...
首页> 外文期刊>Oriental pharmacy and experimental medicine >Chronic stress aggravates inflammation of nasal mucosa in allergic rhinitis-induced mice model
【24h】

Chronic stress aggravates inflammation of nasal mucosa in allergic rhinitis-induced mice model

机译:慢性应激加剧变应性鼻炎诱发小鼠模型鼻黏膜的炎症

获取原文
   

获取外文期刊封面封底 >>

       

摘要

To investigate the effect of chronic stress on inflammation of nasal mucosa using an unpredictable chronic mild stress (UCMS) model to mimic chronic stress-like disorders. We divided BALB/c mice into four groups: control (n?=?5), UCMS-exposed (n?=?5), AR-induced (n?=?5) and UCMS-exposed/AR-induced groups (n?=?5). We measured cortisol as a marker of chronic stress and cytokines such as IFN-γ and IL-4, IL-5 representing Th1 and Th2 response, respectively, and we also examined the nasal mucous membrane histologically. UCMS exposure was confirmed by an increase in the levels of cortisol. Although there was no significant difference in Th1 cytokine (IFN-γ) levels within the groups, Th2 cytokine (IL-5) levels were significantly increased in stressed groups (UCMS-exposed and UCMS-exposed/AR-induced groups) compared to non-stressed groups (control and AR-induced groups). The histological examination of the nasal mucous membrane after antigen challenge in stressed group revealed severe dilation of blood vessels and injured olfactory hairs on the olfactory mucous membrane and severe swelling in the respiratory epithelium, compared to non-stressed group. These results suggest that chronic stress can aggravate inflammation of nasal mucosa in AR-induced mice model by shifting to the Th2 response by up-regulation of Th2 cytokines expression.
机译:为了研究慢性应激对鼻粘膜炎症的影响,使用不可预测的慢性轻度应激(UCMS)模型来模拟慢性应激样疾病。我们将BALB / c小鼠分为四组:对照组( n ?=?5),暴露于UCMS的小鼠( n ?== ?5),AR诱导( n ?=?5)和UCMS暴露/ AR诱导的组( n ? =?5)。我们测量了皮质醇作为慢性应激的标志物,并分别测定了IFN-γ和IL-4,IL-5分别代表Th1和Th2反应的细胞因子,并从组织学角度检查了鼻黏膜。皮质醇水平升高证实了UCMS暴露。尽管各组之间的Th1细胞因子(IFN-γ)水平没有显着差异,但是与非对照组相比,应激组(UCMS暴露和UCMS暴露/ AR诱导的组)中Th2细胞因子(IL-5)的水平显着增加。应激组(对照组和AR诱导组)。与非应激组相比,应激组抗原刺激后鼻黏膜的组织学检查显示,血管严重扩张,嗅黏膜上的嗅毛受损,呼吸道上皮严重肿胀。这些结果表明,慢性应激可通过上调Th2细胞因子表达转移至Th2反应,从而加重AR诱导的小鼠模型中鼻粘膜的炎症。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号