CAJ | 학술논문

目的：研究YKL-40介导支气管上皮细胞的炎症反应及对支气管平滑肌细胞增殖和迁移的影响。方法：体外培养支气管上皮永生细胞系（BEAS-2B）和原代人支气管上皮细胞（HBECs），用不同浓度的YKL-40刺激BEAS-2B和HBECs不同时间后，用Realtime PCR和ELISA方法检测炎症细胞因子的变化。 YKL-40刺激BEAS-2B和HBECs 6 h后，更换新鲜培养基继续培养18 h后收集细胞培养液，命名为（ YKL-40-BEAS-2B-CM、YKL-40-HBECs-CM），用于培养支气管平滑肌细胞（BSMCs）。24 h后检测BSMCs迁移能力的变化，72 h后检测BSMCs增殖能力的变化。结果：在BEAS-2B和HBECs中，YKL-40均能以浓度和时间依赖方式增强IL-8 mRNA的表达和IL-8的分泌，但对RANTES、Eotaxin，TNF-α没有影响。 YKL-40-BEAS-2B-CM和YKL-40-HBECs-CM刺激BSMCs能显著增强其增殖能力和迁移能力，但去除YKL-40-BEAS-2B-CM和YKL-40-HBECs-CM中的IL-8后，则未见其可以明显提高BSMCs的增殖和迁移能力。结论：YKL-40通过调控支气管上皮表达和分泌IL-8参与了哮喘时的气道炎症反应，进一步通过影响支气管平滑肌细胞的增殖和迁移介导哮喘时的气道重构。抑制IL-8有望成为控制YKL-40介导的哮喘炎症反应和组织重构的有效干预措施。
목적：연구YKL-40개도지기관상피세포적염증반응급대지기관평활기세포증식화천이적영향。방법：체외배양지기관상피영생세포계（BEAS-2B）화원대인지기관상피세포（HBECs），용불동농도적YKL-40자격BEAS-2B화HBECs불동시간후，용Realtime PCR화ELISA방법검측염증세포인자적변화。 YKL-40자격BEAS-2B화HBECs 6 h후，경환신선배양기계속배양18 h후수집세포배양액，명명위（ YKL-40-BEAS-2B-CM、YKL-40-HBECs-CM），용우배양지기관평활기세포（BSMCs）。24 h후검측BSMCs천이능력적변화，72 h후검측BSMCs증식능력적변화。결과：재BEAS-2B화HBECs중，YKL-40균능이농도화시간의뢰방식증강IL-8 mRNA적표체화IL-8적분비，단대RANTES、Eotaxin，TNF-α몰유영향。 YKL-40-BEAS-2B-CM화YKL-40-HBECs-CM자격BSMCs능현저증강기증식능력화천이능력，단거제YKL-40-BEAS-2B-CM화YKL-40-HBECs-CM중적IL-8후，칙미견기가이명현제고BSMCs적증식화천이능력。결론：YKL-40통과조공지기관상피표체화분비IL-8삼여료효천시적기도염증반응，진일보통과영향지기관평활기세포적증식화천이개도효천시적기도중구。억제IL-8유망성위공제YKL-40개도적효천염증반응화조직중구적유효간예조시。
Objective:To investigate YKL-40-mediated inflammation in human bronchial epithelial cells and analyzed the soluble factors secreted by bronchial epithelial cells exposed to YKL-40 that were responsible for increasing proliferation and migration of primary normal human bronchial smooth muscle cells (BSMCs).Methods:YKL-40-induced inflammation was assayed in two human bronchial epithelial cells (BEAS-2B cell line and primary human bronchial epithelial cells ,namely HBECs).In addition,we treated BEAS-2B cells and HBECs with YKL-40,and added the conditioned culture media ( YKL-40-BEAS-2B-CM) and ( YKL-40-HBECs-CM) to BSMCs.The proliferation and migration of BSMCs were determined by premixed WST-1 cell proliferation reagent and QCM chemotaxis migration assay ,respectively.Results: Bronchial epithelial cells treated with YKL-40 resulted in a significant increase of IL-8 production,but have no effect about RANTES ,Eotaxin and TNF-α.YKL-40-BEAS-2B-CM and YKL-40-HBECs-CM induced IL-8 was found to further stimulate proliferation and migration of BSMCs ,and the effects were inhibited after neutralizing IL-8.Conclusion:Through investigating the interaction of airway epithelium and smooth muscle ,our findings implicate that YKL-40 may be involved in the inflammation of asthma by induction of IL-8 from epithelium,subsequently contributing to BSMCs proliferation and migration.Moreover, inhibition of IL-8 signaling is a potential therapeutic target for YKL-40-induced inflammation and remodeling of asthma.