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Weihui Gou, Zhen Zhang, Chunfeng Yang, Yumei Li
Macrophage polarization plays a crucial role in regulating myocardial inflammation and injuries of coxsackievirus B3 (CVB3)-induced viral myocarditis (VM). It has been reported that miR-223 is a potent regulator of inflammatory responses that involved in macrophage polarization. However, the functional roles of miR-223 in CVB3-induced VM still remain unknown. Here, we found that miR-223 expression was significantly down-regulated in heart tissues and heart-infiltrating macrophages of CVB3-infected mice. Up-regulation of miR-223 in vivo protected the mice against CVB3-induced myocardial injuries characterized by the increased body weight and survival, enhanced left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), relieved inflammation, depressed creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and aspartate transaminase (AST) levels, reduced production of interferon (IFN)-γ, interleukin (IL)-6 as well as increased IL-10...
March 7, 2018: Experimental Cell Research
Nannan Zhou, Yan Yue, Sidong Xiong
BACKGROUND: Viral myocarditis is a widespread cardiac disease associated with inflammation and myocardial injury and is predominantly caused by coxsackievirus B3 (CVB3) infection in humans as well as in mice. CVB3-induced myocarditis shows sexually dimorphic sensitivity and is more prevalent in male mice. Our previous studies showed that natural killer (NK) cells played an indispensable role in CVB3-induced myocarditis, and female mice exhibited less pathological cardiac interferon gamma (IFN-γ)+ NK cell infiltration than did male mice...
January 6, 2018: Canadian Journal of Cardiology
Lang Tian, Yeyi Yang, Chunyun Li, Jia Chen, Zhuoying Li, Xin Li, Shentang Li, Fang Wu, Zhangxue Hu, Zuocheng Yang
Coxsackievirus B3 (CVB3) is an important human pathogen linked to cardiac arrhythmias and acute heart failure. CVB3 infection has been reported to induce the formation of autophagosomes that support the viral replication in host cells. Interestingly, our study shows that the accumulation of autophagosomes during CVB3 infection is caused by a blockage of autophagosome-lysosome fusion rather than the induction of autophagosome biogenesis. Moreover, CVB3 decreases the transcription and translation of syntaxin 17 (STX17), a SNARE (soluble N-ethylmaleimide-sensitive factor activating protein receptor) protein involved in autophagosome-lysosome fusion...
February 14, 2018: Cell Death & Disease
Yan Wang, Ying Qin, Tianying Wang, Yang Chen, Xiujuan Lang, Jia Zheng, Shuoyang Gao, Sijia Chen, Xiaoyan Zhong, Yusong Mu, Xiaoyu Wu, Fengming Zhang, Wenran Zhao, Zhaohua Zhong
Enterovirus 71 (EV71) is the primary causative pathogen of hand, foot, and mouth disease (HFMD), affecting children with severe neurological complications. Pyroptosis is a programmed cell death characterized by cell lysis and inflammatory response. Although proinflammatory response has been implicated to play important roles in EV71-caused diseases, the involvement of pyroptosis in the pathogenesis of EV71 is poorly defined. We show that EV71 infection induced caspase-1 activation. Responding to the activation of caspase-1, the expression and secretion of both IL-1β and IL-18 were increased in EV71-infected cells...
February 13, 2018: Scientific Reports
Kapka Miteva, Kathleen Pappritz, Marzena Sosnowski, Muhammad El-Shafeey, Irene Müller, Fengquan Dong, Konstantinos Savvatis, Jochen Ringe, Carsten Tschöpe, Sophie Van Linthout
Inflammation in myocarditis induces cardiac injury and triggers disease progression to heart failure. NLRP3 inflammasome activation is a newly identified amplifying step in the pathogenesis of myocarditis. We previously have demonstrated that mesenchymal stromal cells (MSC) are cardioprotective in Coxsackievirus B3 (CVB3)-induced myocarditis. In this study, MSC markedly inhibited left ventricular (LV) NOD2, NLRP3, ASC, caspase-1, IL-1β, and IL-18 mRNA expression in CVB3-infected mice. ASC protein expression, essential for NLRP3 inflammasome assembly, increased upon CVB3 infection and was abrogated in MSC-treated mice...
