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活性氧和一氧化氮在肥大细胞依赖性炎症过程中的作用。

The role of reactive oxygen species and nitric oxide in mast cell-dependent inflammatory processes.

作者信息

Swindle Emily J, Metcalfe Dean D

机构信息

Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-6961, USA.

出版信息

Immunol Rev. 2007 Jun;217:186-205. doi: 10.1111/j.1600-065X.2007.00513.x.

DOI:10.1111/j.1600-065X.2007.00513.x
PMID:17498060
Abstract

Reactive oxygen species (ROS) and reactive nitrogen oxide species (RNOS), including nitric oxide, are produced in cells by a variety of enzymatic and non-enzymatic mechanisms. At high levels, both types of oxidants are used to kill ingested organisms within phagocytes. At low levels, RNOS may diffuse outside cells where they impact the vasculature and nervous system. Recent evidence suggests that low levels of ROS produced within cells are involved in cell signaling. Along with these physiological roles, many pathological conditions exist where detrimental high-level ROS and RNOS are produced. Many situations in which ROS/RNOS are associated also involve mast cell activation. In innate immunity, such mast cells are involved in the immune response toward pathogens. In acquired immunity, activation of mast cells by cross-linking of receptor-bound immunoglobulin E causes the release of mediators involved in the allergic inflammatory response. In this review, we describe the principle pathways for ROS and RNOS generation by cells and discuss the existence of such pathways in mast cells. In addition, we examine the evidence for a functional role for ROS and RNOS in mast cell secretory responses and discuss evidence for a direct relationship between ROS, RNOS, and mast cells in mast cell-dependent inflammatory conditions.

摘要

活性氧(ROS)和活性氮氧化物(RNOS,包括一氧化氮)通过多种酶促和非酶促机制在细胞内产生。在高水平时,这两种类型的氧化剂都用于杀死吞噬细胞内摄入的生物体。在低水平时,RNOS可能扩散到细胞外,影响血管系统和神经系统。最近的证据表明,细胞内产生的低水平ROS参与细胞信号传导。除了这些生理作用外,还存在许多产生有害高水平ROS和RNOS的病理状况。许多与ROS/RNOS相关的情况也涉及肥大细胞活化。在先天免疫中,此类肥大细胞参与对病原体的免疫反应。在获得性免疫中,受体结合的免疫球蛋白E交联导致肥大细胞活化,从而释放参与过敏性炎症反应的介质。在本综述中,我们描述了细胞产生ROS和RNOS的主要途径,并讨论了肥大细胞中此类途径的存在情况。此外,我们研究了ROS和RNOS在肥大细胞分泌反应中发挥功能作用的证据,并讨论了在肥大细胞依赖性炎症条件下ROS、RNOS与肥大细胞之间存在直接关系的证据。

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