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Rheumatology 2002; 41: 509-517
© 2002 British Society for Rheumatology

Original Papers

Differential function of nitric oxide in murine antigen-induced arthritis

A. Veihelmann,*, A. Hofbauer*,1, F. Krombach1, M. Dorger1, M. Maier, H.-J. Refior and K. Messmer1

Department of Orthopaedics and
1 Institute for Surgical Research, Ludwig Maximilians University of Munich, Munich, Germany

Background. The aim of our study was to investigate the role of inducible nitric oxide synthase (iNOS)-derived nitric oxide (NO) production in different stages of murine antigen-induced arthritis (AiA).

Methods. Clinical, histological and microcirculatory parameters (measured by intravital fluorescence microscopy) were assessed in the knee joint during acute and chronic AiA after inhibition of iNOS with L-N6-(1-iminoethyl)lysine (L-NIL). Plasma concentrations of and were evaluated by the Griess reaction and the expression of iNOS, P- and E-selectin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) by immunohistochemistry.

Results. In both stages of the disease, plasma concentrations of and were increased and iNOS was expressed. In the acute phase, swelling, leucocyte adhesion, leucocyte infiltration and expression of adhesion molecules were increased in arthritic animals treated with L-NIL in comparison with untreated arthritic animals. In the chronic phase, no change in the disease parameters could be detected after L-NIL treatment.

Conclusion. Increased NO production induced by iNOS during the acute phase of AiA can be regarded as a protective response in the prevention of further leucocytic infiltration and joint destruction, whereas it seems to play a subordinate role in chronic AiA.

KEY WORDS: Rheumatoid arthritis, Nitric oxide, iNOS, Synovial microcirculation, L-NIL.

Correspondence to: A. Veihelmann, Department of Orthopaedics, Ludwig Maximilians University of Munich, Marchioninistrasse 15, 81366 Munich, Germany.

*The first two authors contributed equally to this work.


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