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Left ventricular enlargement in coxsackievirus-B3 induced chronic myocarditis - ongoing inflammation and an imbalance of the matrix degrading system


Rutschow, S; Leschka, S; Westermann, D; Puhl, K; Weitz, A; Ladyszenskij, L; Jaeger, S; Zeichhardt, H; Noutsias, M; Schultheiss, H P; Tschope, C; Pauschinger, M (2010). Left ventricular enlargement in coxsackievirus-B3 induced chronic myocarditis - ongoing inflammation and an imbalance of the matrix degrading system. European Journal of Pharmacology, 630(1-3):145-151.

Abstract

Enteroviruses, especially Coxsackie B3 virus (CVB-3), cause acute viral myocarditis, but the detailed mechanisms leading to chronic left ventricular dysfunction and dilatation remain elusive. Myocardial tissues of CVB-3 infected and sham infected male swr/J mice were analyzed after hemodynamic evaluation on days 4, 7, and 28 p.i. by RT-PCR, gelatin zymography, ELISA, immunohisto-chemistry, sirius red staining, and luxol fast blue staining. In the early phase after infection an abnormal diastolic function was the main hemodynamic finding. CVB-3 infection caused impairment of left ventricular function combined with ventricular dilatation 7 and 28 days post-infection. These hemodynamic findings were associated with relevant upregulation of different cytokines (IL-1beta, IL-6, IL-10, INF-gamma, TNF-alpha) in the acute phase with persistent over-expression of IL-6, IL-10, and INF-gamma in the chronic phase. This virus induced myocardial inflammation was linked to a significant induced MMP/TIMP-system (MMP-2,-3,-8, TIMP-1, uPA, tPA - mRNA-expression, MMP-2-activity) in the acute and chronic phase leading to imbalance in the MMP/TIMP-ratio at day 28. This imbalance in the MMP/TIMP-system was significantly correlated to the development of ventricular dilatation. Viral persistence induces chronic myocardial inflammation and an imbalance of the matrix degrading system, associated with the development of left ventricular dysfunction and dilatation in chronic murine myocarditis.

Abstract

Enteroviruses, especially Coxsackie B3 virus (CVB-3), cause acute viral myocarditis, but the detailed mechanisms leading to chronic left ventricular dysfunction and dilatation remain elusive. Myocardial tissues of CVB-3 infected and sham infected male swr/J mice were analyzed after hemodynamic evaluation on days 4, 7, and 28 p.i. by RT-PCR, gelatin zymography, ELISA, immunohisto-chemistry, sirius red staining, and luxol fast blue staining. In the early phase after infection an abnormal diastolic function was the main hemodynamic finding. CVB-3 infection caused impairment of left ventricular function combined with ventricular dilatation 7 and 28 days post-infection. These hemodynamic findings were associated with relevant upregulation of different cytokines (IL-1beta, IL-6, IL-10, INF-gamma, TNF-alpha) in the acute phase with persistent over-expression of IL-6, IL-10, and INF-gamma in the chronic phase. This virus induced myocardial inflammation was linked to a significant induced MMP/TIMP-system (MMP-2,-3,-8, TIMP-1, uPA, tPA - mRNA-expression, MMP-2-activity) in the acute and chronic phase leading to imbalance in the MMP/TIMP-ratio at day 28. This imbalance in the MMP/TIMP-system was significantly correlated to the development of ventricular dilatation. Viral persistence induces chronic myocardial inflammation and an imbalance of the matrix degrading system, associated with the development of left ventricular dysfunction and dilatation in chronic murine myocarditis.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Diagnostic and Interventional Radiology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:25 March 2010
Deposited On:12 Jan 2010 12:57
Last Modified:18 Feb 2018 02:40
Publisher:Elsevier
ISSN:0014-2999
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.ejphar.2009.12.019
PubMed ID:20035743

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