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mTOR regulates metabolic adaptation of APCs in the lung and controls the outcome of allergic inflammation.mTOR调节肺部抗原呈递细胞的代谢适应性,并控制过敏性炎症的结果。
Science. 2017 Sep 8;357(6355):1014-1021. doi: 10.1126/science.aaj2155. Epub 2017 Aug 10.
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Challenges in the Management of Fungal Keratitis.
JAMA Ophthalmol. 2017 Jun 1;135(6):525-526. doi: 10.1001/jamaophthalmol.2017.0722.
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The mTOR signal regulates myeloid-derived suppressor cells differentiation and immunosuppressive function in acute kidney injury.mTOR信号调节急性肾损伤中髓源性抑制细胞的分化和免疫抑制功能。
Cell Death Dis. 2017 Mar 23;8(3):e2695. doi: 10.1038/cddis.2017.86.
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BAMBI inhibits inflammation through the activation of autophagy in experimental spinal cord injury.BAMBI通过激活自噬抑制实验性脊髓损伤中的炎症反应。
Int J Mol Med. 2017 Feb;39(2):423-429. doi: 10.3892/ijmm.2016.2838. Epub 2016 Dec 27.
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Mammalian target of rapamycin inhibition counterbalances the inflammatory status of immune cells in patients with chronic granulomatous disease.雷帕霉素靶蛋白抑制作用可平衡慢性肉芽肿病患者免疫细胞的炎症状态。
J Allergy Clin Immunol. 2017 May;139(5):1641-1649.e6. doi: 10.1016/j.jaci.2016.08.033. Epub 2016 Oct 1.
6
LOX-1 and TLR4 affect each other and regulate the generation of ROS in A. fumigatus keratitis.凝集素样氧化低密度脂蛋白受体1(LOX-1)和Toll样受体4(TLR4)相互影响,并调节烟曲霉性角膜炎中活性氧的产生。
Int Immunopharmacol. 2016 Nov;40:392-399. doi: 10.1016/j.intimp.2016.09.027. Epub 2016 Sep 30.
7
Mammalian Target of Rapamycin Inhibition With Rapamycin Mitigates Radiation-Induced Pulmonary Fibrosis in a Murine Model.雷帕霉素抑制哺乳动物雷帕霉素靶蛋白可减轻小鼠模型中辐射诱导的肺纤维化。
Int J Radiat Oncol Biol Phys. 2016 Nov 15;96(4):857-866. doi: 10.1016/j.ijrobp.2016.07.026. Epub 2016 Jul 28.
8
Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury.肺上皮细胞中MTOR的激活会促进脂多糖诱导的急性肺损伤。
Autophagy. 2016 Dec;12(12):2286-2299. doi: 10.1080/15548627.2016.1230584. Epub 2016 Sep 22.
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Rapamycin increases RSV RNA levels and survival of RSV-infected dendritic cell depending on T cell contact.雷帕霉素可提高呼吸道合胞病毒(RSV)的RNA水平,并取决于T细胞接触情况提高受RSV感染的树突状细胞的存活率。
Toxicol In Vitro. 2016 Oct;36:114-119. doi: 10.1016/j.tiv.2016.07.016. Epub 2016 Jul 25.
10
The Inhibitory Effect of Rapamycin on Toll Like Receptor 4 and Interleukin 17 in the Early Stage of Rat Diabetic Nephropathy.雷帕霉素对大鼠糖尿病肾病早期Toll样受体4及白细胞介素17的抑制作用
Kidney Blood Press Res. 2016;41(1):55-69. doi: 10.1159/000368547. Epub 2016 Feb 7.

小鼠角膜感染期间与雷帕霉素哺乳动物靶标/Toll样受体4信号通路相关的白细胞介素-1β的产生

Production of interleukin-1β related to mammalian target of rapamycin/Toll-like receptor 4 signaling pathway during infection of the mouse cornea.

作者信息

Xu Rui, Lin Jing, Zhao Gui-Qiu, Li Cui, Che Cheng-Ye, Xu Qiang, Liu Min

机构信息

Department of Ophthalmology, the Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong Province, China.

出版信息

Int J Ophthalmol. 2018 May 18;11(5):712-718. doi: 10.18240/ijo.2018.05.02. eCollection 2018.

DOI:10.18240/ijo.2018.05.02
PMID:29862167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5957020/
Abstract

AIM

To elucidate the effect of rapamycin on regulating the production of interleukin (IL)-1β in ()-induced keratitis and to verify whether the expression of IL-1β in keratitis is associated with the mammalian target of rapamycin (mTOR)/Toll-like receptor 4 (TLR4) signaling pathway.

METHODS

Fungal keratitis mouse models of susceptible C57BL/6 mice were established using . The mice were subsequently treated with rapamycin. The protein levels of p-mTOR, TLR4, and IL-1β in normal and infected corneal tissue were measured by Western blot. The TLR4 and IL-1β mRNA levels were determined by real-time polymerase chain reaction (PCR).

RESULTS

In C57BL/6 mice, rapamycin treatment decreased the clinical scores and production of the pro-inflammatory cytokine, IL-1β. The expression of TLR4, stimulated by , was reduced as well when the mTOR signaling pathway was suppressed by rapamycin.

CONCLUSION

Rapamycin is beneficial for the outcome of fungal keratitis and has an inhibitory effect expression of the inflammatory cytokine IL-1β. The inhibitory effect on IL-1β expression can be associated with the mTOR/TLR4 signaling pathway in infection in mice.

摘要

目的

阐明雷帕霉素对调节烟曲霉素诱导的角膜炎中白细胞介素(IL)-1β产生的影响,并验证角膜炎中IL-1β的表达是否与雷帕霉素哺乳动物靶点(mTOR)/Toll样受体4(TLR4)信号通路相关。

方法

使用烟曲霉素建立易感C57BL/6小鼠的真菌性角膜炎小鼠模型。随后用雷帕霉素对小鼠进行治疗。通过蛋白质免疫印迹法检测正常和感染角膜组织中p-mTOR、TLR4和IL-1β的蛋白水平。通过实时聚合酶链反应(PCR)测定TLR4和IL-1β的mRNA水平。

结果

在C57BL/6小鼠中,雷帕霉素治疗降低了临床评分和促炎细胞因子IL-1β的产生。当雷帕霉素抑制mTOR信号通路时,烟曲霉素刺激的TLR4表达也降低。

结论

雷帕霉素对真菌性角膜炎的转归有益,且对炎性细胞因子IL-1β的表达有抑制作用。对IL-1β表达的抑制作用可能与小鼠烟曲霉素感染中的mTOR/TLR4信号通路有关。