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Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication

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Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication. / Lindner, Diana; Li, Jia; Savvatis, Konstantinos; Klingel, Karin; Blankenberg, Stefan; Tschöpe, Carsten; Westermann, Dirk.

In: MEDIAT INFLAMM, Vol. 2014, 2014, p. 519528.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Lindner, D, Li, J, Savvatis, K, Klingel, K, Blankenberg, S, Tschöpe, C & Westermann, D 2014, 'Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication', MEDIAT INFLAMM, vol. 2014, pp. 519528. https://doi.org/10.1155/2014/519528

APA

Lindner, D., Li, J., Savvatis, K., Klingel, K., Blankenberg, S., Tschöpe, C., & Westermann, D. (2014). Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication. MEDIAT INFLAMM, 2014, 519528. https://doi.org/10.1155/2014/519528

Vancouver

Lindner D, Li J, Savvatis K, Klingel K, Blankenberg S, Tschöpe C et al. Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication. MEDIAT INFLAMM. 2014;2014:519528. https://doi.org/10.1155/2014/519528

Bibtex

@article{caa42a858572415b93b55d6a28099ceb,
title = "Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication",
abstract = "Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsackievirus B3 (CVB3) and detected increased gene expression of anti-inflammatory and antiviral cytokines in the heart. Subsequently, we infected cardiac fibroblasts, cardiomyocytes, and macrophages with CVB3. Due to viral infection, the expression of TNF-α, IL-6, MCP-1, and IFN-β was significantly increased in cardiac fibroblasts compared to cardiomyocytes or macrophages. We found that in addition to cardiomyocytes cardiac fibroblasts were infected by CVB3 and displayed a higher virus replication (132-fold increase) compared to cardiomyocytes (14-fold increase) between 6 and 24 hours after infection. At higher virus concentrations, macrophages are able to reduce the viral copy number. At low virus concentration a persistent virus infection was determined. Therefore, we suggest that cardiac fibroblasts play an important role in the pathology of CVB3-induced myocarditis and are another important contributor of virus replication aggravating myocarditis. ",
keywords = "Animals, Cells, Cultured, Coxsackievirus Infections/pathology, Cytokines/genetics, Enterovirus B, Human/genetics, Fibroblasts/immunology, Gene Expression, Genome, Viral, Heart/virology, Macrophages/immunology, Male, Mice, Mice, Inbred C57BL, Myocarditis/pathology, Myocardium/immunology, Myocytes, Cardiac/immunology, Ventricular Function, Left, Viral Load, Virus Replication",
author = "Diana Lindner and Jia Li and Konstantinos Savvatis and Karin Klingel and Stefan Blankenberg and Carsten Tsch{\"o}pe and Dirk Westermann",
year = "2014",
doi = "10.1155/2014/519528",
language = "English",
volume = "2014",
pages = "519528",
journal = "MEDIAT INFLAMM",
issn = "0962-9351",
publisher = "Hindawi Publishing Corporation",

}

RIS

TY - JOUR

T1 - Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication

AU - Lindner, Diana

AU - Li, Jia

AU - Savvatis, Konstantinos

AU - Klingel, Karin

AU - Blankenberg, Stefan

AU - Tschöpe, Carsten

AU - Westermann, Dirk

PY - 2014

Y1 - 2014

N2 - Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsackievirus B3 (CVB3) and detected increased gene expression of anti-inflammatory and antiviral cytokines in the heart. Subsequently, we infected cardiac fibroblasts, cardiomyocytes, and macrophages with CVB3. Due to viral infection, the expression of TNF-α, IL-6, MCP-1, and IFN-β was significantly increased in cardiac fibroblasts compared to cardiomyocytes or macrophages. We found that in addition to cardiomyocytes cardiac fibroblasts were infected by CVB3 and displayed a higher virus replication (132-fold increase) compared to cardiomyocytes (14-fold increase) between 6 and 24 hours after infection. At higher virus concentrations, macrophages are able to reduce the viral copy number. At low virus concentration a persistent virus infection was determined. Therefore, we suggest that cardiac fibroblasts play an important role in the pathology of CVB3-induced myocarditis and are another important contributor of virus replication aggravating myocarditis.

AB - Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsackievirus B3 (CVB3) and detected increased gene expression of anti-inflammatory and antiviral cytokines in the heart. Subsequently, we infected cardiac fibroblasts, cardiomyocytes, and macrophages with CVB3. Due to viral infection, the expression of TNF-α, IL-6, MCP-1, and IFN-β was significantly increased in cardiac fibroblasts compared to cardiomyocytes or macrophages. We found that in addition to cardiomyocytes cardiac fibroblasts were infected by CVB3 and displayed a higher virus replication (132-fold increase) compared to cardiomyocytes (14-fold increase) between 6 and 24 hours after infection. At higher virus concentrations, macrophages are able to reduce the viral copy number. At low virus concentration a persistent virus infection was determined. Therefore, we suggest that cardiac fibroblasts play an important role in the pathology of CVB3-induced myocarditis and are another important contributor of virus replication aggravating myocarditis.

KW - Animals

KW - Cells, Cultured

KW - Coxsackievirus Infections/pathology

KW - Cytokines/genetics

KW - Enterovirus B, Human/genetics

KW - Fibroblasts/immunology

KW - Gene Expression

KW - Genome, Viral

KW - Heart/virology

KW - Macrophages/immunology

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Myocarditis/pathology

KW - Myocardium/immunology

KW - Myocytes, Cardiac/immunology

KW - Ventricular Function, Left

KW - Viral Load

KW - Virus Replication

U2 - 10.1155/2014/519528

DO - 10.1155/2014/519528

M3 - SCORING: Journal article

C2 - 25374444

VL - 2014

SP - 519528

JO - MEDIAT INFLAMM

JF - MEDIAT INFLAMM

SN - 0962-9351

ER -