Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis. Issue 4 (1st April 2022)

• Record Type: Journal Article
• Authors: Wu, Linghe; Fiet, Mitchell D.; Raaijmakers, Daan R.; Woudstra, Linde; van Rossum, Albert C.; Niessen, Hans W. M.; Krijnen, Paul A. J.
• Is Part Of: International journal of experimental pathology. Volume 103:Issue 4(2022)
• Page Start: 149
• Page End: 155
• Publication Date: 2022-04-01
• Subjects: atria -- Coxsackievirus B3 -- in situ hybridization -- inflammation -- viral myocarditis; Pathology, Experimental -- Periodicals; 616.07
• DOI: 10.1111/iep.12438
• Languages: English
• ISSNs: 0959-9673

Abstract

Abstract: Atrial dysfunction is a relatively common complication of acute myocarditis, although its pathophysiology is unclear. There is limited information on myocarditis‐associated histological changes in the atria and how they develop in time. The aim of this study therefore was to investigate inflammation, fibrosis and viral genome in the atria in time after mild CVB3‐induced viral myocarditis (VM) in mice. C3H mice ( n = 68) were infected with 10 5 PFU of Coxsackievirus B3 (CVB3) and were compared with uninfected mice ( n = 10). Atrial tissue was obtained at days 4, 7, 10, 21, 35 or 49 post‐infection. Cellular infiltration of CD45+ lymphocytes, MAC3+ macrophages, Ly6G+ neutrophils and mast cells was quantified by (immuno)histochemical staining. The CVB3 RNA was determined by in situ hybridization, and fibrosis was evaluated by elastic van Gieson (EvG) staining. In the atria of VM mice, the numbers of lymphocytes on days 4 and 7 ( p < .05) and days 10 ( p < .01); macrophages on days 7 ( p < .01) and 10 ( p < .05); neutrophils on days 4 ( p < .05); and mast cells on days 4 and 7 ( p < .05) increased significantly compared with control mice and decreased thereafter to basal levels. No cardiomyocyte death was observed, and the CVB3 genome was detected in only one infected mouse on Day 4 post‐infection. No significant changes in the amount of atrial fibrosis were found between VM and control mice. A temporary increase in inflammation is induced in the atria in the acute phase of CVB3‐induced mild VM, which may facilitate the development of atrial arrhythmia and contractile dysfunction.