Fairweather D, Rose N R
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Lupus. 2005;14(9):646-51. doi: 10.1191/0961203305lu2192oa.
Inflammatory heart disease is a rising concern worldwide. Similar mechanisms link autoimmune diseases, including the association of increased disease with proinflammatory cytokines and the importance of regulatory mechanisms in the control of chronic inflammation. Many pathogens including bacteria, protozoa and viruses have been associated with heart disease in patients, and are able to induce similar disease in animal models. Recognition of pathogens by the innate immune system leads to release of proinflammatory cytokines that both reduce infection and increase chronic inflammatory heart disease. Elevated levels of proinflammatory cytokines are able to overcome tolerance to chronic disease, indicating that environmental factors are important in determining progression to chronic heart disease. Understanding the mechanisms leading to chronic heart disease will be critical for developing effective therapies to reduce cardiac dysfunction and heart failure.
炎症性心脏病在全球范围内日益受到关注。自身免疫性疾病存在相似的机制，包括疾病增加与促炎细胞因子的关联以及调节机制在控制慢性炎症中的重要性。许多病原体，包括细菌、原生动物和病毒，都与患者的心脏病有关，并且能够在动物模型中诱发类似疾病。先天免疫系统对病原体的识别会导致促炎细胞因子的释放，这些因子既能减少感染，又会增加慢性炎症性心脏病。促炎细胞因子水平的升高能够克服对慢性病的耐受性，这表明环境因素在决定向慢性心脏病发展的过程中很重要。了解导致慢性心脏病的机制对于开发有效的治疗方法以减少心脏功能障碍和心力衰竭至关重要。
