生物标志物在支气管肺发育不良发生风险中的研究进展

陈祥菲, 曲书强

中国儿童保健杂志 ›› 2022, Vol. 30 ›› Issue (2) : 176-180.

PDF(556 KB)
PDF(556 KB)
中国儿童保健杂志 ›› 2022, Vol. 30 ›› Issue (2) : 176-180. DOI: 10.11852/zgetbjzz2021-0030
综述

生物标志物在支气管肺发育不良发生风险中的研究进展

  • 陈祥菲, 曲书强
作者信息 +

Research progress in biomarkers in the risk of bronchopulmonary dysplasia

  • CHEN Xiang-fei, QU Shu-qiang
Author information +
文章历史 +

摘要

支气管肺发育不良(BPD)主要见于极低或超低出生体重儿,或是上呼吸机时间长、下呼吸机困难的新生儿;是新生儿致死的原因之一,严重影响儿童的健康状况,也给家庭和社会造成了沉重的经济负担。目前在治疗上,国内外还没有特异性药物和有效的干预措施,因此预防和评估本病的发生显得至关重要;目前分子生物标志物对BPD的发生及风险评估是国内外学者研究的热点,具有重要的指导作用和现实意义,本文针对分子生物标志物对BPD的发生风险和评估展开综述,以期为临床如何预测和评估BPD的发生提供新思路。

Abstract

Bronchopulmonary dysplasia (BPD) is mainly found in very low or extra-low birth weight infants, or newborns who take a long time on ventilator and have difficulty in removing ventilator. BPD is one of the causes of neonatal mortality, which seriously affects the health status of children and also causes a heavy economic burden to families and society. At present, there are no specific drugs and effective interventions at home and abroad, so prevention and assessment of the occurrence of this disease are crucial. The occurrence and risk assessment of BPD by molecular biomarkers is currently a hot topic of researches at home and abroad, which plays an important guiding role and has practical significance. This paper reviews the risk and assessment of molecular biomarkers for the development of BPD, in order to provide new ideas on how to predict and assess the occurrence of BPD.

关键词

支气管肺发育不良 / 生物标志物 / 早产儿

Key words

bronchopulmonary / dysplasia biomarkers / premature infants

引用本文

导出引用
陈祥菲, 曲书强. 生物标志物在支气管肺发育不良发生风险中的研究进展[J]. 中国儿童保健杂志. 2022, 30(2): 176-180 https://doi.org/10.11852/zgetbjzz2021-0030
CHEN Xiang-fei, QU Shu-qiang. Research progress in biomarkers in the risk of bronchopulmonary dysplasia[J]. Chinese Journal of Child Health Care. 2022, 30(2): 176-180 https://doi.org/10.11852/zgetbjzz2021-0030
中图分类号: R725.6   