February 12, 2018: Scientific Reports
Olli H Laitinen, Emma Svedin, Sebastian Kapell, Minna M Hankaniemi, Pär G Larsson, Erna Domsgen, Virginia M Stone, Juha A E Määttä, Heikki Hyöty, Vesa P Hytönen, Malin Flodström-Tullberg
Enteroviruses (EVs), such as the Coxsackie B-viruses (CVBs), are common human pathogens, which can cause severe disease including meningitis, myocarditis and neonatal sepsis. EVs encode two proteases (2Apro and 3Cpro), which perform the proteolytic cleavage of the CVB polyprotein and also cleave host cell proteins to facilitate viral replication. The 2Apro cause direct damage to the infected heart and tools to investigate 2Apro and 3Cpro expression may contribute new knowledge on virus-induced pathologies. Here, we developed new antibodies to CVB-encoded 2Apro and 3Cpro; Two monoclonal 2Apro antibodies and one 3Cpro antibody were produced...
February 6, 2018: Journal of Virological Methods
Fangqiang Song, Fanpo Kong, Hongqing Zhang, Yongqin Zhou, Ming Li
Inflammation and oxidative stress are implicated in the pathogenesis of acute viral myocarditis (AVM). Ulinastantin (UTI), an inhibitor of serine protease widely used in treatment of pancreatitis and various inflammatory disorders, displays cardioprotective properties in experimental animals. Although the specific mechanism through which UTI regulates cardiac function is not well explored, evidence suggests that UTI might activate nuclear factor E2-related factor 2 (Nrf2) signaling. In this study, we investigated the role of Nrf2 in mediating UTI's cardioprotection in a mouse model of AVM...
January 30, 2018: Inflammation
Yaping Wang, Liangliang Jia, Jian Shen, Yidong Wang, Zurong Fu, Sheng-An Su, Zhejun Cai, Jian-An Wang, Meixiang Xiang
Cathepsin B (CatB) is a cysteine proteolytic enzyme widely expressed in various cells and mainly located in the lysosomes. It contributes to the pathogenesis and development of many diseases. However, the role of CatB in viral myocarditis (VMC) has never been elucidated. Here we generated the VMC model by intraperitoneal injection of coxsackievirus B3 (CVB3) into mice. At day 7 and day 28, we found CatB was significantly activated in hearts from VMC mice. Compared with the wild-type mice receiving equal amount of CVB3, genetic ablation of CatB (Ctsb-/-) significantly improved survival, reduced inflammatory cell infiltration, decreased serum level of cardiac troponin I, and ameliorated cardiac dysfunction, without altering virus titers in hearts...
January 23, 2018: PLoS Pathogens
Francesca Pennino, Antonio Nardone, Paolo Montuori, Sara Aurino, Ida Torre, Andrea Battistone, Roberto Delogu, Gabriele Buttinelli, Stefano Fiore, Concetta Amato, Maria Triassi
Human enteroviruses (HEVs) occur in high concentrations in wastewater and can contaminate receiving environmental waters, constituting a major cause of acute waterborne disease worldwide. In this study, we investigated the relative abundance, occurrence, and seasonal distribution of polio and other enteroviruses at three wastewater treatment plants (WWTPs) in Naples, Southern Italy, from January 2010 to December 2014. Influent and effluent samples from the three WWTPs were collected monthly. One hundred and sixty-one of the 731 wastewater samples collected (22...
