感染和动脉样硬化:新兴的机械主义范式
1Cardiovascular Research Foundation, Washington Hospital Center, Washington, DC 20010, USA. sxe2@mhg.edu
Circulation
|July 27, 1999
概括
感染可能通过引起细胞变化导致动脉样硬化. 动脉样硬化风险随着传染病原体的数量增加而增加,并且根据宿主而异.
科学领域:
- 心血管科学 心血管科学
- 传染病免疫学 传染病免疫学
背景情况:
- 动脉样硬化发展是复杂的,感染成为潜在的促成因素.
- 在动物模型中,某些特定的病原体,如Chlamydia pneumoniae和cytomegalovirus已被证明会使动脉样硬化恶化.
研究的目的:
- 探索传染病原体和动脉样硬化的发展之间的联系.
- 了解病原体负载和宿主免疫反应如何影响动脉样硬化风险.
主要方法:
- 审查有关传染病原体和动脉样硬化的现有调查.
- 从动物模型和人类研究中分析数据,将病原体与疾病进展联系起来.
主要成果:
- 传染剂诱导细胞和分子变化,支持动脉生成.
- 多种病原体与动脉样硬化有关,风险与感染数量相关.
- 宿主易感性有所不同,受免疫反应的有效性 (幽默与细胞) 和潜在的自身免疫成分的影响.
结论:
- 虽然最终的因果证据尚未得到证实,但证据表明感染有助于动脉样硬化.
- 主体免疫反应和病原体负载是感染相关动脉样硬化的关键因素.
- 进一步的研究对于阐明机制和制定预防策略至关重要.
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