title: Th17 cells contribute to viral replication in coxsackievirus B3-induced acute viral myocarditis.
abstract: Acute viral myocarditis (AVMC) is characterized by virus-triggered myocardial inflammation, and Coxsackievirus B3 (CVB3) is the primary pathogen. We previously proved that Th17 cells, besides having proinflammatory effects, were involved in AVMC by enhancing humoral response. However, the relationship between Th17 cells and CVB3 replication remains unknown. In this experiment, we infected BALB/c mice with CVB3 for establishing AVMC models and then found that, with the increase of viral replication, the expressions of splenic Th17 cells, serum IL-17, and cardiac IL-17 mRNA were elevated significantly, accompanied by the progressive cardiac injuries of AVMC. Furthermore, on day 5, the peak time for viral replication, correlation was positive between cardiac IL-17 mRNA and CVB3 RNA (correlation index = 0.835; p < 0.01). Although the expressions of Th1 and CD8(+) T cells, which could secrete the antiviral cytokine IFN-γ and damage the heart, were also elevated, along with Th17 cells, in AVMC, the neutralization of IL-17 further upregulated the percentages of splenic Th1 and CD8(+) T cells and the levels of cardiac IFN-γ mRNA. The cardiac pathological changes were obviously improved after neutralization, with reduced viral replication followed by decreases in the cardiac inflammatory cytokines IL-17, TNF-α, and IL-1β. These data suggest that Th17 cells contribute to CVB3 replication in AVMC, and that IL-17 might be an important target for regulating the balance of antiviral immunities.
authors.affiliation: Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Miao
authors.initials: M
authors.lastname: Yu
authors.forename: Qiong-Wen
authors.initials: QW
authors.lastname: Lin
authors.forename: Ai-Lin
authors.initials: AL
authors.lastname: Cao
authors.forename: Xian
authors.initials: X
authors.lastname: Yu
authors.forename: Ji-Hua
authors.initials: JH
authors.lastname: Dong
authors.forename: Jin-Ping
authors.initials: JP
authors.lastname: Wang
authors.forename: Jing-Hui
authors.initials: JH
authors.lastname: Zhang
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: He-Ping
authors.initials: HP
authors.lastname: Guo
authors.forename: Xiang
authors.initials: X
authors.lastname: Cheng
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002469:Cell Separation; D003384:Coxsackievirus Infections / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D029822:Enterovirus B, Human / Q000502:physiology; D005434:Flow Cytometry; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology* / Q000473:pathology / Q000821:virology; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D014779:Virus Replication / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D012333:RNA, Messenger