Pathogenic role of the damage-associated molecular patterns S100A8 and S100A9 in coxsackievirus B3-induced myocarditis
Background: The alarmins S100A8 and S100A9 are damage-associated molecular patterns, which play a pivotal role in cardiovascular diseases, inflammation, and viral infections. We aimed to investigate their role in Coxsackievirus B3 (CVB3)-induced myocarditis. Methods and Results: S100A8 and S100A9 mR...
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| Main Authors: | , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
November 20, 2017
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| In: |
Circulation. Heart failure
Year: 2017, Volume: 10, Issue: 11 |
| ISSN: | 1941-3297 |
| DOI: | 10.1161/CIRCHEARTFAILURE.117.004125 |
| Online Access: | Verlag, teilw. kostenfrei, Volltext: http://dx.doi.org/10.1161/CIRCHEARTFAILURE.117.004125 Verlag, teilw. kostenfrei, Volltext: http://circheartfailure.ahajournals.org.ezproxy.medma.uni-heidelberg.de/content/10/11/e004125 
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| Author Notes: | Irene Müller, Thomas Vogl, Kathleen Pappritz, Kapka Miteva, Konstantinos Savvatis, David Rohde, Patrick Most, Dirk Lassner, Burkert Pieske, Uwe Kühl, Sophie Van Linthout, Carsten Tschöpe |
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| 245 | 1 | 0 | |a Pathogenic role of the damage-associated molecular patterns S100A8 and S100A9 in coxsackievirus B3-induced myocarditis |c Irene Müller, Thomas Vogl, Kathleen Pappritz, Kapka Miteva, Konstantinos Savvatis, David Rohde, Patrick Most, Dirk Lassner, Burkert Pieske, Uwe Kühl, Sophie Van Linthout, Carsten Tschöpe |
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| 520 | |a Background: The alarmins S100A8 and S100A9 are damage-associated molecular patterns, which play a pivotal role in cardiovascular diseases, inflammation, and viral infections. We aimed to investigate their role in Coxsackievirus B3 (CVB3)-induced myocarditis. Methods and Results: S100A8 and S100A9 mRNA expression was 13.0-fold (P=0.012) and 5.1-fold (P=0.038) higher in endomyocardial biopsies from patients with CVB3-positive myocarditis compared with controls, respectively. Elimination of CVB3 led to a downregulation of these alarmins. CVB3-infected mice developed an impaired left ventricular function and displayed an increased left ventricular S100A8 and S100A9 protein expression versus controls. In contrast, CVB3-infected S100A9 knockout mice, which are also a complete knockout for S100A8 on protein level, showed an improved left ventricular function, which was associated with a reduced cardiac inflammatory and oxidative response, and lower CVB3 copy number compared with wild-type CVB3 mice. Exogenous application of S100A8 to S100A9 knockout CVB3 mice induced a severe myocarditis similar to wild-type CVB3 mice. In CVB3-infected HL-1 cells, S100A8 and S100A9 enhanced oxidative stress and CVB3 copy number compared with unstimulated infected cells. In CVB3-infected RAW macrophages, both alarmins increased MIP-2 (macrophage inflammatory protein-2) chemokine expression, which was reduced in CVB3 S100A8 knockdown versus scrambled siRNA CVB3 cells. Conclusions: S100A8 and S100A9 aggravate CVB3-induced myocarditis and might serve as therapeutic targets in inflammatory cardiomyopathies. | ||
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| 650 | 4 | |a RAGE | |
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