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首页> 外文期刊>Cytokine >Knockout of toll-like receptor-4 attenuates the pro-inflammatory state of diabetes.
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Knockout of toll-like receptor-4 attenuates the pro-inflammatory state of diabetes.

机译：Toll样受体4的敲除减弱了糖尿病的促炎状态。

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摘要

Type 1 diabetes (T1DM) is associated with increased vascular complications and is a pro-inflammatory state. Recent findings have shown increased TLR2 and 4 expression, signaling, ligands, and functional activation in T1DM subjects compared to controls and further accentuated in T1DM with microvascular complications. Thus, the aim of this study was to examine if genetic deficiency of TLR4 attenuates the increased inflammation associated with T1DM using the streptozotocin-induced diabetic mouse model. C57BL/6 and TLR4(-/-) mice were obtained and studied in the native state and following induction of diabetes using streptozotocin. Diabetic (WT+STZ) mice had increased expression of both TLR2 and TLR4, while TLR4(-/-) STZ mice had increased expression only of TLR2, but not TLR4 compared to the non-diabetic mice TLR2 expression was significantly increased with STZ-induced diabetes and was unaffected by knockout of TLR4. Also, levels of MyD88, IRAK-1 protein phosphorylation, Trif, IRF3, and NF-kappaB activity were significantly reduced in TLR4(-/-) +STZ mice compared to the WT+STZ mice. WT+STZ mice exhibited significantly increased levels of serum and macrophage IL-1beta, IL-6, KC/IL-8, IP-10, MCP-1, IFN beta and TNF-alpha compared to WT mice and this was significantly attenuated in TLR4(-/-) +STZ mice (P<0.01). Thus, TLR4 contributes to the pro-inflammatory state and TLR4KO attenuates inflammation in diabetes.
机译：1型糖尿病（T1DM）与血管并发症增加相关，并且属于促炎状态。最近的研究结果显示，与对照组相比，T1DM受试者中TLR2和4的表达，信号传导，配体和功能激活增加，而在T1DM中伴有微血管并发症则进一步加剧。因此，本研究的目的是使用链脲佐菌素诱导的糖尿病小鼠模型检查TLR4的遗传缺陷是否能减轻与T1DM相关的炎症反应。获得C57BL / 6和TLR4（-/-）小鼠，并在天然状态下和使用链脲佐菌素诱导糖尿病后进行研究。与非糖尿病小鼠相比，糖尿病（WT + STZ）小鼠的TLR2和TLR4均表达增加，而TLR4（-/-）STZ小鼠仅TLR2的表达升高，而与非糖尿病小鼠相比TLR2的表达却显着增加。诱发糖尿病，不受TLR4基因敲除的影响。而且，与WT + STZ小鼠相比，TLR4（-/-）+ STZ小鼠的MyD88，IRAK-1蛋白磷酸化，Trif，IRF3和NF-κB活性水平显着降低。与WT小鼠相比，WT + STZ小鼠的血清和巨噬细胞IL-1beta，IL-6，KC / IL-8，IP-10，MCP-1，IFNβ和TNF-α的水平显着增加，并且在WT + STZ小鼠中显着减弱TLR4（-/-）+ STZ小鼠（P <0.01）。因此，TLR4促成促炎状态，而TLR4KO减轻了糖尿病中的炎症。

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