Cytokines in the placenta of Pakistani newborns with and without intrauterine growth retardation
Cytokines in the placenta of Pakistani newborns with and without intrauterine growth retardation
复制标题
DOI：
10.1203/01.pdr.0000196332.37565.7d
复制
发表时间：
2006-02-01
影响因子：
3.6
通讯作者：
Hanson, LÅ
中科院分区：
文献类型：
--
作者：
Amu, S;Hahn-Zoric, M;Hanson, LÅ
虽然宫内发育迟缓（IUGR）是新生儿死亡率和发病率增加的主要危险因素，但其背后的机制尚不清楚。我们分析了巴基斯坦IUGR非常常见的有和无IUGR婴儿的细胞因子基因表达和基因多态性。研究了45对IUGR和55对对照母婴对。用RT-PCR从胎盘定量IL-10、IL-8、TNF-α、TGF-β、IL-6、IL-4、IL-1 β、IL-12、IFN-γ和GAPDH的mRNA。从基因组DNA中确定细胞因子和细胞因子受体基因多态性，包括-108711-10、-308TNFA、-174IL6、+915TGFB1、内含子2 IL 1 RN、+36TNFR 1、150 V IL 4 RA和-159CD14。结果显示：IUGR组胎盘蜕膜组织中IL-10、IL-12显著降低，TGF-β显著升高，滋养层细胞中IL-10显著降低，TGF-β显著升高，IL-1 β、IL-6、IL-8、IL-10、IL-12、TNF-α和TGF-β水平均显著高于非IUGR组。我们发现，与非IUGR婴儿相比，IUGR婴儿的母亲血清中IL-1 β和IUGR婴儿血清中TGF-β的水平显着降低。我们注意到，IL-10 mRNA在蜕膜中的表达下调，而TGF-β mRNA在IUGR胎盘中的表达上调，这些胎盘来自具有IUGR多个危险因素的人群。我们认为胎盘中的低IL-10可能与IUGR的发病机制有关，并且可能是可以治疗的。
Although intrauterine growth retardation (IUGR) is a major risk factor for increased neonatal mortality and morbidity, the mechanisms behind it are not clear. We analyzed cytokine gene expression and gene polymorphisms in infants with and without IUGR in Pakistan, where IUGR is very common. 45 IUGR and 55 control mother/infant pairs were studied. mRNA for IL-10, IL-8, TNF-alpha, TGF-beta, IL-6, IL-4, IL-1 beta, IL-12, IFN-gamma and GAPDH was quantified with RT-PCR from placenta. Cytokine and cytokine receptor gene polymorphisins for -108711-10, -308TNFA, -174IL6, +915TGFB1, intron 2 IL1RN, +36TNFR1, 150V IL4RA and -159CD14 were determined from genomic DNA. The serum levels of IL-1 beta, IL-6, IL-8, IL-10, IL-12, TNF-alpha and TGF-beta were measured.There was a significant decrease of IL-10 and IL-12, but increase of TGF-beta in the decidua and similarly decrease of IL-10 but increase of TGF-beta in the trophoblasts of the IUGR placentas compared with the non-IUGR placentas. We found significantly lower levels of IL-1 beta in serum from the mothers of the IUGR infants and of TGF-beta in serum of the infants with IUGR compared with the non-IUGR infants. We note that the IL-10 mRNA expression in the decidua was down-regulated, but the TGF-beta mRNA up-regulated in IUGR placentas of mothers from a population with multiple risk factors for IUGR. We propose that the low IL-10 in the placenta may be involved in the pathogenesis of IUGR and might possibly be treatable.