Smoking and nicotine exposure delay development of collagen-induced arthritis in mice

IntroductionRecent epidemiological studies have implicated smoking as an environmental risk factor for the development of rheumatoid arthritis (RA). The aim of the present study is the evaluation of the role of cigarette smoke (CS) in the pathogenesis of collagen-induced arthritis in mice.

Methods: DBA/1 mice exposed to CS for 16 weeks (n=25) and mice exposed to nicotine in drinking water (n=10) were immunized with collagen type II (CII).

Severity of arthritis was evaluated clinically and morphologically and compared to control mice (n=35). Intensity of inflammation was evaluated by serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels.

Additionally, antibody response to CII (anti-CII) and citrullinated peptides (aCCP) was measured.

Results: Clinical evaluation of arthritis showed a delayed onset of arthritis in CS-exposed mice compared to non-smoking controls (P<0.05). Histological index and weight changes were comparable between the groups, however smoking mice presented less weight loss during the acute phase of the disease and gained weight significantly faster in the recovery phase (P<0.05).

Similar results were obtained in the mice exposed to nicotine. Nicotine also showed a direct anti-inflammatory effect diminishing IL-6 production by stimulated splenocytes in vitro (P<0.001).

Additionally, smoking mice had lower levels of aCCP and anti-CII antibodies compared to non-smoking (P<0.05).

Conclusions: Neither smoking nor nicotine exposure aggravates development of CII-induced arthritis in mouse model. Moreover, CS exposure was associated with a lower level of anti-CII antibodies, providing a possible explanation for a delay of arthritis onset in this group.

Author: Sofia Silfversward LindbladPiotr MydelIng-Marie JonssonRobert SeniorAndrej TarkowskiMaria Bokarewa
Credits/Source: Arthritis Research &Therapy 2009, 11:R88

Published on: 2009-06-11

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