参考文献

[1] Jensen EA, Dysart K, Gantz MG, et al. The diagnosis of bronchopulmonary dysplasia in very preterm infants. an evidence-based approach[J]. Am J Respir Crit Care Med, 2019,200(6):751-759.
[2] Lapcharoensap W, Bennett MV, Xu X, et al. Hospitalization costs associated with bronchopulmonary dysplasia in the first year of life[J]. J Perinatol, 2020,40(1):130-137.
[3] Maturu P, Wei-Liang Y, Androutsopoulos VP, et al. Quercetin attenuates the hyperoxic lung injury in neonatal mice: implications for bronchopulmonary dysplasia(BPD)[J]. Food Chem Toxicol, 2018,114:23-33.
[4] Yen E, Weinberger BI, Laumbach RJ, et al. Exhaled breath condensate nitrite in premature infants with bronchopulmonary dysplasia[J]. J Neonatal Perinatal Med, 2018,11(4):399-407.
[5] Kalikstad B, Kultima HG, Andersstuen TK, et al. Gene expression profiles in preterm infants on continuous long term oxygen therapy suggest reduced oxidative stress dependent signaling during hypoxia[J]. Mol Med Rep, 2017,15(4):1513-1526.
[6] El-Saie A, Shivanna B. Novel strategies to reduce pulmonary hypertension in infants with bronchopulmonary dysplasia[J]. Front Pediatr, 2020,8:201.
[7] Kim BI, Lee HE, Choi CW, et al. Increase in cord blood soluble e-selectin and tracheal aspirate neutrophils at birth and the development of new bronchopulmonary dysplasia[J]. J Perinat Med, 2004,32(3):282-287.
[8] Sun Y, Chen C, Zhang X, et al. High neutrophil-to-lymphocyte ratio is an early predictor of bronchopulmonary dysplasia[J]. Front Pediatr, 2019,7:464.
[9] Kandasamy J, Roane C, Szalai A, et al. Serum eotaxin-1 is increased in extremely-low-birth-weight infants with bronchopulmonary dysplasia or death[J]. Pediatr Res, 2015,78(5):498-504.
[10] 陈瑛,彭晓艳,韩同英,等.早产儿嗜酸性粒细胞增多症与支气管肺发育不良的相关性[J]. 中华新生儿科杂志, 2021,36(1):14-19.
[11] 邱纪玲,王晓彤,周灏雯,等.间充质干细胞条件培养液修复多种疾病损伤的潜能[J]. 中国组织工程研究, 2019,23(29):4743-4748.
[12] Jaimes Y, Naaldijk Y, Wenk K, et al. Mesenchymal stem cell-derived microvesicles modulate lipopolysaccharides-induced inflammatory responses to microglia cells[J]. Stem Cells, 2017,35(3):812-823.
[13] Porzionato A, Zaramella P, Dedja A, et al. Intratracheal administration of clinical-grade mesenchymal stem cell-derived extracellular vesicles reduces lung injury in a rat model of bronchopulmonary dysplasia[J]. Am J Physiol Lung Cell Mol Physiol,2019,316(1):L6-L19.
[14] Willis GR, Fernandez-Gonzalez A, Anastas J, et al. Mesenchymal stromal cell exosomes ameliorate experimental bronchopulmonary dysplasia and restore lung function through macrophage immunomodulation[J]. Am J Respir Crit Care Med, 2018,197(1):104-116.
[15] LaGrandeur RG, Singhal M, Bany-Mohammed F, et al. Pilot feasibility study to detect mesenchymal stem cell biomarkers of bronchopulmonary dysplasia in the tracheal aspirate fluid of preterm infants[J]. J Neonatal Perinatal Med, 2018,11(1):1-10.
[16] Möbius MA, Thébaud B. Bronchopulmonary dysplasia: where have all the stem cells gone? Origin and (potential) function of resident lung stem cells[J]. Chest, 2017,152(5):1043-1052.
[17] Sakaguchi S, Sakaguchi N, Asano M, et al. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases[J]. Journal of Immunology, 1995, 155(3):1151.
[18] 肖天津,张乐平,古中东,等.Treg细胞和il-12在肺结核合并老年慢性支气管炎患者外周血中的表达及意义[J]. 分子诊断与治疗杂志, 2016,8(3):188-191.
[19] 林晴晴,谭卉晗,吴永芳,等.脐血tgf-β1、treg细胞数量水平对早产儿支气管肺发育不良的预测价值[J]. 分子诊断与治疗杂志, 2020,12(8):1052-1055.
[20] Cai H, Wang J, Mo Y, et al. Salidroside suppresses group 2 innate lymphoid cell-mediated allergic airway inflammation by targeting il-33/st2 axis[J]. Int Immunopharmacol, 2020,81:106243.
[21] Ding W, Zou GL, Zhang W, et al. Interleukin-33: its emerging role in allergic diseases[J]. Molecules,2018,23(7):1665.
[22] de Kleer IM, Kool M, de Bruijn MJ, et al. Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung[J]. Immunity, 2016,45(6):1285-1298.
