CAJ | 학술논문

目的：通过体外实验研究IL-31对肺泡Ⅱ型上皮细胞A549表达趋化因子C-C趋化因子配体2（CCL2）的影响，探讨IL-31在支气管哮喘气道炎症中的作用。方法体外培养肺泡Ⅱ型上皮细胞 A549，用不同浓度（10、50、100 ng/mL）IL-31作用A549细胞、相同浓度（10 ng/mL）IL-31作用A549细胞不同时间（12、24、36 h），收集细胞，提取细胞总RNA，荧光定量PCR法分析趋化因子CCL2 mRNA的表达情况。结果不同浓度IL-31作用于A549细胞后，趋化因子CCL2的表达较正常未处理组明显增加，差异有统计学意义（P＜0.05）；10 ng/mL IL-31作用A549细胞后，不同时间段CCL2的表达均增高，且差异有统计学意义（P＜0.05）。结论 IL-31作用于肺泡Ⅱ型上皮细胞A549后，趋化因子CCL2的表达明显增高，表明IL-31可能诱导肺组织细胞分泌趋化因子参与哮喘气道炎症过程。
목적：통과체외실험연구IL-31대폐포Ⅱ형상피세포A549표체추화인자C-C추화인자배체2（CCL2）적영향，탐토IL-31재지기관효천기도염증중적작용。방법체외배양폐포Ⅱ형상피세포 A549，용불동농도（10、50、100 ng/mL）IL-31작용A549세포、상동농도（10 ng/mL）IL-31작용A549세포불동시간（12、24、36 h），수집세포，제취세포총RNA，형광정량PCR법분석추화인자CCL2 mRNA적표체정황。결과불동농도IL-31작용우A549세포후，추화인자CCL2적표체교정상미처리조명현증가，차이유통계학의의（P＜0.05）；10 ng/mL IL-31작용A549세포후，불동시간단CCL2적표체균증고，차차이유통계학의의（P＜0.05）。결론 IL-31작용우폐포Ⅱ형상피세포A549후，추화인자CCL2적표체명현증고，표명IL-31가능유도폐조직세포분비추화인자삼여효천기도염증과정。
Objective To explore the effect of of IL-31 on airway inflammation of bronchial asthma by studying the effect of IL-31 on the expression of CCL2 in typeⅡalveolar epithelial cells A549 in vitro. Methods The typeⅡalveolar epithelial cells A549 were cultured in vitro,with the different-concentration IL-31 solution including 10,50,100 ng/mL acting on them and the same concentration IL-31(10 ng/mL)acting on the them for different times including 12,24 h and 36 h,and then collected the cells and extracted the total cellular RNA. The mRNA expression of chemokine CCL2 were measured by fluorescent real-time PCR assay. Results Compared with the normal treatment group ,the mRNA expression of chemokine CCL2 was significantly increased with different concentrations of IL-31 impacting on the A549 cells. The difference was statistically significant (P<0.05);The mRNA expression of chemokine CCL2 was increased with 10 ng/mL IL-31 impacting on the A549 cells at different time periods. The dif-ference had statistical significance(P<0.05). Conclusion The expression of chemokine CCL2 is obviously increased with the impact of IL-31 acting in type II alveolar epithelial cells A549 ,which indicates that IL-31 may probably induce lung tissue cells to secrete chemokines involving in asthmatic airway inflammation.