IL-13 protects mice from lipopolysaccharide-induced lethal endotoxemia: correlation with down-modulation of TNF-alpha, IFN-gamma, and IL-12 production
العنوان: | IL-13 protects mice from lipopolysaccharide-induced lethal endotoxemia: correlation with down-modulation of TNF-alpha, IFN-gamma, and IL-12 production |
---|---|
المؤلفون: | T Muchamuel, S Menon, P Pisacane, M C Howard, D A Cockayne |
المصدر: | The Journal of Immunology. 158:2898-2903 |
بيانات النشر: | The American Association of Immunologists, 1997. |
سنة النشر: | 1997 |
مصطلحات موضوعية: | Immunology, Immunology and Allergy |
الوصف: | IL-13 is a potent down-modulator of macrophage proinflammatory activity in vitro, similar in this context to the anti-inflammatory cytokines IL-4 and IL-10. Since IL-10 effectively confers protection to mice from LPS-induced lethal endotoxemia through inhibition of proinflammatory cytokine production, we investigated whether IL-13 may also be capable of providing protection in this experimental model of endotoxic shock. A single injection of recombinant murine IL-13 (rmIL-13; 0.5-10 microg) significantly increased survival in a dose-dependent manner when a lethal i.p. injection of endotoxin was administered to BALB/c mice. This effect appeared to be IL-13 specific, since survival was not affected in mice that received heat-inactivated rmIL-13. rmIL-13 provided significant protection to mice even when given 30 min after LPS injection; however, this protection decreased in a time-dependent manner as the administration of rmIL-13 was delayed by 1, 2, and 5 h following LPS injection. The protective effect of IL-13 was correlated with significant decreases in the production of the inflammatory mediators TNF-alpha, IFN-gamma, and IL-12 as well as a decrease in the anti-inflammatory mediator IL-10. Our data suggest that IL-13 provides protection from LPS-induced lethal endotoxemia in a manner that is similar to but independent from that of IL-10, and therefore can be added to the list of cytokine immunomodulators that might be beneficial in the treatment of septic shock. |
تدمد: | 1550-6606 0022-1767 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::e46ad03667357cc2aa5c1474f8307e01 https://doi.org/10.4049/jimmunol.158.6.2898 |
رقم الأكسشن: | edsair.doi...........e46ad03667357cc2aa5c1474f8307e01 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15506606 00221767 |
---|