IL-10 deficiency prevents IL-5 overproduction and eosinophilic inflammation in a murine model of asthma-like reaction

Eosinophilic inflammation and bronchial mucus secretion are among the chara cteristic pathalogical changes in asthmatic reaction, which is mediated by Th2 type responses. Although it belongs to Th2 cytokines especially in the mouse, IL-10 is often considered an inhibitory cytokine for both Th1 and Th 2 cells. In the present study, using a murine asthma model induced by ovalb umin (OVA), we demonstrated that endogenous IL-10 is critical for the devel opment of asthma-like responses. Specifically, in comparison with wild-type controls, IL-10 gene knockout (KO) mice showed significantly reduced IL-5 production, eosinophilic inflammation and mucus production without notable changes in IL-4 and IgE responses following i.p. sensitization and subseque nt intranasal challenge with OVA. In addition, Th1-related cytokine (IFN-ga mma and IL-12) production in IL-10 KO mice was significantly higher than th at in wild-type mice. The results suggest that endogenous IL-10 plays an im portant role in promoting pulmonary eosinophilic inflammatory reaction and mucus production during asthmatic reaction. The data also argue that IL-10 may be more influential in the development of IL-5-producing Th2 cells whic h differ from typical Th2 cells producing both IL-4 and IL-5.