Regulation of Nlrp3 inflammasome by dietary metabolites.
Regulation of Nlrp3 inflammasome by dietary metabolites.
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DOI：
10.1016/j.smim.2015.10.004
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发表时间：
2015-09
影响因子：
7.8
通讯作者：
Dixit VD
中科院分区：
文献类型：
--
作者：
Camell C;Goldberg E;Dixit VD
先天免疫细胞和能量代谢之间的双向交流现在被广泛认为是调节体内平衡以及因调节失调的炎症而出现的慢性疾病的手段。大量营养素来自饮食或内源性途径，这些途径产生代谢物并将其转移到能量或生物合成途径中，调节炎症反应的启动、持续和停止。NLRP3炎症体是一种结构多样的代谢损伤相关分子模式(DAMP)的重要先天感受器，与热量过多、肥胖和衰老相关的一系列炎症性疾病有关。因此，了解免疫-代谢相互作用的调节机制及其在慢性病发病机制中的作用，有可能减少疾病的病理，提高老年人的生活质量，促进健康寿命的延长。就像免疫细胞的特殊亚群通过产生负调节细胞因子来抑制炎症一样；特定的免疫调节代谢物可以抑制炎症小体介导的免疫激活。在这里，我们强调能量底物、替代燃料和代谢阻尼剂在调节NLRP3炎症体中的作用，并讨论可能影响无菌炎症性疾病的潜在饮食干预。
The bidirectional communication between innate immune cells and energy metabolism is now widely appreciated to regulate homeostasis as well as chronic diseases that emerge from dysregulated inflammation. Macronutrients-derived from diet or endogenous pathways that generate and divert metabolites into energetic or biosynthetic pathways-regulate the initiation, duration and cessation of the inflammatory response. The NLRP3 inflammasome is an important innate sensor of structurally diverse metabolic damage-associated molecular patterns (DAMPs) that has been implicated in a wide range of inflammatory disorders associated with caloric excess, adiposity and aging. Understanding the regulators of immune-metabolic interactions and their contribution towards chronic disease mechanisms, therefore, has the potential to reduce disease pathology, improve quality of life in elderly and promote the extension of healthspan. Just as specialized subsets of immune cells dampen inflammation through the production of negative regulatory cytokines; specific immunoregulatory metabolites can deactivate inflammasome-mediated immune activation. Here, we highlight the role of energy substrates, alternative fuels and metabolic DAMPs in the regulation of the NLRP3 inflammasome and discuss potential dietary interventions that may impact sterile inflammatory disease.