The mechanisms that cause the inflammation of airway and lung tissue in asthma have been studied extensively. It is noted that type 1 T helper cell (Th1)-related cytokines could decrease the accumulation of eosinophils in lung tissue and relieve airway constriction. But the therapeutic mechanisms of Th1 cytokines remain unclear. In this study, interleukin-12 (IL-12) DNA plasmid as a therapeutic reagent was delivered intravenously. Bronchoalveolar lavage (BAL) fluids were collected from IL-12 treated and control mice, and analyzed for cell composition and eotaxin level. The results showed that IL-12 DNA plasmid could effectively inhibit eosinophilia and airway inflammation in vivo. The level of eotaxin in BAL fluid also decreased. To further investigate the effect of Th1-related cytokines such as IL-12 or interferon-γ (IFN-γ) on the eotaxin level produced by lung cells, primary lung cell culture was established. The results demonstrated that both IL-12 and IFN-γ could suppress eotaxin secretion from IL-13 or IL-4 stimulated primary lung cell culture. Moreover, the inhibitory effect of IL-12 could not be reversed by the administration of anti-IFN-γ antibody. All the evidences suggested that IL-12 could regulate airway inflammation by suppressing the eotaxin secretion of lung tissue through an IFN-γ independent mechanism.
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