December 16, 2017: Food and Environmental Virology
Honghui Yang, Yan Chen, Chuanyu Gao
Viral myocarditis is one of the major causes of congestive heart failure and dilated cardiomyopathy. Recent reports have demonstrated an essential role of cytokines, like interleukin-13 (IL-13), in the pathogenesis of viral myocarditis, while the underlying mechanisms remain poorly defined. Here, using a coxsackie virus B3 (CVB3)-infection model in BALB/C mice, we showed that IL-13 protected mouse heart function in viral myocarditis, seemingly through reduction in T lymphocyte immunity and induction of M2 macrophage polarization...
November 21, 2017: Oncotarget
Su-Xia Ma, Zhi-Feng Bai, Wei Wang, Hui-Ying Wu
BACKGROUND: This study aims to investigate the regulative role of microRNA-93 (miR-93) in mouse cardiac microvascular endothelial cells (CMECs) injury and inflammatory response by negatively targeting SPP1 gene via the NF-κB signaling pathway. METHODS: Healthy Balb/c mice were recruited to establish mouse model with myocarditis using CVB3 virus. Mice were grouped into the normal, blank, negative control (NC), miR-93 inhibitor, miR-93 mimic, SPP1 shRNA and miR-93 mimic + SPP1 shRNA groups...
December 12, 2017: Journal of Cellular Biochemistry
Ye Qiu, Xin Ye, Huifang Mary Zhang, Paul Hanson, Guangze Zhao, Lei Tong, Ronald Xie, Decheng Yang
Nuclear factor of activated T cells 5 (NFAT5)/Tonicity enhancer binding protein (TonEBP) is a transcription factor induced by hypertonic stress in the kidney. However, the function of NFAT5 in other organs has rarely been studied, even though it is ubiquitously expressed. Indeed, although NFAT5 was reported to be critical for heart development and function, its role in infectious heart diseases has remained obscure. In this study, we aimed to understand the mechanism by which NFAT5 interferes with infection of Coxsackievirus B3 (CVB3), a major cause of viral myocarditis...
December 2017: PLoS Pathogens
Andreas Koenig, Iwona Buskiewicz, Sally A Huber
Sexual bias is a hallmark in various diseases. This review evaluates sexual dimorphism in clinical and experimental coxsackievirus B3 (CVB3) myocarditis, and how sex bias in the experimental disease changes with increased age. Coxsackieviruses are major causes of viral myocarditis, an inflammation of the heart muscle, which is more frequent and severe in men than women. Young male mice infected with CVB3 develop heart-specific autoimmunity and severe myocarditis. Females infected during estrus (high estradiol) develop T-regulatory cells and when infected during diestrus (low estradiol) develop autoimmunity similar to males...
2017: Frontiers in Immunology
Irene Müller, Thomas Vogl, Kathleen Pappritz, Kapka Miteva, Konstantinos Savvatis, David Rohde, Patrick Most, Dirk Lassner, Burkert Pieske, Uwe Kühl, Sophie Van Linthout, Carsten Tschöpe
BACKGROUND: The alarmins S100A8 and S100A9 are damage-associated molecular patterns, which play a pivotal role in cardiovascular diseases, inflammation, and viral infections. We aimed to investigate their role in Coxsackievirus B3 (CVB3)-induced myocarditis. METHODS AND RESULTS: S100A8 and S100A9 mRNA expression was 13.0-fold ( P =0.012) and 5.1-fold ( P =0.038) higher in endomyocardial biopsies from patients with CVB3-positive myocarditis compared with controls, respectively...
November 2017: Circulation. Heart Failure
Shi-Zhong Ma, Shu-Hua Luan, Ling-Juan Zhu, Xue Zhang, Xin-Sheng Yao
Two new phenolics, 1,3-di-O-p-coumaroyl-2',6'-di-O-acetylsucrose (1) and quercetin 3-O-β-D-apiofuranoyl-(1→2)-α-L-rhamnopyranoside (2), along with nine known compounds (3-11), were isolated from the whole plants of Antenoron filiforme var. neofiliforme. Their chemical structures were characterized on the basis of various spectroscopic techniques. This is the first report of the isolation of phenylpropanoid sucrose (1, 3-4) from the genus Antenoron. The bioassay results showed that compound 11 exhibited antiviral activity against the Coxsackie virus B3 (CVB3)...
