Adhesion molecules during immune response to exercise

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.