Ykl-40 Sirna Downregulates The Expression Of Eotaxin, Il-5, Gm-Csf In An Epithelial Cell Model Of Asthma

Background: YKL-40 is highly expressed in airway inflammation and remodeling, and higher YKL-40 levels 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 a important role in eosinophilic airway inflammation. Objectives: YKL-40 could be an attractive target in the design of asthma therapies. Methods: 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. Results: The YKL-40 protein levers in cells transfected with siRNA-YKL-40 (YKL40- 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). Conclusions: This finding could extend