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(Journal of Leukocyte Biology. 2000;68:119-124.)
© 2000 by Society for Leukocyte Biology

The effects of NO synthase inhibitors on murine collagen-induced arthritis do not support a role of NO in the protective effect of IFN-

Laboratory of Immunobiology, Rega Institute, University of Leuven, Faculty of Medicine, B-3000 Leuven, Belgium

Correspondence: Dr. A. Billiau, Rega Institute, University of Leuven, Laboratory of Immunobiology, Minderbroedersstraat 10, B-3000 Leuven, Belgium. E-mail: Alfons.Billiau{at}rega.kuleuven.ac.be

DBA/1 mice deficient in expressing the interferon- (IFN-) membrane receptor (IFN-R KO mice) are more susceptible to collagen-induced arthritis (CIA) than wild-type mice, indicating that endogenous IFN- plays a protective role in the pathogenesis of CIA. In IFN-R KO mice, nitric oxide (NO) production during CIA is impaired. Because NO is known to exert immunosuppressive and anti-inflammatory effects in certain model systems, the protective effect of IFN- might be mediated by NO. Here, we tested in wild-type mice whether inhibition of NO production by metabolic inhibitors, aminoguanidine (AG) and L-N-(1-iminoethyl)lysine (L-NIL), could mimic the ablation of the IFN- receptor. A high-dose regimen of AG supplied in the drinking water inhibited NO production, disease development, and anticollagen antibody production but was also associated with transient body weight loss. At a dose and time regimen that still inhibited NO production but did not cause body weight loss, AG failed to affect disease scores. Treatment with L-NIL, which more specifically than AG affects inducible NO production, caused a slight increase in anticollagen antibody production although not significantly affecting disease occurrence. These data indicate that the diminished capacity of the IFN-R KO mice to produce NO following immunization with collagen is unlikely to account for their higher susceptibility to CIA.

Key Words: interferon- • nitric oxide • collagen-induced arthritis

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