Vaginal host immune-microbiome interactions in a cohort of primarily African-American women who ultimately underwent spontaneous preterm birth or delivered at term.
Vaginal host immune-microbiome interactions in a cohort of primarily African-American women who ultimately underwent spontaneous preterm birth or delivered at term.
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DOI：
10.1016/j.cyto.2020.155316
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发表时间：
2021-01
期刊：
影响因子：
3.8
通讯作者：
Gomez-Lopez N
中科院分区：
文献类型：
--
作者：
Florova V;Romero R;Tarca AL;Galaz J;Motomura K;Ahmad MM;Hsu CD;Hsu R;Tong A;Ravel J;Theis KR;Gomez-Lopez N
最近的研究表明，阴道微生物组的改变可以评估自发性早产（PTB）的风险，PTB是全球新生儿发病率和死亡率的主要原因。然而，局部免疫反应与阴道微生物组之间的关系仍然知之甚少。在此，我们描述了最终接受PTB的女性和足月分娩的女性的阴道宿主免疫-微生物组相互作用。在一项病例对照研究中，收集了52名孕妇（其中18名接受了PTB，34名足月分娩）10-32周的阴道液样本。使用敏感和特异性免疫测定法测定33种免疫介质的浓度。本研究利用了先前发表的16 S rRNA基因序列和这些受试者的细菌分类数据。利用线性混合效应模型来测试阴道免疫介质浓度和细菌菌落类型相对丰度之间的关联。1)在整个研究人群中，CXCL 10、CCL 2、CCL 3、SLP 1和VEGF的阴道浓度与阴道微生物组的非乳杆菌属、社区状态IV型（CST IV）成员负相关; 2）CXCL 10特别地与15种细菌性阴道炎类型负相关，其中大多数是CST IV的典型成员，如阴道加德纳菌（Gardnerella vagulosa）、巨球菌属（Megaspaera spp.）、和阴道奇异菌; 3）双孢菌属，也是CST IV的成员，与VEGF、CCL 2、CCL 3、SLPI和CXCL 10的阴道浓度呈负相关; 4）当将PTB病例与足月对照进行比较时，CCL 26、CCL 22、CCL 2、CXCL 10和IL-16，尤其是CCL 26与CST IV的五个典型成员呈负相关：Sneathia sanguinegens、微小微单胞菌、韦荣球菌科、BVAB 2和Gemella spp.;与足月对照组相比，血红色Sneathia sanguinegens与PTB病例中所有五种可溶性免疫介质（CCL 26、CCL 22、CCL 2、CXCL 10和IL-16）的负相关性更强。阴道宿主免疫-微生物组相互作用的评估显示，特异性可溶性免疫介质（主要是CXCL 10）与阴道微生物组的CST IV的典型成员呈负相关。特别是，在最终接受PTB的女性中，与足月分娩的女性相比，Sneathia sanguinegens与不同的免疫介质（包括CXCL 10和CCL 26）具有更强的负相关性。这些发现为了解正常和复杂妊娠中的阴道宿主免疫-微生物组相互作用提供了见解。
Recent studies suggest that alterations in the vaginal microbiome allow for the assessment of the risk for spontaneous preterm birth (PTB), the leading cause of neonatal morbidity and mortality worldwide. However, the associations between the local immune response and the vaginal microbiome are still poorly understood. Herein, we characterize the vaginal host immune-microbiome interactions in women who ultimately underwent PTB and in those who delivered at term. Vaginal fluid samples from 52 pregnant women (of whom 18 underwent PTB and 34 delivered at term) were collected from 10–32 weeks in a case-control study. Concentrations of 33 immune mediators were determined using sensitive and specific immunoassays. The previously published 16S rRNA gene sequence and bacterial phylotype data of these subjects were utilized in this study. Linear mixed effects models were utilized to test associations between vaginal immune mediator concentrations and bacterial phylotype relative abundances. 1) In the overall study population, vaginal concentrations of CXCL10, CCL2, CCL3, SLP1 and VEGF negatively correlated with non-Lactobacillus, Community State Type IV (CST IV) members of the vaginal microbiome; 2) CXCL10, in particular, negatively correlated with 15 bacterial phylotypes, most of which are typical members of CST IV, such as Gardnerella vaginalis, Megasphaera spp., and Atopobium vaginae; 3) Gemella spp., also members of CST IV, negatively correlated with vaginal concentrations of VEGF, CCL2, CCL3, SLPI, and CXCL10; 4) when comparing PTB cases to term controls, five soluble immune mediators (CCL26, CCL22, CCL2, CXCL10, and IL-16), especially CCL26, were negatively correlated with five typical members of CST IV: Sneathia sanguinegens, Parvimonas micra, Veillonellaceae, BVAB2, and Gemella spp.; and 5) Sneathia sanguinegens had stronger negative associations with all five soluble immune mediators (CCL26, CCL22, CCL2, CXCL10, and IL-16) in PTB cases than in term controls. The assessment of vaginal host immune-microbiome interactions revealed that specific soluble immune mediators, mainly CXCL10, negatively correlated with typical members of CST IV of the vaginal microbiome. Sneathia sanguinegens, in particular, had stronger negative associations with different immune mediators, including CXCL10 and CCL26, in women who ultimately underwent PTB compared to those who delivered at term. These findings provide insight into the vaginal host immune-microbiome interactions in normal and complicated pregnancies.
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阴道营养不良增加了早产胎儿膜破裂，新生儿败血症的风险，并因红霉素而加剧。
影响因子：
9.3
作者：
Brown RG;Marchesi JR;Lee YS;Smith A;Lehne B;Kindinger LM;Terzidou V;Holmes E;Nicholson JK;Bennett PR;MacIntyre DA
通讯作者：
MacIntyre DA
影响因子：
5.2
作者：
Anton L;Sierra LJ;DeVine A;Barila G;Heiser L;Brown AG;Elovitz MA
通讯作者：
Elovitz MA
影响因子：
3.7
作者：
Aagaard K;Riehle K;Ma J;Segata N;Mistretta TA;Coarfa C;Raza S;Rosenbaum S;Van den Veyver I;Milosavljevic A;Gevers D;Huttenhower C;Petrosino J;Versalovic J
通讯作者：
Versalovic J
影响因子：
2.8
作者：
Fettweis, Jennifer M.;Brooks, J. Paul;Buck, Gregory A.
通讯作者：
Buck, Gregory A.
影响因子：
3.6
作者：
Berard, Alicia R.;Perner, Michelle;Burgener, Adam D.
通讯作者：
Burgener, Adam D.