Finding the priority and cluster of inflammatory biomarkers for infectious preterm birth: a systematic review.

IF 4.4 3区 医学 Q2 IMMUNOLOGY
Jiayi Li, Jianrong Ge, Na Ran, Changwu Zheng, Yumeng Fang, Danna Fang, Qian Yang, Yeling Ma
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引用次数: 0

Abstract

Infectious preterm birth (PTB) is one of the most important causes of perinatal death. It is difficult to find reliable biomarkers accurate to gestational weeks for infectious PTB prediction clinically. Infectious PTB is found usually accompanied with immune imbalance. Thus, the systematic study to find the priority of inflammatory biomarkers and innovative inflammatory clusters for infectious PTB prediction is urgently needed.This systematic study that focused on the inflammatory clusters and infectious PTB in the PubMed database was analyzed by using the criteria of the Population, Intervention, Comparison, Outcome, and Study design (PICOS) framework according to the recommendations of preferred reporting items for systematic reviews and meta-analysis (PRISMA).The network meta-analyzed results showed that the prioritization of the inflammatory factors for infectious PTB prediction is soluble tumor necrosis factor receptor 2 (sTNFR2) > tumor necrosis factor α (TNFα) > interleukin-10 (IL-10) > interleukin-6 (IL-6) > C-reactive protein (CRP) > interleukin-1β (IL-1β). Furthermore, the results also indicated that global consideration of multiple inflammatory factors, such as CRP/IL-1β/IL-6 biomarker cluster in gestational 27-34 weeks, and the tumor necrosis factor/nerve growth factor (TNF/NGF) family during gestational 25-33 weeks, were potential biomarker clusters that specific for infectious PTB prediction.This study systematically pointed out prioritization of the inflammatory factors for infectious PTB prediction. The results also provided evidence that maternal inflammatory clusters can predict infectious PTB occurrence at accurate gestational week. The global consideration of multiple inflammatory factors at accurate gestational age is highlighted.

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发现感染性早产炎症生物标志物的优先级和集群:系统综述。
感染性早产(PTB)是围产期死亡的重要原因之一。临床上很难找到准确到妊娠周的可靠生物标志物来预测感染性肺结核。感染性肺结核通常伴有免疫失衡。因此,迫切需要系统研究炎症生物标志物和创新炎症簇在感染性肺结核预测中的优先地位。本系统研究的重点是PubMed数据库中的炎症聚集性肺结核和感染性肺结核,根据系统评价和荟萃分析(PRISMA)首选报告项目的建议,采用人群、干预、比较、结果和研究设计(PICOS)框架的标准进行分析。网络meta分析结果显示,预测感染性PTB的炎症因子优先顺序为可溶性肿瘤坏死因子受体2 (sTNFR2) >肿瘤坏死因子α (TNFα) >白细胞介素-10 (IL-10) >白细胞介素-6 (IL-6) > c反应蛋白(CRP) >白细胞介素-1β (IL-1β)。此外,结果还表明,全球考虑多种炎症因子,如妊娠27-34周的CRP/IL-1β/IL-6生物标志物簇,妊娠25-33周的肿瘤坏死因子/神经生长因子(TNF/NGF)家族,是特异性预测感染性肺结核的潜在生物标志物簇。本研究系统地指出了炎症因子在感染性肺结核预测中的优先级。结果还提供了证据,证明母体炎症簇可以准确预测妊娠周感染性肺结核的发生。全球考虑多种炎症因素在准确胎龄突出。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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