- Paper Report
- Open Access
L-arginine in the control of lung chemokine production
- Undurti Das1
© Biomed Central Ltd 2001
- Received: 24 April 2001
- Published: 14 September 2001
- Acute lung injury, chemokines, nitric oxide
In experimental animals, acute lung injury (ALI) can be induced by lipopolysaccharide (LPS) administration. Accumulation of polymorphonuclear neutrophils (PMNs) during ALI involves chemoattractant cytokines such as cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein (MIP). LPS-induced PMN accumulation can be prevented by antibodies to these cytokines. Nitric oxide (NO) also prevents PMN accumulation in ALI. Nuclear factor ?B (NF?B) is a transcriptional regulator of CINC-1 and MIP-2; when bound to inhibitory factor ?B (I?B), NF?B is prevented from translocating to the nucleus and exerting its transcriptional effects. In this study the authors studied the effect of L-arginine, the precursor of NO, on modulation of NF?B expression.
L-arginine attenuated LPS-induced CINC-1 and MIP-2 production. Prior administration of L-arginine inhibited LPS-induced increases in NF?B binding of DNA, and maintained levels of free I?B after stimulation with LPS. These actions of L-arginine were abolished by an NO synthase inhibitor, this suggests that L-arginine and NO, the products of NO synthase action on L-arginine, are involved in regulation of NF?B. These results indicate that L-arginine would be useful in the prevention of ALI induced by LPS, and may prevent ALI induced by other agents.
Animal study, northern blotting, ELISA