Mechanisms of degranulation in neutrophils.
Mechanisms of degranulation in neutrophils.
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DOI：
10.1186/1710-1492-2-3-98
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发表时间：
2006-09-15
期刊：
影响因子：
--
通讯作者：
Lacy P
中科院分区：
文献类型：
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作者：
Lacy P
中性粒细胞是在一系列疾病和病症中引起组织损伤的关键炎性细胞。作为骨髓来源的白色血细胞，它们响应趋化信号从血流迁移到组织炎症部位，并通过经历受体介导的呼吸爆发和脱粒诱导炎症。嗜中性粒细胞脱颗粒是肺部疾病的主要致病因素，包括哮喘的严重窒息发作。然而，控制中性粒细胞脱粒的机制还不清楚。最近的观察表明，从中性粒细胞释放颗粒取决于细胞内信号传导途径的激活，包括β-抑制蛋白、Rho鸟苷三磷酸酶Rac 2、可溶性NSF附着蛋白（SNAP）受体、酪氨酸激酶的src家族和酪氨酸磷酸酶MEG 2。其中一些观察结果表明，从中性粒细胞脱粒是选择性的，并依赖于非冗余信号通路。本文综述了近年来有关中性粒细胞释放颗粒源性介质的机制的研究进展。
Neutrophils are critical inflammatory cells that cause tissue damage in a range of diseases and disorders. Being bone marrow-derived white blood cells, they migrate from the bloodstream to sites of tissue inflammation in response to chemotactic signals and induce inflammation by undergoing receptor-mediated respiratory burst and degranulation. Degranulation from neutrophils has been implicated as a major causative factor in pulmonary disorders, including severe asphyxic episodes of asthma. However, the mechanisms that control neutrophil degranulation are not well understood. Recent observations indicate that granule release from neutrophils depends on activation of intracellular signalling pathways, including β-arrestins, the Rho guanosine triphosphatase Rac2, soluble NSF attachment protein (SNAP) receptors, the src family of tyrosine kinases, and the tyrosine phosphatase MEG2. Some of these observations suggest that degranulation from neutrophils is selective and depends on nonredundant signalling pathways. This review focuses on new findings from the literature on the mechanisms that control the release of granule-derived mediators from neutrophils.