Involvement of inducible nitric oxide synthase and mitochondrial dysfunction in the pathogenesis of enterovirus 71 infection
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Dejian Dang1, Chao Zhang1, Rongguang Zhang1,2, Weidong Wu2,3, Shuaiyin Chen1, Jingchao Ren2,3, Peng Zhang1, Guangyuan Zhou3, Demin Feng4, Tiantian Sun1, Ying Li1, Qiaoli Liu1, Mengchen Li1, Yuanlin Xi1, Yuefei Jin1 and Guangcai Duan1,2
1Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, People's Republic of China
2Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang, People's Republic of China
3School of Public Health, Xinxiang Medical University, Xinxiang, People's Republic of China
4The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China
Guangcai Duan, email: [email protected]
Yuefei Jin, email: [email protected]
Keywords: hand foot mouth disease, enterovirus71, inducible nitric oxide synthase, mitochondrial damage, BALB/c mice
Received: July 22, 2017 Accepted: August 28, 2017 Published: September 23, 2017
Enterovirus71 (EV71) is recognized as the main causative agent of severe hand, foot and mouth disease (HFMD). However, the pathogenesis of EV71 infection has not been well characterized. Clinical evidence indicated that inducible nitric oxide synthase (iNOS) induction in the lung of HFMD patients contributes to the severe symptoms of pulmonary edema. In the present study, we recruited 142 subjects including HFMD patients and controls, and serum level of nitric oxide (NO) was determined. Next, cellular and animal model were used to further investigate the roles of iNOS and mitochondria damage during EV71 infection. Serum NO level in HFMD patients with mild or severe symptoms was higher than that in controls, and there was a trend towards an increase in the serum NO level of severe cases relative to mild cases. EV71 infection caused apoptosis and increased levels of NO, iNOS, superoxide dismutase (SOD) activity and malondialdehyde (MDA), and degraded mitochondrial membrane potential (ΔΨm) in vitro. Pathological alterations of mitochondrial morphology were observed in vitro and in vivo. Furthermore, the expression of iNOS levels in target organs including brain, spinal cord, skeletal muscle, lung and heart were increased with the progression of the pathogenesis of EV71 infection in mice. Taken together, iNOS and mitochondrial damage participate in the pathogenesis of EV71 infection.
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