Gabriel H H, Kindermann W
Institute for Sports and Preventive Medicine, Faculty of Medicine, University of the Saarland, Saarbrücken, Germany.
Can J Physiol Pharmacol. 1998 May;76(5):512-23. doi: 10.1139/cjpp-76-5-512.
Cell-cell and cell-matrix contacts are dependent on cell surface density, localization, and avidity state of adhesion molecules. These adhesion molecules are involved in all steps of the leukocyte's adhesion process. Selectins, molecules of the immunoglobulin superfamily, and integrins are necessary for an initial tethering, triggering, firm attachment, and transendothelial migration of leukocytes. Hormones, cytokines, other pro-inflammatory agents, and shedded receptors like the LPS-receptor significantly alter the adhesion process. Infectious and noninfectious inflammatory processes are capable of inducing an altered adhesion of leukocytes to endothelial cells. The result is a preferential homing of leukocytes to sites of inflammation. Acute bouts of exercise may induce a release or secretion of many of the aforementioned substances involved in the adhesion process. The acute immune response to exercise is strongly influenced by the activation of the sympathetic nervous system and the hypothalamo-pituitary-adrenal axis. During the first 10-30 min of exercise an almost maximal increase of T and B lymphocytes, monocytes, and NK cells from the marginal pool into the blood circulation is induced. This demargination of cells is likely an effect mediated by beta 2 adrenergic receptors and probably due to a change of the avidity state of adhesion molecules. Strenuous exercise is associated with an increase of serum cortisol resulting in a delayed neutrocytosis and lymphocytopenia. Both phenomena are due to altered circulation patterns. It will be discussed how far adhesion molecules might contribute to this effect. Furthermore an evaluation of contradicting experimental results about surface expression of selectins and integrins will be provided.
细胞间和细胞与基质的接触取决于粘附分子的细胞表面密度、定位和亲和力状态。这些粘附分子参与白细胞粘附过程的所有步骤。选择素、免疫球蛋白超家族分子和整合素对于白细胞的初始 tethering、触发、牢固附着和跨内皮迁移是必需的。激素、细胞因子、其他促炎剂以及诸如 LPS 受体等脱落受体可显著改变粘附过程。感染性和非感染性炎症过程能够诱导白细胞与内皮细胞的粘附改变。结果是白细胞优先归巢至炎症部位。急性运动发作可能会诱导许多上述参与粘附过程的物质的释放或分泌。运动的急性免疫反应受到交感神经系统和下丘脑 - 垂体 - 肾上腺轴激活的强烈影响。在运动的最初 10 - 30 分钟内，可诱导边缘池中的 T 和 B 淋巴细胞、单核细胞和 NK 细胞几乎最大程度地增加进入血液循环。这种细胞的边缘池迁移可能是由β2 肾上腺素能受体介导的效应，可能是由于粘附分子亲和力状态的改变。剧烈运动与血清皮质醇增加相关，导致中性粒细胞增多和淋巴细胞减少延迟。这两种现象都是由于循环模式改变所致。将讨论粘附分子在多大程度上可能促成这种效应。此外还将提供对关于选择素和整合素表面表达的相互矛盾的实验结果的评估。
