title: Expression of IL-23/Th17 pathway in a murine model of Coxsackie virus B3-induced viral myocarditis.
abstract: BACKGROUND
  The IL-23/Th17 pathway is implicated in the pathogenesis of a number of chronic inflammatory and autoimmune diseases. Whether it regulates the viral myocarditis (VMC) is unknown.
  
  
  RESULTS
  To examine the pathogenesis role of IL-23/Th17 axis in VMC, we used male BALB/c mice to induced VMC by Coxsackie virus B3 (CVB3) peritoneal injection. IL-23, IL-17, and signal transducer and activator of transcription 3 (STAT3) mRNA in the myocardium of VMC mice were assessed by semi-quantitative RT-PCR. IL-23 and IL-17 protein from blood serum were evaluated by ELISA. Phosphorylated-STAT3 (p-STAT3) protein expression in the myocardium was evaluated by immunohistochemical staining. Flow cytometric analysis was used to evaluate the frequencies of Th17 subsets. Isolated CD4+ T cells from VMC mice were cultured with recombinant IL-23(rIL-23) in vitro. In addition, a STAT3-specific inhibitor (S3I-201) was used to test whether regulation of STAT3 could be partly responsible for Th17 diminution. Results showed that expression of IL-23, IL-17, STAT3 mRNA and protein increased in VMC mice. When purified CD4+ T cells derived from VMC mice were cultured in vitro with rIL-23, the frequency of Th17 cells was dramatically increased, accompanied by significantly enhanced production of IL-17 in the supernatants of cultured CD4+ T cells. S3I-201 significantly restrained Th17 cell proliferation.
  
  
  CONCLUSIONS
  The IL-23/Th17 pathway axis is strongly expressed in murine VMC, identifying a novel pathway of potential significance in viral myocarditis.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Yang
authors.forename: Wei-Feng
authors.initials: WF
authors.lastname: Wu
authors.forename: Yu-Luan
authors.initials: YL
authors.lastname: Yan
authors.forename: Yu
authors.initials: Y
authors.lastname: Pang
authors.forename: Qing
authors.initials: Q
authors.lastname: Kong
authors.forename: Yan-Lan
authors.initials: YL
authors.lastname: Huang
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003384:Coxsackievirus Infections / Q000276:immunology / Q000473:pathology*; D004770:Enterovirus / Q000276:immunology / Q000472:pathogenicity*; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D053759:Interleukin-23 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology
chemical_list: D020381:Interleukin-17; D053759:Interleukin-23; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse