Contribution of TNFα, IL-1β and CINC-1 for articular incapacitation, edema and cell migration in a model of LPS-induced reactive arthritis

• Published in: Cytokine (Philadelphia, Pa.) Vol. 36; no. 1; pp. 83 - 89
• Main Authors: Bressan, Elisângela, De Queiroz Cunha, Fernando, Tonussi, Carlos Rogério
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01-10-2006
• Subjects: Antibody; Arthritis; Chemokine; Cytokine; Escherichia coli; Inflammation; LPS; Pain; Chemokine; Pain; Antibody; Cytokine; Arthritis; Inflammation; LPS
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2006.11.007

The protective effect of anti-CINC-1, -TNFα and -IL-1β antisera on articular inflammatory incapacitation, articular diameter and synovial fluid cell content, which are correlated to nociception, edema and cell migration, respectively, were evaluated in a rat model of LPS-induced reactive arthritis. In this model,
Escherichia coli lipopolysaccharide (LPS; 30
ng) was injected in a knee-joint previously primed with carrageenan (300
μg). Articular incapacitation was evaluated hourly by the automated registering of the knee-joint function during animal walking, and the knee-joint edema was evaluated by measuring the articular diameter increase. After 6
h, the animals were euthanized for collecting synovial fluid for the evaluation of cell migration. LPS produced dose-dependent incapacitation and edema. Anti-TNFα, -IL-1β, and -CINC-1 antisera (20 and 40
μl) were used as pretreatment into knee-joint before LPS injection. At higher dose, Anti-TNFα and anti-CINC-1 were able to inhibit incapacitation, articular edema and mononuclear (MON) migration. Anti-IL1β did not affect incapacitation at any dose, although inhibited edema and cell migration. Surprisingly, the higher dose of anti-IL1β antisera did not inhibit cell migration, although inhibited articular edema. These findings corroborate the role TNFα has in different forms of arthritis, but points out the idea that CINC-1 (the homologue for human IL-8) may constitute a promising target for reactive arthritis management. Indeed, the potent antiedematogenic effect, and principally the anti-migration effect of anti-CINC-1, raises the possibility of a better control of disease progression than with anti-IL-1β therapies.