Influenza A Virus Induces Interleukin-27 through Cyclooxygenase-2 and Protein Kinase A Signaling

Liu, Li; Cao, Zhongying; Chen, Jing; Li, Rui; Cao, Yanhua; Zhu, Chengliang; Wu, Kailang; Liu, Fang; Zhu, Ying

doi:10.1074/jbc.m111.308064

Cited by 66 publications

(83 citation statements)

References 51 publications

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“…The blot is a representative of three experiments with similar results. *p , 0.05. inhibits IAV replication by activating STAT1/2 phosphorylation and PKR phosphorylation (20). We also showed that IL-27 protein levels were elevated in patients with HBV infection and that HBV enhances the expression of IL-27 in several cell types, including THP-1, HepG2, Huh7, and HEK293T cells (36).…”

Section: Il-27 Enhances the Expression Of Ifn-l1 Receptors Il-28r1 Anmentioning

confidence: 68%

“…IL-27 has therapeutic potential through various mechanisms: inhibiting replication of HIV (12) and hepatitis C virus (HCV) (13), enhancing antitumor immune responses (14), directing antiproliferative effects on tumors (15)(16)(17), and reducing the inflammation associated with experimental autoimmune arthritis (18,19). We recently demonstrated that during influenza A virus (IAV) infection, IL-27 is strongly induced through cyclooxygenase-2 (COX-2)-and protein kinase A (PKA)-signaling pathways (20).…”

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confidence: 99%

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IL-27, a Cytokine, and IFN-λ1, a Type III IFN, Are Coordinated To Regulate Virus Replication through Type I IFN

Cao

Zhang

et al. 2014

The Journal of Immunology

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IL-27, a member of the IL-12 family, plays a critical role in the control of innate and adaptive immune responses. IFN-λ1, a member of the type III IFN family, shows antiviral abilities. In this study, we investigated the effects of IL-27 and IFN-λ1 on the replication of hepatitis B virus (HBV), a major pathogen associated with a high risk for cirrhosis, liver failure, and hepatocellular carcinoma. We revealed that HBV infection activates IL-27 expression and IFN-λ1 production and demonstrated that viral-activated IL-27 and IFN-λ1 are coordinated to inhibit HBV replication. Initially, HBV infection upregulates IL-27 expression, which, in turn, stimulates IFN-λ1 production through regulating ERK1/2 signaling and by enhancing NF-κB nuclear translocation to bind to the IFN-λ1 promoter. Moreover, IL-27–activated IFN-λ1 upregulates IFN-λ1 receptor (IL-28R1 and IL-10Rβ) activity, resulting in the activation of the STAT1/2 pathway, which, in turn, induces the expression of IFN-stimulated genes, including IFN-inducible dsRNA-activated protein kinase, oligoadenylate synthetase 1, and IFN-induced GTP-binding protein 1 and, finally, inhibits HBV protein expression and viral capsid–associated DNA replication. More interestingly, we also revealed that type I IFN (IFN-α) is also involved in the downregulation of HBV replication mediated by IL-27. Thus, we identified a previously unknown mechanism by which IL-27 and IFN-λ1 are coordinated to regulate virus replication through type I IFN.

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Section: Il-27 Enhances the Expression Of Ifn-l1 Receptors Il-28r1 Anmentioning

confidence: 68%

mentioning

confidence: 99%

IL-27, a Cytokine, and IFN-λ1, a Type III IFN, Are Coordinated To Regulate Virus Replication through Type I IFN

Cao

Zhang

et al. 2014

The Journal of Immunology

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“…Similarly, a previous study demonstrated that IL-27 has INF-like response as it induces antiviral genes including PKR, 2'-5' Oligoadenylate synthase and myxovirus protein 1 (Frank et al, 2010).Indeed, IL-27 was shown to be a potent inducer of IFN-gamma, which inhibits the viral replication (Tang et al, 2003). IL-27 was shown recently to inhibit human influenza virus, HIV, and HCV replication by inducing an IFN-like response (Fakruddin et al, 2007;Imamichi et al, 2008;Frank et al, 2010;Liu et al, 2012).The effect of SNP of IL27p28 (especially c.-964A/G (rs153109) on progression of various diseases such asassociation between HBV and HCC (Peng et al, 2013), HBV susceptibility and response to HCV genotype 1 therapy (Zicca et al, 2014) has been evaluated. Here we examined the effect of IL-27-p28.rs153109 SNP on the ability of patients infected with HCV genotype 4a to spontaneously resolve their infection.…”

Section: Introductionmentioning

confidence: 84%

Association of Interleukin-27 rs 153109 Single Nucleotide Polymorphism with Spontaneous Resolution of Hepatitis C Virus - Genotype 4a Infection in Egyptian Patients

