ObjectiveTo 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. MethodsSixty 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. ResultsIn 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. ConclusionsIL-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.
ObjectiveTo detect expressions of interleukin-17 (IL-17) and interleukin-27 (IL-27) proteins in liver tissue of hepatic alveolar echinococcosis. MethodsThe edge liver tissues (from the lesion edge 0.5 cm) and the normal liver tissues (from the lesion edge 5 cm) of 20 patients with hepatic alveolar echinococcosis in the Affiliated Hospital of Qinghai University were collected and stored at-80℃ freezer. The immunohistochemical method was used to detect the expressions of IL-17 and IL-27 proteins in these two tissues. ResultThe positive rates of IL-17 and IL-27 protein expressions in the edge liver tissues were significantly higher than those in the normal liver tissues[IL-17:80.0% (16/20) versus 10.0% (2/20), χ2=12.36, P < 0.01; IL-27:85.0% (17/20) versus 20.0% (4/20), χ2=12.36, P < 0.01]. ConclusionHigh expressions of IL-17 and IL-27 protein in edge liver tissue might participate in progress of hepatic alveolar echinococcosis.
Objective To investigate expression level of interleukin-27 (IL-27)and its impact on virus replication in lung after infected with respiratory syncytial virus (RSV). Methods In vivo,7-week aged female C57 mice were infected with RSV and sacrificed on day 0,0.5,1,2,4,6,8 (n=5).The left lung was extracted for RNA,and then real-time PCR was used to detect the mRNA levels of IL-27p28,IL-27EBI3, RSV-M protein and interferon-β (IFN-β).The right lung was used for HE staining.In vitro, human lung epithelial cells (A549)were infected with RSV,and stimulated with different concentrations of recombinant human interleukin 27 (rhIL-27)in doses of 0,1ng/mL,10ng/mL,and 50ng/mL.After 24 hours,the mRNA expression of interferon induced transmembrane protein 3 (IFITM3),IFN-β,and RSV-M protein were determined by real-time PCR.IFITM3 and STAT1/pSTAT1 protein expression levels were detected by Western blot. Results The viral load in the lungs of mice peaked on 4 day post infection (DPI),then gradually decreased,and almost returned to normal on 8 DPI.IFN-β increased transiently 12 hours after infection,and then quickly returned to normal baseline.IL-27 p28/EBI3 levels peaked on 1 DPI,then gradually decreased to normal on 4 DPI.Stimulating RSV-infected A549 cells with rhIL-27 of 10ng/mL and 50ng/mL significantly inhibited viral replication,enhanced IFTIM3 mRNA expression,and induced STAT1 phosphorylation.However,rhIL-27 stimulation did not affect IFN-β mRNA expression. Conclusions The IL-27 mRNA expression increases after RSV infection.The inhibition of IL-27 on RSV replication might be related to up-regulation of STAT1 phosphorylation and IFITM3 protein expression.