Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Online research Club (http://www.onlineresearchclub.org/), Nagasaki, Japan.
Rev Med Virol. 2020 Jan;30(1):e2084. doi: 10.1002/rmv.2084. Epub 2019 Nov 10.
Degranulation of mast cells (MCs) releases several mediators such as vascular endothelial growth factor (VEGF), chymase, tryptase, histamine, and cytokines, which all have important roles in the severity of dengue infection. We aimed to investigate the role of MCs in severity of dengue.
We searched for relevant studies in 10 databases on 15 August 2016. Meta-analysis (MA) was conducted by R version 3.5.0.
We included 24 studies. in vivo and in vitro studies showed higher MC products released from infected mice/cells with dengue virus. In addition, when administering MC stabilizers or antihistaminic drugs, there was a decrease in vascular/capillary permeability. In human and at early stages, studies revealed an insignificant difference in VEGF levels in dengue fever (DF) versus dengue hemorrhagic fever (DHF) (standardized mean difference [SMD] 0.145; 95% confidence interval [CI], -0.348-0.638). Meanwhile, at acute stages and compared with healthy controls, high heterogeneity with an inconclusive difference in VEGF levels were noted in DF and DHF. However, pooled serum and plasma levels of VEGF were increased significantly in dengue shock syndrome (DSS) versus healthy controls (SMD 0.65; 95% CI, 0.3-0.95). There were also significantly higher chymase levels in DHF patients compared with DF during the acute phase (MD -6.531; 95% CI, -12.2 to -0.9).
VEGF and chymase levels are mediators in dengue pathogenesis. However, limited data were available to support their role in severe dengue cases. Further studies are needed to evaluate the function of other mediators in dengue severity.
肥大细胞(MCs)脱颗粒会释放血管内皮生长因子(VEGF)、糜蛋白酶、类胰蛋白酶、组胺和细胞因子等多种介质,这些介质在登革热感染的严重程度中都具有重要作用。我们旨在研究 MCs 在登革热严重程度中的作用。
我们于 2016 年 8 月 15 日在 10 个数据库中搜索了相关研究。使用 R 版本 3.5.0 进行荟萃分析(MA)。
我们纳入了 24 项研究。体内和体外研究表明,感染登革病毒的小鼠/细胞释放的 MC 产物更高。此外,当给予 MC 稳定剂或抗组胺药物时,血管/毛细血管通透性降低。在人类和早期,研究表明登革热(DF)与登革出血热(DHF)之间 VEGF 水平无显著差异(标准化均数差 [SMD] 0.145;95%置信区间 [CI],-0.348-0.638)。同时,在急性期,与健康对照组相比,DF 和 DHF 中 VEGF 水平的异质性很高,且差异无统计学意义。然而,在登革休克综合征(DSS)与健康对照组相比,血清和血浆 VEGF 水平显著升高(SMD 0.65;95%CI,0.3-0.95)。在急性期,DHF 患者的糜蛋白酶水平也显著高于 DF 患者(MD-6.531;95%CI,-12.2 至-0.9)。
VEGF 和糜蛋白酶水平是登革热发病机制中的介质。然而,目前可用的数据不足以支持它们在重症登革热病例中的作用。需要进一步研究来评估其他介质在登革热严重程度中的作用。