Exercise and inflammation
Exercise and inflammation
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DOI：
10.1152/japplphysiol.00414.2007
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发表时间：
2007-07-01
影响因子：
3.3
通讯作者：
Febbraio, Mark A.
中科院分区：
文献类型：
--
作者：
Febbraio, Mark A.
本系列综述的目的是强调在过去五到十年中，关于体育锻炼和炎症之间相互作用的知识取得的巨大进步。许多年前，人们认识到，与久坐不动的生活方式相比，定期适度的运动可以降低感染风险，而长时间的高强度运动会增加感染风险;所谓的“J形模型”（16）。然而，直到最近，体力活动，炎症和免疫力之间的确切联系仍然是未知的，因为这一领域的研究及其结论主要基于描述性数据分析。事实上，在千年之交发表的一篇关于运动和免疫功能的综合评论中，Pedersen和霍夫曼戈茨（18）认识到了这一点，并评论说：“运动免疫学未来工作的重点应该超越描述性的现象学研究，研究观察到的影响的潜在神经，激素，细胞因子和生化机制。”必须指出的是，该领域的研究人员已经注意到了这一信息，这可以从本系列综述中清楚地观察到。在本系列的第一篇中，Gleeson（7）回顾了与运动和锻炼中的免疫功能相关的文献。Gleeson博士实验室的一项新的令人兴奋的进展是Toll样受体（TLR）在运动期间人体免疫反应中的作用。TLR是已知在检测果蝇和哺乳动物中的感染中起重要作用的模式识别受体的进化的保守家族（9）。在兰开斯特等人的一篇论文中，(13)作者证明，体力活动降低了TLR 1、TLR 2和TLR 4的表达，并得出结论，TLR功能在体内生理条件下受到调节。有趣的是，已知体育锻炼会增加循环热休克蛋白（23），已知其会激活TLR 2和TLR 4（1），突出了免疫系统对体育锻炼的反应的复杂性。运动和免疫功能的主题在库珀（4）的评论中继续，他提出了运动消除免疫危险类型的压力的理论，这种压力有时会失调并对健康有害。这一观点与Matzinger（14）的观点一致，他是第一个挑战免疫功能的“自我与非自我”理论的人，这是一种基于免疫系统更关注破坏分子而不是外来分子的想法提出的免疫模型。在他的评论中，库珀博士提供了“危险理论”在剧烈运动背景下的各种实例。例如，他指出，食物致敏免疫细胞在体内平衡中相对无害。然而，在运动过敏反应的情况下，这些细胞从脾脏等仓库重新分布到中央循环中，在那里它们不再无害。
the purpose of this review series is to highlight the tremendous advancement in knowledge that has taken place over the last five to ten years regarding the interaction between physical exercise and inflammation. Many years ago, it was recognized that regular, moderate exercise reduced the risk of infection compared with a sedentary lifestyle, whereas prolonged, heavy intensity exercise increased infection risk; the so called “J-shaped model”(16). However, the precise nexus between physical activity, inflammation, and immunity has, until recently, been unknown, as studies in this area, and the conclusions they made, were largely based on descriptive data analysis. Indeed, in a comprehensive review on exercise and immune function, published at the turn of the millennium, Pedersen and Hoffman Goetz (18) recognized this and commented,“The focus of future work in exercise immunology should move beyond descriptive, phenomenological studies to studies of underlying neural, hormonal, cytokine, and biochemical mechanisms for the observed effects.” It must be said that researchers in the field have heeded this message, and this can be clearly observed from the present review series.In the first of the series, Gleeson (7) reviews the literature relating to immune function in sport and exercise. One new and exciting development in this field, from work conducted in Dr. Gleeson's laboratory, is the role that Toll-like receptors (TLRs) play in the immune response in humans during exercise. TLR's are an evolutionary, conserved family of pattern recognition receptors known to play an essential role in detecting infection in both Drosophila and mammals (9). In a paper by Lancaster et al.(13), the authors demonstrated that physical activity decreased the expression of TLR1, TLR2, and TLR4 and concluded that TLR function is subject to modulation under physiological conditions in vivo. Intriguingly, physical exercise is known to increase circulating heat shock proteins (23), which are known to activate TLR2 and TLR4 (1), highlighting the complexity of the immune system in response to physical exercise. The theme of exercise and immune function is continued in the review by Cooper (4), who proposes the theory that exercise elicits an immunological danger type of stress that, on occasions, becomes dysregulated and detrimental to well-being. This view is consistent with that of Matzinger (14), who was the first to challenge the “self versus non-self” theory of immune function, a proposed model of immunity based on the idea that the immune system is more concerned with molecules that do damage rather than those that are foreign. In his review, Dr. Cooper provides various instances of the “danger theory” in the context of strenuous exercise. For example, he points out that food-sensitizing immune cells are relatively innocuous in homeostasis. However, in cases of exercise anaphylaxis, these cells are redistributed from depots such as the spleen into the central circulation where they are no longer harmless.