SuXiaoqiong 1 Δ , PanJue 1 Δ , JinJianjun 2 , XuKan 3 , DengZhi 4 , ChenZhihong 1
  • 1. Department of Respiratory Medicine, Zhongshan Hospital Fudan University, Shanghai, 200032, China;
  • 2. ;
  • 3. ;
  • 4. ;
ChenZhihong, Email: czh60@hotmail.com
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Objective To observe whether interleukin-27 (IL-27) intervention could diminish allergic airway inflammation of mouse asthma induced by ovalbumin (OVA) and to investigate the related molecular mechanisms. Methods Sixty female C57/6J mice were randomly divided into six groups, a control group, an asthma group, two IL-27 prevention groups and two IL-27 treatment groups. Based on being sensitized and challenged with OVA in the asthma model, two kinds of IL-27 intervention asthma models were set up, one of which was low-dose multiple prevention model, the other was high-dose few times treatment model. HE stain and inflammation score were done for the lungs. CD4+ T cells were purified from mice spleen and cultured under Th2 medium with/without IL-27. Interleukin-4 (IL-4) was measured by ELISA. CD4+ T cells were cultured under different stringent Th2 medium and stimulated by IL-27. The level of total signal transducer and activator of transcription-1 (STAT1) protein and phos-STAT1 were tested by Western blot. Results In low-dose multiple prevention group, IL-27 inhibited inflammation around bronchial and vascular obviously, the inflammation score was lower than the asthma group (P < 0.05), while the treatment group had no obvious statistical significance (P > 0.05). IL-27 repressed Th2 differentiation of naïve CD4+ T cells which was independent of interferon-γand IL-10. This effect was via STAT1 signaling pathway. CD4+ T cells from asthma mice or cultured under high-IL-4 inducing medium were found impairment of STAT1 phosphorylation. Conclusions IL-27 could inhibit Th2 differentiation of naïve CD4+ T cells, but not in already committed Th2-CD4+ T cells. The inhibition effect of IL-27 for airway inflammation is obvious in prevention group, while the treatment group shows obviously resistance to inhibitory effect of IL-27. Already committed Th2-CD4+ T cells existed in asthma airway might be the reason for IL-27 resistance.

Citation: SuXiaoqiong, PanJue, JinJianjun, XuKan, DengZhi, ChenZhihong. Intranasal Administration of Interleukin-27 Alleviates Airway Allergic Inflammation of Ovalbumin-induced Mouse Asthma Model via STAT1 Signal Pathway. Chinese Journal of Respiratory and Critical Care Medicine, 2015, 14(5): 442-448. doi: 10.7507/1671-6205.2015110 Copy

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