Wang Jia, Kong Lingwen, Luo Qingli, Li Bei, Wu Jinfeng, Liu Baojun, Wu Xiao, Dong Jingcheng
Lab of Integrative Medicine for Lung, Inflammation and Cancers, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, China.
Inflammation. 2014 Dec;37(6):1984-2005. doi: 10.1007/s10753-014-9931-0.
We investigated the effects of respiratory syncytial virus (RSV) infections on ovalbumin (OVA)-challenged mice via regulation of Th17/Treg cell responses. BALB/c mice were challenged with OVA, followed by RSV infections twice. In OVA-challenged mice, the secretion of Th2/Th17-type cytokines, airway hyperresponsiveness and inflammation were significantly inhibited by initial RSV infection. Moreover, the in vivo findings demonstrated that initial RSV infection reversed the imbalance of Th17/Treg responses. In contrast, RSV re-infection strengthened Th2/Th17-type cytokine secretion, airway hyperresponsiveness, and inflammation, especially for lymphocyte infiltration in OVA-challenged mice. Meanwhile, RSV re-infection enhanced the imbalanced Th17/Treg responses. Upon all results reveal that RSV-induced respiratory infections may lead to dual effects pertaining to allergic airway inflammation by regulation of Th17/Treg responses.
我们通过调节Th17/Treg细胞反应，研究了呼吸道合胞病毒（RSV）感染对卵清蛋白（OVA）激发的小鼠的影响。用OVA激发BALB/c小鼠，随后进行两次RSV感染。在OVA激发的小鼠中，初次RSV感染显著抑制了Th2/Th17型细胞因子的分泌、气道高反应性和炎症。此外，体内研究结果表明，初次RSV感染逆转了Th17/Treg反应的失衡。相比之下，RSV再次感染增强了Th2/Th17型细胞因子的分泌、气道高反应性和炎症，尤其是在OVA激发的小鼠中淋巴细胞浸润。同时，RSV再次感染加剧了Th17/Treg反应的失衡。所有结果表明，RSV诱导的呼吸道感染可能通过调节Th17/Treg反应，对过敏性气道炎症产生双重影响。
