Abstract 19779: Nod2 Knock Down Improves Left Ventricular Function and Attenuates Pathophysiological Key Mechanisms in Experimental Coxsackievirus B3-induced Myocarditis

Introduction: Nucleotide binding oligomerization domain 2 (NOD2) is a cytoplasmatic pattern recognition receptor belonging to the NOD-like receptor family, which is part of the innate immune system. Hypothesis: Since NOD2 recognises ssRNA and Coxsackievirus B3 (CVB3) is a ssRNA virus, we hypothesised that NOD2 regulates cardiac inflammatory signaling in CVB3-induced myocarditis. Methods: Gene expression was analyzed on endomyocardial biopsies (EMBs) taken from ejection fraction- and age-matched CVB3+ (n=10) and CVB3- control (n=7) patients and on EMBs from CVB3+patients who spontaneously eliminated CVB3 (n=6). NOD2 -/- mice and wild-type (wt) C57BL/6 mice were i.p. infected with 5 x 105 p.f.u. of CVB3. Seven days after infection, mice were hemodynamically characterized, and left ventricles (LV) were isolated. Results: NOD2 mRNA expression was 3.7-fold (p Conclusions: NOD2 knock down improves LV function and attenuates pathophysiological key mechanisms in acute CVB3-induced myocarditis mice. Modulation of NOD2 might represent a promising therapeutic strategy to treat viral myocarditis.