Lu Xiao-Xia, McCoy Karen S, Hu Wei-Kun, Xu Jia-Li, Wang Hai-Qin, Chen Peng, Chen He-Bin
Department of Pulmonary Medicine, Wuhan Women and Children Health Care Center, Wuhan, 430030, China.
Department of Pediatrics, Division of Pulmonary Medicine, Nationwide Children's Hospital and The Ohio State University School of Medicine and Public Health, Columbus, 43085, USA.
J Huazhong Univ Sci Technolog Med Sci. 2013 Aug;33(4):479-484. doi: 10.1007/s11596-013-1145-4. Epub 2013 Aug 1.
This study investigated the expression of interleukin-17 (IL-17) and T cell immunoglobulin mucin and domain-containing molecule-3 (Tim-3) in bronchoalveolar lavage fluid (BALF) of asthmatic mice and the effect of dexamethasone (DEX) on these factors. Thirty-six mice were randomly divided into three groups: normal group, asthmatic group and DEX group. The mouse model of asthma was established by sensitization with ovalbumin in both the asthmatic and DEX groups. The levels of IL-6, IL-10, IL-17 and TGF-β were measured in BALF by enzyme-linked immunesorbent assay (ELISA). The mRNA expression level of Tim-3 was detected by reverse transcription polymerase chain reaction (RT-PCR). The ratio of Tim-3+CD4+ cells to total CD4+ cells in BALF was determined by flow cytometry. Differential inflammatory cells in BALF were detected. The correlations among IL-17, IL-6, IL-10, Tim-3 and inflammatory cells were analyzed. The results showed that the levels of IL-17, IL-6 and Tim-3 were substantially increased and the IL-10 level decreased in BALF in the asthmatic mice, which was significantly reversed by DEX treatment. IL-17 expression was positively correlated with IL-6 and Tim-3 expression and the number of inflammatory cells but negatively with IL-10 expression. These results indicate that the increased expression of IL-17 and Tim-3 in BALF may be implicated in the occurrence and development of asthmatic inflammation; the mechanism by which DEX suppresses asthmatic airway inflammation involves down-regulation of IL-17 and Tim-3 levels.
本研究调查了哮喘小鼠支气管肺泡灌洗液（BALF）中白细胞介素-17（IL-17）和含T细胞免疫球蛋白粘蛋白结构域分子-3（Tim-3）的表达以及地塞米松（DEX）对这些因子的影响。36只小鼠随机分为三组：正常组、哮喘组和DEX组。哮喘组和DEX组均通过卵清蛋白致敏建立哮喘小鼠模型。采用酶联免疫吸附测定（ELISA）法检测BALF中IL-6、IL-10、IL-17和转化生长因子-β（TGF-β）的水平。通过逆转录聚合酶链反应（RT-PCR）检测Tim-3的mRNA表达水平。采用流式细胞术测定BALF中Tim-3+CD4+细胞与总CD4+细胞的比例。检测BALF中的差异炎症细胞。分析IL-17、IL-6、IL-10、Tim-3与炎症细胞之间的相关性。结果显示，哮喘小鼠BALF中IL-17、IL-6和Tim-3水平显著升高，IL-10水平降低，DEX治疗可显著逆转上述变化。IL-17表达与IL-6和Tim-3表达以及炎症细胞数量呈正相关，与IL-10表达呈负相关。这些结果表明，BALF中IL-17和Tim-3表达增加可能与哮喘炎症的发生发展有关；DEX抑制哮喘气道炎症的机制涉及下调IL-17和Tim-3水平。
