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Stabilin-1 mediates beneficial monocyte recruitment and tolerogenic macrophage programming during CVB3-induced viral myocarditis

Pathological innate and adaptive immune response upon viral infection may lead to cardiac injury and dysfunction. Stabilin-1 is a scavenger receptor that regulates several aspects of the innate immunity. Whether stabilin-1 affects the inflammatory response during viral myocarditis (VM) is entirely u...

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Main Authors: Carai, Paolo (Author) , Papageorgiou, Anna Pia (Author) , Van Linthout, Sophie (Author) , Deckx, Sophie (Author) , Velthuis, Sebastiaan (Author) , Lutgens, Esther (Author) , Wijnands, Erwin (Author) , Tschöpe, Carsten (Author) , Schmuttermaier, Christina (Author) , Kzhyshkowska, Julia (Author) , Jones, Elizabeth Anne Vincent (Author) , Heymans, Stephane (Author)
Format: Article (Journal)
Language:English
Published: April 2022
In: Journal of molecular and cellular cardiology
Year: 2022, Volume: 165, Pages: 31-39
ISSN:1095-8584
DOI:10.1016/j.yjmcc.2021.12.009
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1016/j.yjmcc.2021.12.009
Verlag, kostenfrei, Volltext: https://www.sciencedirect.com/science/article/pii/S0022282821002364
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Author Notes:Paolo Carai, Anna Pia Papageorgiou, Sophie Van Linthout, Sophie Deckx, Sebastiaan Velthuis, Esther Lutgens, Erwin Wijnands, Carsten Tschöpe, Christina Schmuttermaier, Julia Kzhyshkowska, Elizabeth Anne Vincent Jones, Stephane Heymans
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Summary:Pathological innate and adaptive immune response upon viral infection may lead to cardiac injury and dysfunction. Stabilin-1 is a scavenger receptor that regulates several aspects of the innate immunity. Whether stabilin-1 affects the inflammatory response during viral myocarditis (VM) is entirely unknown. Here, we assess the role of stabilin-1 in the pathogenesis of VM and its suitability as a therapeutic target. Genetic loss of stabilin-1 increased mortality and cardiac necrosis in a mouse model of human Coxsackievirus B3 (CVB3)-induced myocarditis. Absence of stabilin-1 significantly reduced monocyte recruitment and strongly reduced the number of alternatively activated anti-inflammatory macrophages in the heart, enhancing a pro-inflammatory cardiac niche with a detrimental T lymphocyte response during VM. Yeast two-hybrid screening, confirmed by affinity chromatography, identified fibronectin as a stabilin-1 interacting partner. Absence of stabilin-1 specifically decreased monocyte adhesion on extracellular fibronectin in vitro. Loss of Type III repeats Extra Domain A (EDA) of fibronectin during VM also increased the mortality and cardiac necrosis as in stabilin-1 knockout mice, with reduced monocytic cardiac recruitment and increased T lymphocyte response. Collectively, stabilin-1 has an immune-suppressive role of limiting myocardial damage during VM, regulating anti-inflammatory monocyte-recruitment to the site of inflammation.
Item Description:Online verfügbar: 28. Dezember 2021, Artikelversion: 30. Dezember 2021
Gesehen am 12.03.2024
Physical Description:Online Resource
ISSN:1095-8584
DOI:10.1016/j.yjmcc.2021.12.009

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