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, Jahrgang 2014, 2014, S. 519528.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -