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Induction of murine experimental autoimmune myocarditis – technical details, implementation and evaluation

Dudu, Felicia Luminita ; Fueriu, Razvan Mihai ; Jakobsson, Gabriel LU ; Vlad, Mihaela Loredana ; Lazar, Alexandra Gela ; Manea, Simona Adriana ; Manea, Adrian and Schiopu, Alexandru LU orcid (2025) In Romanian Journal of Cardiology / Revista Romana de Cardiologie 35(3). p.194-204
Abstract

Introduction: Myocarditis is a complex cardiac disorder with multifactorial etiology, characterized by myocardial inflammation, cardiomyocyte damage, and fibrosis. Left untreated, myocarditis may lead to acute and chronic heart failure and life-threatening arrhythmias. Reliable experimental models of myocarditis are required to study the underlying pathological mechanisms of the disease and to develop efficient therapies. Materials and Methods: Experimental autoimmune myocarditis (EAM) was induced by immunizing 9-week-old female BALB/c mice with a specific peptide derived from the cardiac α-myosin heavy chain (α-MHC) which is the major autoantigen recognized by heart-specific autoantibodies in myocarditis. The immunization activates an... (More)

Introduction: Myocarditis is a complex cardiac disorder with multifactorial etiology, characterized by myocardial inflammation, cardiomyocyte damage, and fibrosis. Left untreated, myocarditis may lead to acute and chronic heart failure and life-threatening arrhythmias. Reliable experimental models of myocarditis are required to study the underlying pathological mechanisms of the disease and to develop efficient therapies. Materials and Methods: Experimental autoimmune myocarditis (EAM) was induced by immunizing 9-week-old female BALB/c mice with a specific peptide derived from the cardiac α-myosin heavy chain (α-MHC) which is the major autoantigen recognized by heart-specific autoantibodies in myocarditis. The immunization activates an anti-α-MHC immune response, which triggers an inflammatory reaction leading to cardiomyocyte damage and myocardial injury. The mice received two immunizations with 100 μL of an emulsion containing α-MHC peptide emulsified 1:1 in Complete Freund’s Adjuvant (CFA) supplemented with 4 mg/mL inactivated Mycobacterium tuberculosis (M. tuberculosis), administered subcutaneously on Days 0 and 7. Results: We highlight the essential steps for the successful preparation of the peptide-adjuvant emulsion, a key factor in the effective implementation of the model, and mouse immunization. We also demonstrate how the inflammatory, fibrotic, and functional consequences on the myocardium should be evaluated. Conclusion: This efficient and reproducible murine EAM model allows experimental research on the pathophysiology and treatment of myocarditis.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
cardiac α-myosin heavy chain peptide, experimental autoimmune myocarditis, immune response, inflammation
in
Romanian Journal of Cardiology / Revista Romana de Cardiologie
volume
35
issue
3
pages
11 pages
publisher
Sciendo
external identifiers
  • scopus:105014194202
ISSN
1220-658X
DOI
10.2478/rjc-2025-0026
language
English
LU publication?
yes
id
a920320c-f976-4e12-bb75-65fb49b69e66
date added to LUP
2025-11-17 12:57:35
date last changed
2025-11-17 12:58:39
@article{a920320c-f976-4e12-bb75-65fb49b69e66,
  abstract     = {{<p>Introduction: Myocarditis is a complex cardiac disorder with multifactorial etiology, characterized by myocardial inflammation, cardiomyocyte damage, and fibrosis. Left untreated, myocarditis may lead to acute and chronic heart failure and life-threatening arrhythmias. Reliable experimental models of myocarditis are required to study the underlying pathological mechanisms of the disease and to develop efficient therapies. Materials and Methods: Experimental autoimmune myocarditis (EAM) was induced by immunizing 9-week-old female BALB/c mice with a specific peptide derived from the cardiac α-myosin heavy chain (α-MHC) which is the major autoantigen recognized by heart-specific autoantibodies in myocarditis. The immunization activates an anti-α-MHC immune response, which triggers an inflammatory reaction leading to cardiomyocyte damage and myocardial injury. The mice received two immunizations with 100 μL of an emulsion containing α-MHC peptide emulsified 1:1 in Complete Freund’s Adjuvant (CFA) supplemented with 4 mg/mL inactivated Mycobacterium tuberculosis (M. tuberculosis), administered subcutaneously on Days 0 and 7. Results: We highlight the essential steps for the successful preparation of the peptide-adjuvant emulsion, a key factor in the effective implementation of the model, and mouse immunization. We also demonstrate how the inflammatory, fibrotic, and functional consequences on the myocardium should be evaluated. Conclusion: This efficient and reproducible murine EAM model allows experimental research on the pathophysiology and treatment of myocarditis.</p>}},
  author       = {{Dudu, Felicia Luminita and Fueriu, Razvan Mihai and Jakobsson, Gabriel and Vlad, Mihaela Loredana and Lazar, Alexandra Gela and Manea, Simona Adriana and Manea, Adrian and Schiopu, Alexandru}},
  issn         = {{1220-658X}},
  keywords     = {{cardiac α-myosin heavy chain peptide; experimental autoimmune myocarditis; immune response; inflammation}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{194--204}},
  publisher    = {{Sciendo}},
  series       = {{Romanian Journal of Cardiology / Revista Romana de Cardiologie}},
  title        = {{Induction of murine experimental autoimmune myocarditis – technical details, implementation and evaluation}},
  url          = {{http://dx.doi.org/10.2478/rjc-2025-0026}},
  doi          = {{10.2478/rjc-2025-0026}},
  volume       = {{35}},
  year         = {{2025}},
}