Th17/Treg失衡在肺炎支原体肺炎患儿中的作用及其机制
| 作者: |
1杜许芳,
1周炯英
1 常熟市第二人民医院儿科，江苏 常熟 215500 |
| 通讯: |
杜许芳
Email: duxufang516@163.com |
| DOI: | 10.3978/j.issn.2095-6959.2016.12.023 |
摘要
目的：探讨Th17/Treg失衡在肺炎支原体肺炎患儿中的作用及其机制。方法：纳入2013年6月至2015年1月我院收治的60例肺炎支原体肺炎急性期患儿和30例同期体检的健康儿童为研究对象。流式细胞术分析两组儿童外周血Th17和Treg的百分率，ELISA分析Th17和Treg特异性细胞因子IL-17和IL-10的分泌水平，定量PCR测定Th17和Treg特异性转录因子RORγt和Foxp3 mRNA的表达水平，以及Notch信号分子(Notch1，Hes1和Hey1)的表达水平。结果：与健康儿童相比，肺炎支原体肺炎急性期患儿外周血的Th17的百分率，IL-17分泌水平以及特异性转录因子RORγt的表达水平均明显增高，差异均具有统计学意义(P<0.05)，而急性期患儿外周血的Treg的百分率，IL-10分泌水平以及特异性转录因子Foxp3的表达水平均较健康儿童明显降低，差异均具有统计学意义(P<0.05)。进一步分析显示急性期患儿Notch1、Hes1和Hey1的表达水平均明显高于健康儿童，其差异均具有统计学意义(P<0.05)。结论：Th17/Treg失衡参与儿童支原体肺炎的发生发展，Notch信号通路可能通过调节免疫细胞分化和细胞因子分泌参与Th17/Treg失衡。
关键词：
肺炎支原体肺炎
Th17
Treg
机制
Role and mechanism of Th17/Treg imbalance in children with mycoplasma pneumoniae pneumonia
CorrespondingAuthor: DU Xufang Email: duxufang516@163.com
DOI: 10.3978/j.issn.2095-6959.2016.12.023
Abstract
Objective: To explore the role and mechanism of Th17/Treg imbalance in children with mycoplasma pneumoniae pneumonia. Methods: 90 children were enrolled in this study from June 2013 to January 2015 at our hospital, among whom 60 cases were diagnosed with mycoplasma pneumoniae pneumonia and 30 cases were healthy children. The percentage of Th17 and Treg cells in both groups were analyzed by flow cytometry, the corresponding cytokines of IL-17 and IL-10 and the mRNA levels of specific transcriptional factors of Th17 and Treg (RORγ and Foxp3) were analyzed in both groups by ELISA and PCR, respectively. What’s more, the Notch signaling molecules (Notch1 and Hes1) were further investigated. Results: The percentage of Th17, the level of the associated cytokine (IL-17) and the mRNA level of transcriptional factor (RORγ) were all significantly higher in children with mycoplasma pneumoniae pneumonia than those healthy children (P<0.05), While, the percentage of Treg, the level of associated cytokine IL-10 and the mRNA level of transcriptional factor (Foxp3) were all significantly lower in children with mycoplasma pneumoniae pneumonia than those in healthy children (P<0.05). Furthermore, the mRNA levels of the Notch signaling molecules (Notch1 and Hes1) were both significantly increased in children with mycoplasma pneumoniae pneumonia by comparison with those in healthy children (P<0.05). Conclusion: Th17/Treg imbalance participates in the development of mycoplasma pneumoniae pneumonia in children. Notch signaling pathway may participate in Th17/Treg imbalance by regulating their differentiation and cytokine secretion.