Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis

Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardi...

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Bibliographic Details
Published in:Journal of immunology research 2017-01, Vol.2017 (2017), p.1-17
Main Authors: Lindner, Diana, Blankenberg, Stefan, Escher, Felicitas, Klingel, Karin, Gotzhein, Frauke, Becher, Peter Moritz, Westermann, Dirk
Format: Article
Language:English
Subjects:
Acute Disease
Animals
Biomarkers
Cardiology
Cardiomyocytes
Cardiomyopathy
Chronic illnesses
Collagen
Cytokines
Cytokines - genetics
Cytokines - metabolism
Disease Models, Animal
Enterovirus
Enterovirus B, Human
Fibroblasts
Fibroblasts - metabolism
Fibrosis
Gene expression
Heart failure
Hemodynamics
Hypertension
Immunoglobulins
Immunology
Infections
Inflammation
Inflammation Mediators - metabolism
Investigations
Laboratory animals
Male
Mice
Myocarditis - pathology
Myocarditis - physiopathology
Myocarditis - virology
Picornaviridae
Rodents
Time Factors
Ventricular Dysfunction
Ventricular Remodeling
Viral infections
Virus Replication
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Summary:Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardiac function. Material and Methods. We infected C57BL/6J mice with Coxsackievirus B3 and determined the hemodynamic function 7 as well as 28 days after infection. Subsequently, we analyzed viral burden and viral replication in the cardiac tissue as well as the expression of cytokines and matrix proteins. Furthermore, cardiac fibroblasts were infected with virus to investigate if viral infection alone induces profibrotic signaling. Results. Severe cardiac inflammation was determined and cardiac fibrosis was consistently colocalized with inflammation during the acute phase of myocarditis. Declined cardiac inflammation but no significantly improved hemodynamic function was observed 28 days after infection. Interestingly, cardiac fibrosis declined to basal levels as well. Both cardiac inflammation and fibrosis were reversible, whereas the hemodynamic function remains impaired after healed viral myocarditis in C57BL/6J mice.
ISSN:2314-8861
2314-7156
DOI:10.1155/2017/6590609