Gao Meng, Liu Liang-Xiao, Wu Fu-Ling, Zhang Xuejing, Li Ying-Ying, Shi Tao, Li De-Zhi, Han Ting-Ting
Department of Pediatrics, Binzhou Medical University Hospital, Binzhou, China.
Department of Pediatrics, Binzhou Medical University Hospital, Binzhou, China AND Department of Pediatrics, College of Clinical Medicine, Binzhou Medical University, Binzhou, China.
Iran J Allergy Asthma Immunol. 2017 Oct;16(5):386-395.
Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and hospitalization that lead to high morbidity and mortality among young infants. T helper 17 (Th17) cells and regulatory T cells (Tregs) play essential roles in the pathogenesis of autoimmune, cancer, and inflammatory diseases. However, whether changes in T-cell subsets are related to the systemic immune responses in RSV-caused bronchiolitis merit further investigation. Three-week-old Sprague Dawley (SD) rats were randomly divided into the normal control (NC) and RSV bronchiolitis (RSV-B) groups. An RSV-B model was successfully established using nasal drip containing RSV. Furthermore, pathological changes in the lung tissues were observed using hematoxylin and eosin staining. Flow cytometry determined the levels of Th17 and Treg subsets. The related cytokines were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of related transcription factors, such as RORγt and FOXP3, were examined using real-time quantitative PCR and western blot analysis. The RSV-B group exhibited pulmonary interstitial hyperemia and edema, inflammatory cell infiltration, wide alveolar septa, and bronchial collapse and deformation. The percentage of Th17 cells in RSV-B group was about 2.3 fold higher than that of NC group, and the concentration of IL-17, IL-23 and RORγt was higher than in NC group. In contrast, the percentage of Treg cells in the RSV-B group was approximately 0.7 fold lower than that in the NC group, and the levels of IL-10, TGF-β, and FOXP3 in the RSV-B group were lower than those in the NC group. The above results were statistically significant. The changes of Th17/Treg, and their associated cytokines, specific transcription factors, are present in RSV bronchiolitis model rats, which may play an important role in the pathogenesis of RSV bronchiolitis.
呼吸道合胞病毒（RSV）是导致细支气管炎和住院的主要原因，这些情况在幼儿中会导致高发病率和死亡率。辅助性T细胞17（Th17）和调节性T细胞（Tregs）在自身免疫性疾病、癌症和炎症性疾病的发病机制中发挥着重要作用。然而，T细胞亚群的变化是否与RSV引起的细支气管炎中的全身免疫反应相关，值得进一步研究。将三周龄的Sprague Dawley（SD）大鼠随机分为正常对照组（NC）和RSV细支气管炎（RSV-B）组。通过滴鼻给予含RSV的溶液成功建立了RSV-B模型。此外，使用苏木精和伊红染色观察肺组织的病理变化。流式细胞术测定Th17和Treg亚群的水平。使用酶联免疫吸附测定（ELISA）测量相关细胞因子。使用实时定量PCR和蛋白质印迹分析检测相关转录因子如RORγt和FOXP3的表达水平。RSV-B组表现出肺间质充血和水肿、炎性细胞浸润、肺泡间隔增宽以及支气管塌陷和变形。RSV-B组中Th17细胞的百分比比NC组高约2.3倍，IL-17、IL-23和RORγt的浓度高于NC组。相反，RSV-B组中Treg细胞的百分比比NC组低约0.7倍，RSV-B组中IL-10、TGF-β和FOXP3的水平低于NC组。上述结果具有统计学意义。Th17/Treg及其相关细胞因子、特异性转录因子的变化存在于RSV细支气管炎模型大鼠中，这可能在RSV细支气管炎的发病机制中起重要作用。