Fawzy

Wahid²,

Nazmy³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Background: HCV is a major global health problem. IL-27 is a member of the IL-6/IL-12 cytokine family with a broad range of anti-inflammatory properties. Recent studies highlighted the effect of a SNP in the IL-27 promoter region on modulating the progression of infectious diseases and individual responses to therapy. Aim of the work: The present study investigated the potential role of (-964 A/G) SNP in the promoter region of IL-27p28 gene (alleles rs153109) on the outcome of HCV infection among genotype 4a infected patients. Materials and Methods: HCV genotyping confirmed that all of the HCV-infected patients had genotype 4a infection. Genomic DNA was extracted from 111 patients with chronic HCV infection, 42 spontaneous resolvers (SR) and 16 healthy controls. IL-27p28.rs153109 genotyping was assessed using PCR-RFLP then confirmed by DNA sequencing. Results: The frequency of IL-27-p28.rs153109AA, AG, and GG genotypes among chronically infected subjects were 74.8 %, 25.2%, and 0% while among the SR, they were 57.1%, 35.7%, and 7.14%, respectively. Our data show the unique presence of G/G genotype in the SR group (3 patients; 7.14%). Moreover, the "G" allele frequencies among chronic and resolved subjects were 12.6% and 25.0%, respectively (p=0.0136). Importantly, subjects with the GG genotype were more likely to clear their HCV infection than those with the AA genotype (p=0.0118). Conclusions: HCV genotype 4a subjects with the IL-27-p28.rs153109 A/G and G/G genotype were more likely to clear their HCV infection. Therefore, we propose IL-27p28.rs153109SNPas a genetic biomarker for predicting HCV infection outcome.

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“…41 Another research claimed that IL-27 is a novel anti-HIV cytokine that inhibits HIV replication by activating multiple interferon-inducible genes in macrophages. 42 Furthermore, Le Texier and associates showed that IL-27 along with TGFβ1 play a role in model of rodent cardiac allograft tolerance that their expression correlates with inhibition of Th17 differentiation and with expansion of regulatory CD4+ CD25+ T cells. 18 It also has been proposed that IL-27 can show as effective therapeutic agent suppresses differentiation of Th17 cells in autoimmune diseases like Sjögren syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…41 The role of IL-27 in the pathogenesis of other viral infections show its prominent role in removing viruses, for example; study of the role of IL-27 in influenza virus type A replication and gene expression showed inhibition and antiviral function of IL-27 which enforced by activation of STAT1/2/3. 42 Wang and associates carried out a gene expression profiling study and found that IL-27 serum levels were significantly higher in HBV-infected patients in comparing with healthy controls. 7 Zhu and associates determined the correlation between HBV infection and IL-27 gene expression, using semiquantitative RT-PCR and ELISA method which results showed that IL-27 was significantly elevated in patients as compared to healthy individuals.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Zare

Karimi²,

Rashki³

et al. 2017

Exp Clin Transplant

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Objectives: Hepatitis B viral infection is among the most common causes of cirrhosis and hepatocellular carcinoma and a frequent viral indication for liver transplant. Cytokine-mediated immunity plays a critical role in introducing and promoting hepatitis B virus outcomes and in graft microenvironment. Interleukin 27 is a heterodimeric cytokine and a member of interleukin-6/interleukin-12 family. Interleukin-27 shows a broad range of pro-and antiinflammatory properties and plays a determining role during immune responses in combating hepatitis B virus. Therefore, in this study, the possible association between expressions of interleukin-27 gene with hepatitis B virus infection was evaluated in liver transplant patients. Materials and Methods: In a cross-sectional study from liver transplant patients with the risk of hepatitis B virus infection who admitted to Namazi Hospital affiliated to Shiraz University of Medical Sciences, 50 patients were selected and subgrouped to 25 hepatitis B virus-infected and 25 noninfected ones between years 2011 and 2013. The 25 healthy controls also were enrolled in this study. The presence of hepatitis B virus infection was assessed using polymerase chain reaction and enzyme-linked immunosorbent assay protocols in liver transplant patients. In addition, the interleukin-27 gene expression level was analyzed using an in-house-SYBER Green real time polymerase chain reaction method. The rate of interleukin-27 gene expression level was statistically analyzed in studied patient groups and controls using the Livak (2-ΔΔCT ) method. Results:The expression level of interleukin-27 gene was increased 10.27-and 2.36-fold in hepatitis B virusinfected and uninfected liver transplanted patients compared with healthy controls. Conclusion: Hepatitis B virus infection can lead to overexpression of interleukin-27 gene in liver transplant patients compared with uninfected ones and controls. However, further studies are needed to characterize the effective antihepatitis B virus effects of interleukin-27 in liver transplant patients.

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Influenza A Virus Induces Interleukin-27 through Cyclooxygenase-2 and Protein Kinase A Signaling

Cited by 66 publications

References 51 publications

IL-27, a Cytokine, and IFN-λ1, a Type III IFN, Are Coordinated To Regulate Virus Replication through Type I IFN

IL-27, a Cytokine, and IFN-λ1, a Type III IFN, Are Coordinated To Regulate Virus Replication through Type I IFN

Association of Interleukin-27 rs 153109 Single Nucleotide Polymorphism with Spontaneous Resolution of Hepatitis C Virus - Genotype 4a Infection in Egyptian Patients

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