[23] Tang X. Interleukin-33 (IL-33) increases hyperoxia-induced bronchopulmonary dysplasia in newborn mice by regulation of inflammatory mediators[J]. Med Sci Monit, 2018,24:6717-6728.
[24] 蒋燕,曾雯,胡旭红,等.血清白介素-33表达在支气管肺发育不良中的临床价值研究[J]. 成都医学院学报, 2020, 15 (3):70-73.
[25] Fu P, Ebenezer DL, Ha AW, et al. Nuclear lipid mediators: role of nuclear sphingolipids and sphinosine-1-phosphate signaling in epigenetic regulation of inflammation and gene expression[J]. Other, 2018,119(8):6337-6353.
[26] Hendricks-Muñoz KD, Xu J, Voynow JA. Tracheal aspirate VEGF and sphingolipid metabolites in the preterm infant with later development of bronchopulmonary dysplasia[J]. Pediatr Pulmonol, 2018,53(8):1046-1052.
[27] Viswanathan N, Ha AW, Dong Y, et al. Expression profiling of genes regulated by sphingosine kinase1 signaling in a murine model of hyperoxia induced neonatal bronchopulmonary dysplasia[J]. BMC Genomics, 2017,18(1):664.
[28] Petrache I, Berdyshev EV. Ceramide signaling and metabolism in pathophysiological states of the lung[J]. Annu Rev Physiol, 2016,78:463-480.
[29] Presa N, Gomez-Larrauri A, Rivera IG, et al. Regulation of cell migration and inflammation by ceramide 1-phosphate[J]. Biochim Biophys Acta, 2016,1861(5):402-409.
[30] van Mastrigt E, Zweekhorst S, Bol B, et al. Ceramides in tracheal aspirates of preterm infants: marker for bronchopulmonary dysplasia[J]. PLoS One, 2018,13(1):e0185969.
[31] König K, Guy KJ, Walsh G, et al. Association of bnp, ntprobnp, and early postnatal pulmonary hypertension in very preterm infants[J]. Pediatr Pulmonol, 2016,51(8):820-824.
[32] Montaner A, Pinillos R, Galve Z, et al. Brain natriuretic propeptide as an early marker of bronchopulmonary dysplasia or death in the preterm newborn[J]. Klin Padiatr, 2017,229(4):223-228.
[33] Méndez-Abad P, Zafra-Rodríguez P, Lubián-López S, et al. NtproBNP is a useful early biomarker of bronchopulmonary dysplasia in very low birth weight infants[J]. Eur J Pediatr, 2019,178(5):755-761.
[34] Naeem B, Ayub A, Aly AM, et al. Urinary nt-proBNP as a potential noninvasive biomarker for screening of pulmonary hypertension in preterm infants: a pilot study[J]. J Perinatol, 2020,40(4):628-632.
[35] Vaz M, Hwang SY, Kagiampakis I, et al. Chronic cigarette smoke-induced epigenomic changes precede sensitization of bronchial epithelial cells to single-step transformation by KRAS mutations[J]. Cancer Cell, 2017,32(3):360-376.
[36] Agudelo Garcia PA, Hoover ME, Zhang P, et al. Identification of multiple roles for histone acetyltransferase 1 in replication-coupled chromatin assembly[J]. Nucleic Acids Res, 2017,45(16):9319-9335.
[37] Wang J, Jing Y, Wang X, et al. Changing expression profiles of mrna, lncrna, circrna, and miRNA in lung tissue reveal the pathophysiological of bronchopulmonary dysplasia (bpd) in mouse model[J]. J Cell Biochem, 2019,120(6):9369-9380.
[38] 李娟,蔡成,龚小慧,等.长链非编码RNA malat1与细胞凋亡诱导因子在早产儿支气管肺发育不良中表达及意义[J]. 临床儿科杂志, 2019,37(8):583-586.
[39] Mo W, Li Y, Chang W, et al. The role of lncRNA h19 in MAPK signaling pathway implicated in the progression of bronchopulmonary dysplasia[J]. Cell Transplant, 2020,29:963689720918294.doi:10.1177/0963689720918294
[40] Saliminejad K, Khorshid HRK, Fard SS, et al. An overview of micrornas: biology, functions, therapeutics, and analysis methods[J]. J Cell Physiol, 2019,234(5):5451-5465.
[41] Drury RE, O′Connor D, Pollard AJ. The clinical application of micrornas in infectious disease[J]. Front Immunol, 2017,8:1182.
[42] Yang Y, Qiu J, Kan Q, et al. MicroRNA expression profiling studies on bronchopulmonary dysplasia: a systematic review and meta-analysis[J]. Genet Mol Res, 2013,12(4):5195-206.
[43] Gong X, Qiu J, Qiu G, et al. Adrenomedullin regulated by mirna-574-3p protects premature infants with bronchopulmonary dysplasia[J].Bioscience Reports, 2020,40(5):BSR20191879.doi:10.1042/BSR20191879.

PDF(556 KB)

Accesses

Citation

Detail

段落导航
相关文章

/