Simone Filardo, Marisa Di Pietro, Silvio Romano, Rosa Sessa
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引用次数: 0
摘要
肺炎衣原体是人类呼吸道感染(包括社区获得性肺炎)的病原体,并与动脉粥样硬化性心血管疾病有关。本系统综述旨在回答有关肺炎双球菌参与动脉粥样硬化发病机制、其细胞和分子机制以及是否有证据表明两者之间存在因果关系等重要问题。我们在 PubMed/Medline、Scopus 和 Web of Science 等数据库中检索了 2003 年至 2023 年底发表的所有综述文章。共纳入了 27 篇综述、系统综述和带有荟萃分析的系统综述。总体而言,目前的证据表明,肺炎双球菌是导致动脉粥样硬化的一个生物学上可信的候选病因,尽管它并不完全符合科赫的 4 个假设;氧化应激和炎症是肺炎双球菌最有可能介导的致病机制。然而,目前还不清楚造成慢性炎症的持久型肺炎球菌如何参与这一病因学研究。未来,新设计的用于肺炎双球菌基因组操作的转化系统必将有助于扩大我们对这种病原体在动脉粥样硬化中作用的认识。
Updating the relationship of Chlamydia pneumoniae with atherosclerotic cardiovascular diseases: a systematic review of reviews.
Chlamydia pneumoniae is the etiologic agent of respiratory tract infections in humans, including community-acquired pneumonia, and has been associated with atherosclerotic cardiovascular diseases. The present systematic review of reviews aimed at answering important questions on the involvement of C. pneumoniae in the pathogenesis of atherosclerosis, its cellular and molecular mechanisms, and whether there is evidence of a causal relationship. The databases PubMed/Medline, Scopus, and Web of Science were searched for all review articles published from 2003 to the end of 2023. A total of 27 reviews, systematic reviews, and systematic reviews with metanalysis were included. Overall, current evidence suggests that C. pneumoniae is a biologically plausible candidate for the causation of atherosclerosis, albeit not all the 4 Koch postulates are fulfilled; oxidative stress and inflammation are the most likely pathogenic mechanisms mediated by C. pneumoniae. However, it is still unclear how the persistent form, responsible for chronic inflammation, fits into this etiopathogenetic scenario. In the future, the newly-designed transformation systems for the genomic manipulation of C. pneumoniae will surely help expand our knowledge on the role of this pathogen in atherogenesis.
期刊介绍:
The publication, diffusion and furtherance of research and study on all aspects of basic and clinical Microbiology and related fields are the chief aims of the journal.