ArticlePloS one2011
Direct gene transfer with IP-10 mutant ameliorates mouse CVB3-induced myocarditis by blunting Th1 immune responses.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Machine learning-based mortality prediction for pediatric fulminant myocarditis using cytokine profiles.Scientific reports · 2026Article
- Zika virus infection in neonatal mice disrupts connexin 43 and induces cardiac inflammation, implicating viral myocarditis in neonatal pathogenesis.Journal of virology · 2025Article
- Antiviral and immunoregulatory effects of curcumin on coxsackievirus B3-infected hepatitis.Virus research · 2023Article
- Multidisciplinary diagnostic approach for fulminant myocarditis related to coronavirus disease 2019 messenger RNA vaccines: a case report.European heart journal. Case reports · 2023Article
- An Albumin-Binding Domain Peptide Confers Enhanced Immunoprotection Against Viral Myocarditis by CVB3 VP1 Vaccine.Frontiers in immunology · 2021Article
- Case report of severe myocarditis in an immunocompromised child with Respiratory Syncytial Virus infection.BMC pediatrics · 2018Article
- The cholinergic anti-inflammatory pathway ameliorates acute viral myocarditis in mice by regulating CD4Virulence · 2018Article
- Transmissible endoplasmic reticulum stress from myocardiocytes to macrophages is pivotal for the pathogenesis of CVB3-induced viral myocarditis.Scientific reports · 2017Article
- New Insights into the Immunobiology of Mononuclear Phagocytic Cells and Their Relevance to the Pathogenesis of Cardiovascular Diseases.Frontiers in immunology · 2017Review
- Phosphodiesterase Type 5 Inhibitor Sildenafil Decreases the Proinflammatory Chemokine CXCL10 in Human Cardiomyocytes and in Subjects with Diabetic Cardiomyopathy.Inflammation · 2016Article
- Phosphodiesterase type 5 inhibitors: back and forward from cardiac indications.Journal of endocrinological investigation · 2016Review
- The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart.Journal of immunology research · 2016Review
- Inhibition of Histone Deacetylase Activity Aggravates Coxsackievirus B3-Induced Myocarditis by Promoting Viral Replication and Myocardial Apoptosis.Journal of virology · 2015Article
- Tenascin-C aggravates autoimmune myocarditis via dendritic cell activation and Th17 cell differentiation.Journal of the American Heart Association · 2014Article
- Advances in monoclonal antibody application in myocarditis.Journal of Zhejiang University. Science. B · 2013Review
- Increased systemic Th17 cytokines are associated with diastolic dysfunction in children and adolescents with diabetic ketoacidosis.PloS one · 2013Article
- Update on coxsackievirus B3 myocarditis.Current opinion in rheumatology · 2012Review
- Regulatory T cells and Th17 cells in viral infections: implications for multiple sclerosis and myocarditis.Future virology · 2012Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocarditis is an inflammation of the myocardium that often follows the enterovirus infections, with coxsackievirus B3 (CVB3) being the most dominant etiologic agent. We and other groups previously reported that chemokine IP-10 was significantly induced in the heart tissue of CVB3-infected mice and contributed to the migration of massive inflammatory cells into the myocardium, which represents one of the most important mechanisms of viral myocarditis. To evaluate the direct effect of IP-10 on the inflammatory responses in CVB3 myocarditis, herein an IP-10 mutant deprived of chemo-attractant function was introduced into mice to antagonize the endogenous IP-10 activity, and its therapeutic effect on CVB3-induced myocarditis was evaluated. METHODOLOGY/PRINCIPAL
findingsThe depletion mutant pIP-10-AT, with an additional methionine after removal of the 5 N-terminal amino acids, was genetically constructed and intramuscularly injected into BALB/c mice after CVB3 infection. Compared with vector or no treatment, pIP-10-AT treatment had significantly reduced heart/body weight ratio and serum CK-MB level, increased survival rate and improved heart histopathology, suggesting an ameliorated myocarditis. This therapeutic effect was not attributable to an enhanced viral clearance, but to a blunted Th1 immune response, as evidenced by significantly decreased splenic CD4(+)/CD8(+)IFN-γ(+) T cell percentages and reduced myocardial Th1 cytokine levels. CONCLUSION/SIGNIFICANCE: Our findings constitute the first preclinical data indicating that interfering in vivo IP-10 activity could ameliorate CVB3 induced myocarditis. This strategy may represent as a new therapeutic approach in treating viral myocarditis.
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