CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.

Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investi...

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Main Authors: Irene Müller, Kathleen Pappritz, Konstantinos Savvatis, Kerstin Puhl, Fengquan Dong, Muhammad El-Shafeey, Nazha Hamdani, Isabell Hamann, Michel Noutsias, Carmen Infante-Duarte, Wolfgang A Linke, Sophie Van Linthout, Carsten Tschöpe
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0182643&type=printable
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author Irene Müller
Kathleen Pappritz
Konstantinos Savvatis
Kerstin Puhl
Fengquan Dong
Muhammad El-Shafeey
Nazha Hamdani
Isabell Hamann
Michel Noutsias
Carmen Infante-Duarte
Wolfgang A Linke
Sophie Van Linthout
Carsten Tschöpe
author_facet Irene Müller
Kathleen Pappritz
Konstantinos Savvatis
Kerstin Puhl
Fengquan Dong
Muhammad El-Shafeey
Nazha Hamdani
Isabell Hamann
Michel Noutsias
Carmen Infante-Duarte
Wolfgang A Linke
Sophie Van Linthout
Carsten Tschöpe
author_sort Irene Müller
collection DOAJ
description Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.
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spelling doaj-art-8adfa9f2ae684b97a588dc84787a2dc82025-08-20T02:46:01ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01128e018264310.1371/journal.pone.0182643CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.Irene MüllerKathleen PappritzKonstantinos SavvatisKerstin PuhlFengquan DongMuhammad El-ShafeeyNazha HamdaniIsabell HamannMichel NoutsiasCarmen Infante-DuarteWolfgang A LinkeSophie Van LinthoutCarsten TschöpeStudies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0182643&type=printable
spellingShingle Irene Müller
Kathleen Pappritz
Konstantinos Savvatis
Kerstin Puhl
Fengquan Dong
Muhammad El-Shafeey
Nazha Hamdani
Isabell Hamann
Michel Noutsias
Carmen Infante-Duarte
Wolfgang A Linke
Sophie Van Linthout
Carsten Tschöpe
CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
PLoS ONE
title CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
title_full CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
title_fullStr CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
title_full_unstemmed CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
title_short CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
title_sort cx3cr1 knockout aggravates coxsackievirus b3 induced myocarditis
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0182643&type=printable
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