Sánchez-Caraballo Andrés, García-Solano Valentina, González-Rangel Sonia Karina, Grattz-Lamadrid Valeria, Munera-Gomez Marlon
Health Faculty, Medical Research Group (GINUMED), University Corporation Rafael Nuñez, Cartagena, Colombia.
Group of Clinical and Experimental Allergy (GACE), IPS Universitaria, University of Antioquia, Medellín, Colombia.
Rev Alerg Mex. 2024 Feb 1;71(1):61. doi: 10.29262/ram.v71i1.1379.
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.
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.
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 , , and , 71,47%, 88,24%, and 80,61%, respectively. Other pathogens, such as sp, and , presented a moderate identity with a maximum value of 65,79%.
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.
心血管疾病是遗传与环境相互作用的结果，这种相互作用影响着心脏和血管的完整性。风险因素包括感染。由于病原体蛋白与人类抗原之间的相似性，针对感染因子的炎症反应是自身免疫性心血管疾病的触发因素，因为免疫反应可能因分子模拟而出现交叉反应。
我们在PubMed和谷歌学术搜索引擎中搜索了与自身免疫性心脏病相关的病原体和自身抗原。通过使用PSI-BLAST进行全局比对来确定蛋白质之间的同一性。蛋白质的三维结构通过Uniprot或NCBI获得，如果未找到，则使用瑞士模型服务器通过同源性对结构进行建模。通过Ellipro和免疫表位数据库（IEDB）进行表位预测。此外，使用PYMOL程序以三维形式可视化蛋白质并在结构中定位表位。
共有十种心血管蛋白在其氨基酸序列中与来自10种病原体的抗原具有同一性（30 - 88.24%）。肌动蛋白和热休克蛋白（HSP）家族与[具体病原体1]、[具体病原体2]和[具体病原体3]的同一性水平较高，分别为71.47%、88.24%和80.61%。其他病原体，如[具体病原体4]、[具体病原体5]和[具体病原体6]，呈现出中等同一性，最大值为65.79%。
人类肌动蛋白和热休克蛋白与各种微生物（如细菌、真菌和原生动物）的表位具有高度保守性，这表明分子模拟和交叉反应是动脉粥样硬化、心脏病、风湿性疾病、心肌炎和恰加斯心脏病发展的一种机制。需要进行体外和体内研究来证实计算机模拟分析中获得的结果。
