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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia.

IL-10 protects mice from LPS-induced lethality. To determine the effects of IL-10 on LPS-induced inflammatory responses, six Papio anubis baboons were i.v. injected with a sublethal dose of LPS (Salmonella typhimurium; 500 microg/kg) directly preceded by either human rIL-10 (n = 3, 500 microg/kg) or diluent (n = 3). IL-10 strongly inhibited LPS- induced release of TNF, IL-6, IL-8, and IL-12 (all p < 0.05). By contrast, IL-10 did neither influence the activation of the coagulation system (plasma levels of thrombin/antithrombin III complexes), nor the activation of the fibrinolytic system (plasma levels of tissue-type plasminogen activator, plasminogen activator inhibitor type I, and plasmin/alpha 2-antiplasmin complexes). IL-10 modestly attenuated neutrophilic leukocytosis and neutrophil degranulation (plasma concentrations of elastase/alpha1-antitrypsin complexes) (both p < 0.05). Changes in surface TNF receptor expression on circulating granulocytes were not affected by IL-10. These results suggest that during sublethal endotoxemia the predominant anti-inflammatory effect of IL-10 treatment is inhibition of proinflammatory cytokine release.[1]

References

  1. Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia. van der Poll, T., Jansen, P.M., Montegut, W.J., Braxton, C.C., Calvano, S.E., Stackpole, S.A., Smith, S.R., Swanson, S.W., Hack, C.E., Lowry, S.F., Moldawer, L.L. J. Immunol. (1997) [Pubmed]
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