Stabilin-1 mediates beneficial monocyte recruitment and tolerogenic macrophage programming during CVB3-induced viral myocarditis
| Autor: | 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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| Přispěvatelé: | Medical Biochemistry, ACS - Atherosclerosis & ischemic syndromes, Cardiologie, MUMC+: MA Med Staf Spec Cardiologie (9), RS: Carim - H02 Cardiomyopathy |
| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
EXPRESSION
HOMEOSTASIS Cell Adhesion Molecules Neuronal Stabilin-1 Coxsackievirus Infections ADHESION PREVENTS Monocytes Mice Necrosis PROTEIN SI-CLP ALTERNATIVELY ACTIVATED MACROPHAGES Viral myocarditis Animals FIBROSIS Molecular Biology Fibronectin Inflammation Macrophages толерогенные макрофаги стабилин-1 DYSFUNCTION Enterovirus B Human Fibronectins Disease Models Animal Myocarditis Virus Diseases миокардит CELLS моноциты Cardiology and Cardiovascular Medicine |
| Zdroj: | Journal of molecular and cellular cardiology. 2022. Vol. 165. P. 31-39 Journal of molecular and cellular cardiology, 165, 31-39. Academic Press Inc. Journal of Molecular and Cellular Cardiology, 165, 31-39. ELSEVIER SCI LTD |
| ISSN: | 0022-2828 |
| Popis: | 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. ispartof: Journal Of Molecular And Cellular Cardiology vol:165 pages:31-39 ispartof: location:England status: published |
| Databáze: | OpenAIRE |
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