Contribution of TNFα, IL-1β and CINC-1 for articular incapacitation, edema and cell migration in a model of LPS-induced reactive arthritis
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....
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| Published in: | Cytokine (Philadelphia, Pa.) Vol. 36; no. 1; pp. 83 - 89 |
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| Abstract | 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. |
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| AbstractList | The protective effect of anti-CINC-1, -TNF alpha and -IL-1 beta 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; 30ng) was injected in a knee-joint previously primed with carrageenan (300 is a subset of g). 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 6h, the animals were euthanized for collecting synovial fluid for the evaluation of cell migration. LPS produced dose-dependent incapacitation and edema. Anti-TNF alpha , -IL-1 beta , and -CINC-1 antisera (20 and 40 is a subset of l) were used as pretreatment into knee-joint before LPS injection. At higher dose, Anti-TNF alpha and anti-CINC-1 were able to inhibit incapacitation, articular edema and mononuclear (MON) migration. Anti-IL1 beta did not affect incapacitation at any dose, although inhibited edema and cell migration. Surprisingly, the higher dose of anti-IL1 beta antisera did not inhibit cell migration, although inhibited articular edema. These findings corroborate the role TNF alpha 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-1 beta therapies. 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. |
| Author | De Queiroz Cunha, Fernando Tonussi, Carlos Rogério Bressan, Elisângela |
| Author_xml | – sequence: 1 givenname: Elisângela surname: Bressan fullname: Bressan, Elisângela organization: Department of Pharmacology, CCB, Federal University of Santa Catarina, Campus Trindade, Florianópolis, SC 88040-900, Brazil – sequence: 2 givenname: Fernando surname: De Queiroz Cunha fullname: De Queiroz Cunha, Fernando organization: Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil – sequence: 3 givenname: Carlos Rogério surname: Tonussi fullname: Tonussi, Carlos Rogério email: tonussi@farmaco.ufsc.br organization: Department of Pharmacology, CCB, Federal University of Santa Catarina, Campus Trindade, Florianópolis, SC 88040-900, Brazil |
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