par van der Poll, Tom;Marchant, Arnaud 
;Buurman, Wim;Berman, L;Keogh, C V;Lazarus, D D;Nguyen, L;Goldman, Michel ;Moldawer, L L;Lowry, Stephen F.
Référence The Journal of immunology, 155, 11, page (5397-5401)
Publication Publié, 1995-12
;Buurman, Wim;Berman, L;Keogh, C V;Lazarus, D D;Nguyen, L;Goldman, Michel ;Moldawer, L L;Lowry, Stephen F.Référence The Journal of immunology, 155, 11, page (5397-5401)
Publication Publié, 1995-12
Article révisé par les pairs
| Résumé : | IL-10 production during endotoxic shock is part of a protective mechanism that involves IL-10-induced inhibition of TNF synthesis. We sought to determine the role of IL-10 in septic peritonitis induced by cecal ligation and puncture (CLP). CLP led to a rapid induction of IL-10 mRNA in various organs of C57BI/6 mice. In liver, IL-10 mRNA was detectable within 1 h following CLP, while in spleen and lungs, IL-10 mRNA was detected from 2 to 4 h and onward. IL-10 protein became detectable in plasma 2 h after CLP, reaching peak concentrations after 12 h (12.7 +/- 5.7 ng/ml). Pretreatment (-2 h) with anti-IL-10 mAb resulted in higher plasma TNF levels following CLP when compared with mice treated with control mAb. Plasma IL-1 activity and IFN-gamma remained undetectable in virtually all mice. Anti-IL-10 enhanced mortality after CLP (p < 0.05 by log-rank test). Addition of anti-TNF mAb did not influence the increased mortality associated with anti-IL-10 treatment. Septic peritonitis is associated with sustained production of IL-10 in various organs, which serves to protect the host against lethality. |
