Intra-uterine growth restriction downregulates the hepatic toll like receptor-4 expression and function.
Intra-uterine growth restriction downregulates the hepatic toll like receptor-4 expression and function.
复制标题
子宫内生长限制下调肝脏 Toll 样受体 4 的表达和功能。
DOI：
10.1080/17402520400008905
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发表时间：
2005-03
影响因子：
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通讯作者：
Devaskar, Sherin U
中科院分区：
文献类型：
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作者：
Equils, Ozlem;Singh, Sapna;Karaburun, Semra;Lu, Daning;Thamotharan, Manikkavasagar;Devaskar, Sherin U
母亲饥饿是胎儿宫内生长受限的重要原因 （IUGR），并增加了新生儿感染的风险。我们研究 母体饥饿对Toll样受体（TLR）4在肝脏， 脾和肠组织从产前胎儿的成年IUGR后代获得， 卡路里限制的老鼠肝脏TLR 4蛋白浓度在10 - 20天内未检测到。 在哺乳期限制牛奶摄入的IUGR大鼠 (SM/SP; n = 4，p < 0.05）与正常对照组相比 生长对照（CM/CP; n=4）， 并且在吮吸期间随意摄入牛奶可以部分纠正这种情况 肝TLR 4表达（SM/CP; n = 4）。IUGR没有影响 脾脏（n = 4）或 肠（n = 4）TLR 4 mRNA水平。在肝脏中，IUGR 导致了20%的增长 基线肿瘤坏死因子（TNF）-α mRNA表达（p < 0.03）和70% 与对照组相比，白细胞介素-1 β（IL-1β）mRNA表达增加（p < 0.008） 对照组（CM/CP，n = 7）。LPS诱导的肝 TNF-α释放显著高于对照组， 与CM/CP相比，SM/SP更高。我们认为IUGR失调 TLR 4在后代中的表达和功能，这可能有助于解释 革兰氏阴性脓毒症和炎症性疾病的风险增加， 人口
Maternal starvation is a significant cause of intrauterine growth restriction (IUGR) in the world and increases the risk of infection in the neonate. We examined the effect of maternal starvation on Toll like receptor (TLR)4 expression in hepatic, splenic and intestinal tissues obtained from the adult IUGR offspring of prenatal calorie restricted rats. The hepatic TLR4 protein concentration was undetectable in the IUGR rats that had restricted milk intake during the suckling period (SM/SP; n = 4, p < 0.05) as compared to the normal growth controls (CM/CP; n=4), and access to ad lib milk intake during the sucking period partially corrected the hepatic TLR4 expression (SM/CP; n = 4). IUGR had no effect on the splenic (n = 4) or intestinal (n = 4) TLR4 mRNA levels. In the liver, IUGR led to a 20% increase in baseline tumor necrosis factor (TNF)-α mRNA expression ( p < 0.03) and a 70% increase in interleukin-1β (IL-1β) mRNA expression ( p < 0.008) as compared to the control rats (CM/CP; n = 7). LPS-induced hepatic TNF-α release was significantly higher in SM/SP as compared to CM/CP. We propose that IUGR dysregulates TLR4 expression and function in the offspring, which may help explain the increased risk of Gram-negative sepsis and inflammatory diseases in this population.