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Research ArticleArticle

Antitumor Necrosis Factor Therapy in Rat Chronic Granulomatous Colitis: Critical Dose-Timing Effects on Outcome

Sebastián Videla, Ana García-Lafuente, María Antolín, Jaime Vilaseca, Francisco Guarner, Ernesto Crespo, Guadalupe González, Antonio Salas and Juan R. Malagelada
Journal of Pharmacology and Experimental Therapeutics December 1998, 287 (3) 854-859;
Sebastián Videla
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Ana García-Lafuente
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María Antolín
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Jaime Vilaseca
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Francisco Guarner
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Ernesto Crespo
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Guadalupe González
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Antonio Salas
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Juan R. Malagelada
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Abstract

Inhibition of tumor necrosis fact (TNFα) is of potential benefit in the treatment of chronic inflammatory conditions. However, TNFα plays an important role in host defenses against infection, and blocking TNFα production may also have adverse effects. We tested the efficacy and safety of anti-TNFα therapy in experimental colitis induced by trinitrobenzenesulfonic acid. We cultured colonic wall specimens for bacterial growth and measured native TNFα protein synthesis in colonic tissue at days 0, 1, 4, 10 and 18 after induction of colitis. Anti-TNFα therapy (monoclonal g1 immunoglobulin, 15 mg/kg i.p., every third day) was started on either day 4 or day 10 after induction of colitis. On day 18, we measured the release of inflammatory mediators and scored colonic lesions. In acute lesions, several species of the common flora were grown, including Streptococcus, Staphylococcus, Bacteroides, clostridia and enterobacteria. In chronic lesions, only enterobacteria, clostridia and lactobacilli were isolated. TNFα production by inflamed colonic tissue was increased in both acute and chronic lesions. Anti-TNFα therapy induced a significant decrease in the release of inflammatory mediators and histopathological remission when treatment started on day 10. However, anti-TNFα therapy increased eicosanoid release and lesion scores when treatment started on day 4. In conclusion, acute colonic lesions showed polymicrobial infection. Anti-TNFα therapy induced remission of chronic intestinal inflammation, but early treatment did not prove effective.

Footnotes

  • Send reprint requests to: F. Guarner, M.D., Digestive System Research Unit, Hospital General Vall d’Hebron, Barcelona 08035, Spain.

  • ↵1 This work was supported by grant SAF 96/0056 from Comisión Interministerial de Ciencia y Tecnologı́a (Madrid, Spain) and by Bayer AG (Leverkusen, Germany).

  • Abbreviations:
    TNBS
    trinitrobenzenesulfonic acid
    TNFα
    tumor necrosis factor-α
    IL-1
    interleukin-1
    TXB2
    thromboxane B2
    LTB4
    leukotriene B4
    • Received October 31, 1997.
    • Accepted June 4, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 287, Issue 3
1 Dec 1998
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Research ArticleArticle

Antitumor Necrosis Factor Therapy in Rat Chronic Granulomatous Colitis: Critical Dose-Timing Effects on Outcome

Sebastián Videla, Ana García-Lafuente, María Antolín, Jaime Vilaseca, Francisco Guarner, Ernesto Crespo, Guadalupe González, Antonio Salas and Juan R. Malagelada
Journal of Pharmacology and Experimental Therapeutics December 1, 1998, 287 (3) 854-859;

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Research ArticleArticle

Antitumor Necrosis Factor Therapy in Rat Chronic Granulomatous Colitis: Critical Dose-Timing Effects on Outcome

Sebastián Videla, Ana García-Lafuente, María Antolín, Jaime Vilaseca, Francisco Guarner, Ernesto Crespo, Guadalupe González, Antonio Salas and Juan R. Malagelada
Journal of Pharmacology and Experimental Therapeutics December 1, 1998, 287 (3) 854-859;
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