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Updated: Jun 27, 2025
Noninvasive Assessment of Cardiac Abnormalities in Experimental Autoimmune Myocarditis by Magnetic Resonance Microscopy Imaging in the Mouse
Published on: June 20, 2014
[Molecular mimic between cardiovascular diseases and microorganism antigens]
Andrés Sánchez-Caraballo1,2,3, Valentina García-Solano1, Sonia Karina González-Rangel1
1Health Faculty, Medical Research Group (GINUMED), University Corporation Rafael Nuñez, Cartagena, Colombia.
Introduction:
Cardiovascular diseases are the result of genetic and environmental interaction that conditions the integrity of the heart and blood vessels. Risk factors include infections. The inflammatory response against the infectious agent is a trigger of autoimmune cardiovascular diseases due to the similarity between the pathogen proteins and human antigens, since the immune response can present cross-reactivity caused by molecular mimicry.
Methods:
We performed a search for pathogens involved in autoimmune heart diseases and autoantigens 9 associated with these diseases in the Pubmed and Google Scholar search engines. Identity between proteins was performed through global alignments using PSI-BLAST. The 3D structures of the proteins were obtained by Uniprot or NCBI and, if not found, the structure was modeled by homology using the Swiss Model server. Epitope prediction was performed through Ellipro and the Immunological Epitope Database (IEDB). In addition, the PYMOL program was used to visualize proteins in 3D and position the epitopes in the structure.
Results:
A total of ten cardiovascular proteins showed identity (30-88,24%) in their amino acid sequences with antigens from 10 pathogens. Actin proteins and heat shock protein (HSP) families had higher levels of identity with Trypanosoma Cruzi, Cryptococcus neoformans, and Chlamydia trachomatis, 71,47%, 88,24%, and 80,61%, respectively. Other pathogens, such as Streptococcus pyogenes, Bacillus sp, Magnetospirillum gryphiswaldense, Helicobacter pylori and Chlamydia pneumoniae, presented a moderate identity with a maximum value of 65,79%.
Conclusion:
Human actin and HSPs share a high degree of conservation with epitopes from various microorganisms, such as bacteria, fungi and protozoa, suggesting molecular mimicry and cross-reactivity as a mechanism for the development of atherosclerosis, heart disease rheumatic disease, myocarditis and Chagas heart disease. In vitro and in vivo work is needed to demonstrate the results obtained in the In Silico analysis.
Insights
Infections can trigger autoimmune heart diseases when pathogen proteins mimic human antigens, leading to cross-reactivity. This study identifies shared epitopes between cardiovascular proteins and microbes, suggesting a molecular mimicry mechanism for heart conditions.
Area of Science:
- Molecular biology and immunology
- Cardiovascular research
- Infectious diseases
Context:
- Cardiovascular diseases (CVDs) arise from genetic and environmental factors, with infections posing a significant risk.
- The immune response to pathogens can mistakenly target self-antigens in the heart due to molecular mimicry, initiating autoimmune reactions.
- Understanding the molecular basis of infection-induced autoimmunity is crucial for preventing and treating CVDs.
Purpose:
- To identify pathogens and their antigens that share sequence identity with human cardiovascular proteins.
- To investigate the potential for molecular mimicry and cross-reactivity in the development of autoimmune heart diseases.
- To computationally predict shared epitopes between human heart proteins and microbial antigens.
Summary:
- A computational analysis revealed sequence identity between human cardiovascular proteins (actin and heat shock proteins) and antigens from pathogens like *Cryptococcus neoformans*, *Chlamydia trachomatis*, and *Trypanosoma cruzi*.
- High sequence conservation (up to 88.24%) was observed, particularly for heat shock proteins (HSPs) and actin, with specific microbial agents.
- The findings suggest that molecular mimicry, driven by shared epitopes, may underlie autoimmune conditions such as myocarditis, rheumatic heart disease, and Chagas heart disease.
Impact:
- Provides a mechanistic link between specific infections and the development of various autoimmune cardiovascular diseases.
- Highlights actin and HSPs as potential targets for autoimmune responses triggered by microbial infections.
- Suggests avenues for future in vitro and in vivo research to validate the role of molecular mimicry in these conditions.
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