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运动引起的中性粒细胞脱颗粒和呼吸爆发活性的改变:可能的作用机制。

Exercise-induced alterations in neutrophil degranulation and respiratory burst activity: possible mechanisms of action.

作者信息

Peake Jonathan M

机构信息

School of Human Movement Studies, University of Queensland, St Lucia, QLD 4072, Australia.

出版信息

Exerc Immunol Rev. 2002;8:49-100.

PMID:12690938
Abstract

Neutrophils constitute 50-60% of all circulating leukocytes; they present the first line of microbicidal defense and are involved in inflammatory responses. To examine immunocompetence in athletes, numerous studies have investigated the effects of exercise on the number of circulating neutrophils and their response to stimulation by chemotactic stimuli and activating factors. Exercise causes a biphasic increase in the number of neutrophils in the blood, arising from increases in catecholamine and cortisol concentrations. Moderate intensity exercise may enhance neutrophil respiratory burst activity, possibly through increases in the concentrations of growth hormone and the inflammatory cytokine IL-6. In contrast, intense or long duration exercise may suppress neutrophil degranulation and the production of reactive oxidants via elevated circulating concentrations of epinephrine (adrenaline) and cortisol. There is evidence of neutrophil degranulation and activation of the respiratory burst following exercise-induced muscle damage. In principle, improved responsiveness of neutrophils to stimulation following exercise of moderate intensity could mean that individuals participating in moderate exercise may have improved resistance to infection. Conversely, competitive athletes undertaking regular intense exercise may be at greater risk of contracting illness. However, there are limited data to support this concept. To elucidate the cellular mechanisms involved in the neutrophil responses to exercise, researchers have examined changes in the expression of cell membrane receptors, the production and release of reactive oxidants and more recently, calcium signaling. The investigation of possible modifications of other signal transduction events following exercise has not been possible because of current methodological limitations. At present, variation in exercise-induced alterations in neutrophil function appears to be due to differences in exercise protocols, training status, sampling points and laboratory assay techniques.

摘要

中性粒细胞占所有循环白细胞的50%-60%;它们构成了抗菌防御的第一道防线,并参与炎症反应。为了研究运动员的免疫能力,众多研究调查了运动对循环中性粒细胞数量及其对趋化刺激和激活因子刺激的反应的影响。运动导致血液中中性粒细胞数量呈双相增加,这是由儿茶酚胺和皮质醇浓度升高引起的。中等强度运动可能会增强中性粒细胞的呼吸爆发活性,这可能是通过生长激素和炎症细胞因子IL-6浓度的增加实现的。相比之下,高强度或长时间运动可能会通过循环中肾上腺素( adrenaline )和皮质醇浓度的升高来抑制中性粒细胞脱颗粒和活性氧化剂的产生。有证据表明,运动诱导的肌肉损伤后会发生中性粒细胞脱颗粒和呼吸爆发激活。原则上,中等强度运动后中性粒细胞对刺激的反应性提高可能意味着参与中等强度运动的个体对感染的抵抗力增强。相反,经常进行高强度运动的竞技运动员患病风险可能更高。然而,支持这一概念的数据有限。为了阐明中性粒细胞对运动反应所涉及的细胞机制,研究人员研究了细胞膜受体表达的变化、活性氧化剂的产生和释放,以及最近的钙信号传导。由于目前的方法学限制,无法研究运动后其他信号转导事件可能的改变。目前,运动诱导的中性粒细胞功能改变的差异似乎是由于运动方案、训练状态、采样点和实验室检测技术的不同所致。

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