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Although intrauterine growth retardation (IUGR) is a ma jor 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-α,TGF-β,IL-6,IL-4,IL-1β,IL-12,IFN-γand GAPDH was quantified with RT-PCR from placenta. Cytokine and cytokine receptor gene polymorphisms for -1087IL10,-308TNFA,-174IL6,+915TGFB1,intron 2 IL1RN,+36TNFR1,150V IL4RA and -159CD14 were determined from genomic DNA. The serum levels of IL-1β,IL-6,IL-8,IL-10,IL-12,TNF-αand TGF-βwere measured. There was a significant decrease of IL-10 and IL-12,but increase of TGF-βin the decidua and similarly decrease of IL-10,but increase of TGF-βin the trophoblasts of the IUGR placentas compared with the non-IUGR placentas. We found significantly lower levels of IL-1βin serum from the mothers of the IUGR infants and of TGF-βin 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-βmRNA upregulated 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.
The mechanism of intrauterine growth retardation (IUGR) is a ma jor 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 . MRNA for IL-10, IL-8, TNF-α, TGF-β, IL-6, IL-4, IL-1β, IL-12, IFN- γand GAPDH was quantified with RT-PCR from placenta. Cytokine and cytokine receptor gene polymorphisms for -1087IL10, -308TNFA, -174IL6, +915TGFB1, intron 2 IL1RN, +36 TNFR1, 150V IL4RA and -159CD14 were determined from genomic DNA. The serum levels of was IL-1β, IL-6, IL-8, IL-10, IL-12, TNF-α and TGF-βwere measured. There was a significant decrease of IL-10 and IL- decidua and decreased decrease of IL-10, but increase of TGF-βin the trophoblasts of the IUGR placentas compared with the non-IUGR placentas. We found significantly lower levels of IL-1βin serum from th e mothers of the IUGR infants and of TGF-βin 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-β mRNA upregulated 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 may be treatable.