Microbial-driven preterm labour involves crosstalk between the innate and adaptive immune response.

Microbial-driven preterm labour involves crosstalk between the innate and adaptive immune response.
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DOI:
10.1038/s41467-022-28620-1
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发表时间:
2022-02-21
影响因子:
16.6
通讯作者:
Sykes L
Sykes L
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Chan D;Bennett PR;Lee YS;Kundu S;Teoh TG;Adan M;Ahmed S;Brown RG;David AL;Lewis HV;Gimeno-Molina B;Norman JE;Stock SJ;Terzidou V;Kropf P;Botto M;MacIntyre DA;Sykes L

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关于阴道微生物群在自发性早产(sPTB)中的作用的研究激增,但大多数都是关联性的,没有机制性的见解。在这里,我们展示了一种全面的方法来了解早产的致病因素,该方法基于从133名sPTB高风险女性中收集的纵向阴道微生物群和宫颈阴道液(CVF)免疫表型数据的整合。我们发现,阴道乳酸杆菌的消耗和高细菌多样性导致甘露糖结合凝集素(MBL)、IgM、IgG、C3 b、C5、IL-8、IL-6和IL-1β增加,并增加sPTB的风险。子宫颈缩短通常发生在早产之前,与惰性乳杆菌和IgM、C3 b、C5、C5 a和IL-6水平升高有关。这些数据证明了补体系统在微生物驱动的sPTB中的作用,并为开发活生物治疗剂和补体治疗剂以预防sPTB提供了科学依据。获得机械洞察与自发性早产相关的微生物和免疫因素是重要的预防策略的发展。在这里,作者表明,补体系统与特定的阴道微生物和相关的免疫学变化相结合,有助于这种情况。
There has been a surge in studies implicating a role of vaginal microbiota in spontaneous preterm birth (sPTB), but most are associative without mechanistic insight. Here we show a comprehensive approach to understand the causative factors of preterm birth, based on the integration of longitudinal vaginal microbiota and cervicovaginal fluid (CVF) immunophenotype data collected from 133 women at high-risk of sPTB. We show that vaginal depletion of Lactobacillus species and high bacterial diversity leads to increased mannose binding lectin (MBL), IgM, IgG, C3b, C5, IL-8, IL-6 and IL-1β and to increased risk of sPTB. Cervical shortening, which often precedes preterm birth, is associated with Lactobacillus iners and elevated levels of IgM, C3b, C5, C5a and IL-6. These data demonstrate a role for the complement system in microbial-driven sPTB and provide a scientific rationale for the development of live biotherapeutics and complement therapeutics to prevent sPTB. Gaining mechanistic insight into the microbiological and immunological factors that are associated with spontaneous preterm birth is important for the development of prevention strategies. Here authors show that the complement system in conjunction with specific vaginal microbial and associated immunological changes are contributing to this condition.
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