| Summary: | 碩士 === 國立成功大學 === 生物化學研究所 === 92 === The current paradigm for allergic airway inflammation regards the activated T lymphocyte as the choirmaster of the inflammatory response. It has been shown that T cells secreting IL-10 in the respiratory mucosa can regulate Th2-induced airway hyperreactivity and inflammation. It suggests that IL-10 plays an important inhibitory role in allergic asthma. Our aims, therefore, were to explore if IL-19, a member of IL-10 family which includes IL-10, IL-19, IL-20, MDA-7 (IL-24)， and AK155 (IL-26) was associated with pathogenesis of asthma. Our previous study showed mouse IL-19 induced the production of IL-6 and TNF-α. Mouse IL-19 also induced mouse monocytes apoptosis and production of reactive oxygen species (ROS). To explore IL-19 is associated with pathogenesis of asthma, we employed ELISA to analyze the serum level of IL-19 in the asthma patients and found that IL-19 level in the patients was two-fold over the normal control. Patients with high level of IL-19 also contained high level of IL-4 and IL-13.We further develops an asthma animal model to study the relationship between IL-19 and asthma. IL-19 level in asthma mice was also two-fold over the control mice and the transcript of IL-19 was also induced in the lung of asthma mice. Delivery of IL-19 gene into mice by intramuscular electroporation showed that IL-19 up-regulated IL-4, IL-5 and IL-10 in vivo. IL-13 was not up-regulated by IL-19 in normal mice. However, IL-19 up-regulated IL-13 in asthma mice. In vitro, IL-19 also induced IL-4, IL-5, IL-10 and IL-13 production by the activated T cells. Activation of T cells is required for induction of IL-13 because IL-19 did not induce IL-13 production on unstimulated T cells. Taken together, these results demonstrated that IL-19 may play an important role in pathogenesis of asthma by regulating IL-13 production on activated T cells.
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