Approaches to the pathogenesis of bronchial asthma

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Expression of SOCS family mRNA was examined in lung and spleen in a mouse model of asthma. Augmented expression of SOCS-1 but not SOCS-3 and SOCS-5 was observed in the lung. The expression of SOCS-1 was peaked in the first challenge, when maximum expressions of IL-4 and IFN-g mRNA were observed. The SOCS mRNA expressions were not changed in the spleen. To explore the role of SOCS-1, we examined the effects of exogenous administration of SOCS-1/liposome to the asthma model. The eosinophilic inflammation was significantly diminished following SOCS-1/liposome in comparison with null/liposome administration. Furthermore, prolonged eosinophilic inflammation was observed in an asthma model in SOCS-1^<+/-> mice. These results indicated that SOCS-1 is involved in eosinophilic airway inflammation, and it could promote resolution. of the inflammation.We originally observed IL-12 inhibitory factor in the supernatants from antigen-stimulated splenic T cells obtained from asthma model mice. The estimated molecular weight of inhibitory factor was almost equal to naive mouse IL-10 by HPLC. Since the inhibitory activity was neutralized by addition of anti-IL-10 antibody, we concluded that the factor is IL-10. This means IL-10. is the most important for diminishing IL-12 in mouse model of asthma.