November 21, 2017: Journal of Asian Natural Products Research
Xuejie Wu, Yawen Meng, Chao Wang, Yan Yue, Chunsheng Dong, Sidong Xiong
Semaphorin7A (Sema7A) has been reported to play various roles in nerve axon growth, tumor suppression, and tissue remodeling, as well as regulation of intestinal inflammation diseases. Viral myocarditis (VMC) characterized by viral-myocardial-cell necrosis and inflammatory cell infiltration is a common clinical disease of the cardiovascular system. However, the role of Sema7A in coxsackievirus B3 (CVB3)-induced VMC has not been reported. In this study, we generated an acute VMC mouse model by CVB3 infection, and manipulated Sema7A expression by in vivo polyethyleneimine-mediated Sema7A down-regulation...
January 2018: Journal of Molecular and Cellular Cardiology
Y Zhang, L Sun, H Sun, X Liu, X Luo, C Li, D Sun, T Li
The present study is to measure the expression of microRNA (miRNA or miR)-133b in circulating blood of children with viral myocarditis before and after drug treatment, and to investigate its relationship with the severity of myocardial lesions. A total of 36 children patients with viral myocarditis who received treatments at our hospital between June 2014 and June 2016 were enrolled in the present study, including 21 boys and 15 girls (age range, 9 months - 16 years).Quantitative real-time polymerase chain reaction was used to determine the expression of miR-133b in peripheral blood of patients and cardiomyocytes infected with CVB3...
October 31, 2017: Cellular and Molecular Biology
Denise Hübner, Kristin Jahn, Sandra Pinkert, Janik Böhnke, Matthias Jung, Henry Fechner, Dan Rujescu, Uwe Gerd Liebert, Claudia Claus
Human induced pluripotent stem cell (iPSC) lines are a promising model for the early phase of human embryonic development. Here, their contribution to the still incompletely understood pathogenesis of congenital virus infections was evaluated. The infection of iPSC lines with miscarriage-associated coxsackievirus B3 (CVB3) and measles virus (MV) was compared to the efficient teratogen rubella virus (RV). While CVB3 and MV were found to be cytopathogenic on iPSC lines, RV replicated without impairment of iPSC colony morphology and integrity...
December 8, 2017: ACS Infectious Diseases
Min Li, Kepeng Yan, Lin Wei, Yang Yang, Qian Qian, Wei Xu
Monocyte chemotactic protein-induced protein 1(MCPIP1) is identified as an important inflammatory regulator during immune response. MCPIP1 possesses antiviral activities against several viruses, such as Japanese encephalitis. However, its role on Coxsackievirus B3 (CVB3) infection, a positive-stranded RNA virus, has not been addressed. Here, we reported that MCPIP1 was up-regulated in cardiomyocytes by CVB3 infection and in hearts and pancreas of infected mice. Then we found that overexpression of MCPIP1 inhibited CVB3 replication and knockdown of it promoted virus replication...
October 17, 2017: Medical Microbiology and Immunology
Yanlan Huang, Yong Li, Bin Wei, Weifeng Wu, Xingcui Gao
The cluster of differentiation protein complex, CD80/CD86, regulates Th1/Th2 differentiation in autoimmune disease. In order to establish the effects of CD80/CD86 on Th17 cell differentiation in acute viral myocarditis (VMC), we infected C57BL/6 mice with Coxsackie virus B3 (CVB3) and examined the effects of the treatment with anti-CD80/CD86 monoclonal antibodies (mAbs) on Th17 cell differentiation in vivo. The effects of anti-CD80/CD86 mAbs on Th17 cell differentiation were further evaluated in vitro. The treatment with anti-CD80 mAb induced marked suppression of Th17 cell differentiation and ROR-γt mRNA expression, whereas anti-CD86 mAb alone had no effect, both in vivo and in vitro...
February 2018: Inflammation
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