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

Zeitschrift für Kardiologie
Peter Alter, Bernhard Maisch

Abstract

Apoptosis causes loss of contractile cardiomyocytes in inflammatory heart disease. Despite recent examinations, the influence of virus infection on apoptosis remained ill-defined. 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. 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. Escape mechanisms to protect cardiomyocytes from apoptosis are yet not known for enterovirus infections. Soluble Fas-receptors have to be consid...Continue Reading

Citations

Jun 15, 2006·Clinical Research in Cardiology : Official Journal of the German Cardiac Society·J HademH Drexler
May 16, 2007·Clinical Research in Cardiology : Official Journal of the German Cardiac Society·Angela Kallwellis-OparaMathias Pauschinger
Oct 5, 2011·Laboratory Investigation; a Journal of Technical Methods and Pathology·Linda EbermannAndrea Dörner
Oct 6, 2005·Nature Reviews. Microbiology·J Lindsay WhittonRalph Feuer

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