Open AccessBlockade of interleukin‐17 A protects against coxsackievirus B 3‐induced myocarditis by increasing COX ‐2/ PGE 2 production in the heart
Author(s) -
Xie Yuquan,
Chen Ruizhen,
Zhang Xian,
Yu Yong,
Yang Yingzhen,
Zou Yunzeng,
Ge Junbo,
Chen Haozhu
Publication year - 2012
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00918.x
Subject(s) - viral myocarditis , myocarditis , interleukin 17 , tumor necrosis factor alpha , immunology , pathogenesis , inflammation , interleukin , blockade , coxsackievirus , biology , chemokine , medicine , cytokine , virus , receptor , enterovirus
The T h17/interleukin ( IL )‐17 axis controls inflammation and might be important in the pathogenesis of experimental autoimmune myocarditis ( EAM ) and other autoimmune diseases. However, the mechanism underlying the increased T h17 cell response in coxsackievirus‐induced myocarditis remains unclear. This study aimed to elucidate the regulatory mechanisms affected by blocking IL ‐17 A responses in acute virus‐induced myocarditis ( AVMC ) mice. The results showed that IL ‐17 A and COX ‐2 proteins were significantly increased in the cardiac tissue of acute myocarditis, as were T h17 cells in the spleen. Using anti‐mouse IL ‐17 A b to block IL ‐17 A on day 7 of the viral myocarditis led to decreased expressions of cardiac tumor‐necrosis factor alpha, IL ‐17 A and transforming growth factor beta in AVMC mice compared to isotype control mice. COX ‐2 and prostaglandin E 2 proteins were dramatically elevated, followed by marked reductions in CVB 3 replication and myocardial injury. These results hint that the T h17/ IL ‐17 axis is intimately associated with viral replication in acute myocarditis via induction of COX ‐2 and prostaglandin E 2.