, IκB-α degradation, and NF-κB 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 IκB-α levels, and inhibited NF-κB 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 IκB-α levels and inhibition of NF-κB DNA binding.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number3 24-3
StatePublished - Mar 2001
Externally publishedYes

Fingerprint

Chemokines
Lipopolysaccharides
Arginine
Lung
DNA
Nitric Oxide Synthase
Messenger RNA
Nitric Oxide
Proteins
Vascular System Injuries
Lung Injury
Neutrophils
Leukocytes
Transcription Factors

Keywords

  • Acute lung injury
  • Cytokine-induced neutrophil chemoattractant-1
  • Inhibitory factor κB
  • Macrophage inflammatory protein-2
  • Nitric oxide
  • Nitric oxide synthase
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology (medical)

Cite this

Calkins, C. M., Bensard, D. D., Heimbach, J. K., Meng, X., Shames, B. D., Pulido, E. J., & McIntyre, R. C. (2001). L-Arginine attenuates lipopolysaccharide-induced lung chemokine production. American Journal of Physiology - Lung Cellular and Molecular Physiology, 280(3 24-3).

L-Arginine attenuates lipopolysaccharide-induced lung chemokine production. / Calkins, Casey M.; Bensard, Denis D.; Heimbach, Julie K.; Meng, Xianzhong; Shames, Brian D.; Pulido, Edward J.; McIntyre, Robert C.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 280, No. 3 24-3, 03.2001.

Research output: Contribution to journalArticle

Calkins, CM, Bensard, DD, Heimbach, JK, Meng, X, Shames, BD, Pulido, EJ & McIntyre, RC 2001, 'L-Arginine attenuates lipopolysaccharide-induced lung chemokine production', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 280, no. 3 24-3.
Calkins CM, Bensard DD, Heimbach JK, Meng X, Shames BD, Pulido EJ et al. L-Arginine attenuates lipopolysaccharide-induced lung chemokine production. American Journal of Physiology - Lung Cellular and Molecular Physiology. 2001 Mar;280(3 24-3).
Calkins, Casey M. ; Bensard, Denis D. ; Heimbach, Julie K. ; Meng, Xianzhong ; Shames, Brian D. ; Pulido, Edward J. ; McIntyre, Robert C. / L-Arginine attenuates lipopolysaccharide-induced lung chemokine production. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2001 ; Vol. 280, No. 3 24-3.
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