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The Microbiome and Complement Activation: A Mechanistic Model for Preterm Birth

机译：微生物组和补体激活：早产的机械模型

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Preterm birth (PTB, <37 completed weeks' gestation) is one of the leading obstetrical problems in the United States, affecting approximately one of every nine births. Even more concerning are the persistent racial disparities in PTB, with particularly high rates among African Americans. There are several recognized pathophysiologic pathways to PTB, including infection and/or exaggerated systemic or local inflammation. Intrauterine infection is a causal factor linked to PTB thought to result most commonly from inflammatory processes triggered by microbial invasion of bacteria ascending from the vaginal microbiome. Trials to treat various infections have shown limited efficacy in reducing PTB risk, suggesting that other complex mechanisms, including those associated with inflammation, may be involved in the relationship between microbes, infection, and PTB. The complement system, a key mediator of the inflammatory response, is an innate defense mechanism involved in both normal physiologic processes that occur during pregnancy implantation and processes that promote the elimination of pathogenic microbes. Recent research has demonstrated an association between this system and PTB. The purpose of this article is to present a mechanistic model of inflammation-associated PTB, which hypothesizes a relationship between the microbiome and dysregulation of the complement system. Exploring the relationships between the microbial environment and complement biomarkers may elucidate a potentially modifiable biological pathway to PTB.
机译：早产（PTB，<37完成的周妊娠）是美国的主要产科问题之一，影响每九个诞生中的大约一个。甚至更多的关于PTB的持续种族差异，非洲裔美国人的持续种族差异。 PTB有几种公认的病理物理学途径，包括感染和/或夸张的全身或局部炎症。宫内感染是与PTB思想有关的因果因子，这些因素是从阴道微生物组的微生物侵犯细菌的微生物侵袭引发的炎症过程中最常产生的。治疗各种感染的试验表明，在降低PTB风险时表现出有限的功效，这表明其他复杂机制包括与炎症相关的机制，可能参与微生物，感染和PTB之间的关系。补体系统是炎症反应的关键介质，是妊娠期植入过程中发生的正常生理过程的先天防御机制，促进消除致病微生物的过程。最近的研究表明了该系统与PTB之间的关联。本文的目的是提出炎症相关的PTB的机制模型，其假设微生物组和补体系统的失调之间的关系。探索微生物环境和补体生物标志物之间的关系可以阐明潜在可修饰的生物途径到PTB。

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