Escape from cardiomyocyte apoptosis by enterovirus persistence due to elevated soluble Fas-receptors View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-07

AUTHORS

P. Alter, B. Maisch

ABSTRACT

BACKGROUND: Apoptosis causes loss of contractile cardiomyocytes in inflammatory heart disease. Despite recent examinations, the influence of virus infection on apoptosis remained ill-defined. METHODS: Apoptosis was assessed in left ventricular endomyocardial biopsies by the TUNEL method frompatients with chronic myocarditis and adeno-, cytomegalo- and enterovirus persistence. Soluble Fas-ligands, sFas-receptors, TNF-alpha, IL-6, IL-10 and IFN-gamma were measured using ELISA technique. RESULTS: Elevated (P < 0.05) rates of apoptosis were found in patients with autoimmune myocarditis. Apoptosis was increased (P < 0.05) in the case of cytomegalovirus persistence, but not significantly increased in the presence of adenoviral genome. No evidence for apoptosis, but elevated concentrations of soluble Fas-receptors were found only in the case of enterovirus persistence. In turn, elevated percentages of apoptosis and normal soluble Fas-receptor concentrations were found in patients with chronic myocarditis. Serum levels of soluble Fas-ligands, TNF-alpha, IL-6, IL-10 and IFN-gamma did not predict changes in TUNEL-positivity. CONCLUSIONS: Escape mechanisms to protect cardiomyocytes from apoptosis are yet not known for enterovirus infections. Soluble Fas-receptors have to be considered to counteract binding of soluble Fas-ligands that results in the blockade of apoptosis induction. It is a new finding that soluble Fasreceptors were elevated in the presence of enterovirus genome in the heart. Inhibition of apoptosis can impair virus clearing and prolong its replication with a potential worse outcome. In turn, sufficient protection from apoptosis in autoimmune myocarditis should reduce loss of cardiomyocytes. Therefore, the interaction of the Fas components could provide a new therapeutic target in myocarditis. More... »

PAGES

524-532

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00392-004-0092-2

DOI

http://dx.doi.org/10.1007/s00392-004-0092-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033428860

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15243763


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    "description": "BACKGROUND: Apoptosis causes loss of contractile cardiomyocytes in inflammatory heart disease. Despite recent examinations, the influence of virus infection on apoptosis remained ill-defined.\nMETHODS: Apoptosis was assessed in left ventricular endomyocardial biopsies by the TUNEL method frompatients with chronic myocarditis and adeno-, cytomegalo- and enterovirus persistence. Soluble Fas-ligands, sFas-receptors, TNF-alpha, IL-6, IL-10 and IFN-gamma were measured using ELISA technique.\nRESULTS: Elevated (P < 0.05) rates of apoptosis were found in patients with autoimmune myocarditis. Apoptosis was increased (P < 0.05) in the case of cytomegalovirus persistence, but not significantly increased in the presence of adenoviral genome. No evidence for apoptosis, but elevated concentrations of soluble Fas-receptors were found only in the case of enterovirus persistence. In turn, elevated percentages of apoptosis and normal soluble Fas-receptor concentrations were found in patients with chronic myocarditis. Serum levels of soluble Fas-ligands, TNF-alpha, IL-6, IL-10 and IFN-gamma did not predict changes in TUNEL-positivity.\nCONCLUSIONS: Escape mechanisms to protect cardiomyocytes from apoptosis are yet not known for enterovirus infections. Soluble Fas-receptors have to be considered to counteract binding of soluble Fas-ligands that results in the blockade of apoptosis induction. It is a new finding that soluble Fasreceptors were elevated in the presence of enterovirus genome in the heart. Inhibition of apoptosis can impair virus clearing and prolong its replication with a potential worse outcome. In turn, sufficient protection from apoptosis in autoimmune myocarditis should reduce loss of cardiomyocytes. Therefore, the interaction of the Fas components could provide a new therapeutic target in myocarditis.", 
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