Cell:压力大,能力差!Cell揭秘棕色脂肪细胞应激机制

2020-07-06 生物探索 生物探索

现代社会,每个人都生活中重重压力之下,我们都深知“压力山大”会损害身体健康,使炎症性疾病“雪上加霜”。然而,压力是如何降低机体对疾病的抵抗能力,造成疾病

现代社会,每个人都生活中重重压力之下,我们都深知“压力山大”会损害身体健康,使炎症性疾病“雪上加霜”。然而,压力是如何降低机体对疾病的抵抗能力,造成疾病恶化的呢?压力与炎症又是什么关系呢?应激环境下,体内会分泌皮质醇和肾上腺等激素,这些激素本应减弱炎症反应,为何重压之下,炎症反而加重了呢?这些现象,科学家们仍难以解释。

6月30日,美国耶鲁大学医学院的Andrew Wang课题组在《Cell》在线发表题为Origin and Function of Stress-Induced IL-6 in Murine Models的研究论文。研究揭示了小鼠在压力条件下白介素6(IL-6)的起源与功能。研究发现在应激反应时,棕色脂肪细胞产生大量IL-6引发炎症,IL-6还与自身免疫性疾病、癌症、肥胖症、糖尿病、抑郁症和焦虑症有关。

https://doi.org/10.1016/j.cell.2020.05.054

具体来说,为了研究应激诱导的免疫介质,作者使用小鼠应激模型,筛选了循环中的32种炎性细D胞因子和趋化因子。结果表明 ,IL-6是诱导作用最强的细胞因子,且可介导持久的应激生理效应(图D)。

IL-6由多种细胞类型产生,包括造血细胞、心肌细胞、内皮细胞和脂肪细胞。那么压力条件下,增加的IL-6是由何种细胞产生的呢?

为了确定IL-6的来源,作者利用IL-6缺陷鼠进行混合骨髓嵌合体研究,发现应激诱导的IL-6不是由辐射敏感细胞产生的。之后,作者使用出血模型对多种组织进行IL-6诱导筛选,发现IL-6由棕色脂肪细胞分泌(图D)。

棕色脂肪组织(BAT)在能量代谢和体温调控中发挥重要作用,外周受交感神经的直接支配。作者推测IL-6是通过β-肾上腺素能信号诱导的。为了测试应激诱导的IL-6是否依赖交感神经元,使用6-羟基多巴胺(6-OHDA)阻断BAT交感神经,而不影响中枢神经系统。结果表明,6-OHDA处理后应激诱导的IL-6显著减弱 (图D),并且是β-肾上腺素能受体3(Adrb3)依赖性的(图E)。

考虑到应激时可以产生大量的IL-6,作者推测IL-6对应激生理有协同作用。使用间接量热法,作者检测到阻断IL-6信号,可使小鼠的总能量消耗显著变化(图A)。并且,IL-6在应激过程中会诱导肝脏糖异生,从而增加体内的葡萄糖的生成。

在随后的实验中,作者发现, IL-6可增加内毒素(LPS)炎症模型鼠的死亡率,降低机体对LPS诱导的炎症的适应性。相反,通过药物抑制IL-6,可以抑制小鼠的炎症反应,缓解抑郁症状等。

总的来说,该研究发现棕色脂肪接接受压力信号后,会以Adrb3依赖性方式分泌大量的IL-6,IL-6可通过肝脏糖异生介导血糖升高,从而协助机体作出“战斗或逃跑”反应,但也还会带来炎症等后果。

棕色脂肪细胞不仅能“燃烧你的卡路里”, 发挥减肥的功效,还可以调节体温。但在压力环境下,这种脂肪细胞也能加剧机体炎症。针对棕色脂肪细胞和IL-6的药物,将有助于提高我们承受压力的能力和多种疾病的治疗。

原始出处:

Hua Qing, Reina Desrouleaux, Kavita Israni-Winger, et.al. Origin and Function of Stress-Induced IL-6 in Murine Models. Cell June 30, 2020

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    2020-08-09 维他命
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    2020-12-30 lovetcm
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    2020-07-06 lovetcm
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    2020-07-06 肿肿

    机制研究离临床仍然有距离,不过与临床结合思考,仍然有帮助的,不能仅仅是纯临床思维,转化思维同样重要

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