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伤害感受素/孤啡肽FQ - NOP受体系统在炎症和免疫介导疾病中的作用

Nociceptin/orphanin FQ-NOP receptor system in inflammatory and immune-mediated diseases.

作者信息

Gavioli Elaine C, de Medeiros Iris Ucella, Monteiro Marta C, Calo Girolamo, Romão Pedro R T

机构信息

Department of Biophysic and Pharmacology, Federal University of Rio Grande do Norte, Natal, Brazil.

Laboratory of Clinical Microbiology and Immunology, Faculty of Pharmacy, Federal University of Pará, Belém, Brazil.

出版信息

Vitam Horm. 2015;97:241-66. doi: 10.1016/bs.vh.2014.11.003. Epub 2015 Jan 14.

Abstract

The neuropeptide nociceptin/orphanin FQ (N/OFQ) is the endogenous ligand of the G-protein-coupled receptor NOP. Cells from the immune system express the precursor preproN/OFQ and the NOP receptor, as well as secrete N/OFQ. The activation of the N/OFQ-NOP pathway can regulate inflammatory and immune responses. Several immune activities, including leukocyte migration, cytokine and chemokine production, and lymphocytes proliferation are influenced by NOP activation. It was demonstrated that cytokines and other stimuli such as Toll-like receptor agonist (e.g., lipopolysaccharide) induce N/OFQ production by cells from innate and adaptive immune response. In this context, N/OFQ could modulate the outcome of inflammatory diseases, such as sepsis and immune-mediated pathologies by mechanisms not clearly elucidated. In fact, clinical studies revealed increased levels of N/OFQ under sepsis, arthritis, and Parkinson's disease. Preclinical and clinical studies pointed to the blockade of NOP receptor signaling as successful strategy for the treatment of inflammatory diseases. This review is focused on experimental and clinical data that suggest the participation of N/OFQ-NOP receptor activation in the modulation of the immune response, highlighting the immunomodulatory potential of NOP antagonists in the inflammatory and immunological disturbances.

摘要

神经肽痛敏肽/孤啡肽FQ(N/OFQ)是G蛋白偶联受体NOP的内源性配体。免疫系统的细胞表达前体前痛敏肽/孤啡肽原(preproN/OFQ)和NOP受体,并分泌N/OFQ。N/OFQ-NOP途径的激活可调节炎症和免疫反应。包括白细胞迁移、细胞因子和趋化因子产生以及淋巴细胞增殖在内的多种免疫活动受NOP激活的影响。已证实细胞因子和其他刺激物,如Toll样受体激动剂(如脂多糖)可诱导先天性和适应性免疫反应细胞产生N/OFQ。在这种情况下,N/OFQ可能通过尚未明确阐明的机制调节炎症性疾病的结局,如脓毒症和免疫介导的病理状况。事实上,临床研究显示脓毒症、关节炎和帕金森病患者体内N/OFQ水平升高。临床前和临床研究表明,阻断NOP受体信号传导是治疗炎症性疾病的成功策略。本综述聚焦于实验和临床数据,这些数据提示N/OFQ-NOP受体激活参与免疫反应的调节,强调了NOP拮抗剂在炎症和免疫紊乱中的免疫调节潜力。

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