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目的 YKL-40 is highly expressed in airway inflammation and remodeling,and higher levels of YKL-40 are detected in patients with inflammatory diseases.YKL-40 may participate in the mechanism of inflammatory mediators that regulate eosinophil-mediated airway inflammation and contribute to the pathogenesis of asthma.In the epithelium,YKL-40 could modulate the expression of eotaxin,granulocyte-macrophage colony-stimulating factor(GM-CSF),and interleukin(IL)-5,and the latter played an important role in eosinophilic airway inflammation.Hence,YKL-40 could be an attractive target in the design of asthma therapies.方法 Mouse airway epithelial cells were isolated and identified by immunofluorescent staining.The primary mouse tracheal epithelial cells were cultured with OVA for 48 h and transfected with YKL-40 siRNA.The relative levels of YKL-40,IL-5,GM-CSF,and Eotaxin mRNA transcripts were determined by semi-quantitative RT-PCR,and their proteins were determined by ELISA and Western blot assays,respectively.结果 The levels of YKL-40 protein in cells transfected with siRNA-YKL-40(YKL-40-si)were decreased by 70％compared with the levels in primary mouse tracheal epithelial cells transfected with siRNA-negative control(YKL-40-NC)or non-transfected epithelial cells(YKL-40-0)by Western blotting.The levels of eotaxin,GM-CSF,IL-5 mRNA and protein in cells transfected with siRNA-YKL-40(YKL-40-si)were markedly decreased compared with those in cells transfected with siRNA-negative control(YKL-40-NC)or non-transfected epithelial cells(YKL-40-0).结论 YKL-40 siRNA down-regulates the expression of eotaxin,IL-5,GM-CSF in OVA-stimulated airway epithelial cells.This finding could extend the prospective use of YKL-40 siRNA in asthma research and enlarge the armamentarium for treating asthma.