ADHESION MOLECULES DURING IMMUNE-RESPONSE TO EXERCISE

Cell-cell and cell-matrix contacts are dependent on cell surface densi ty, localization, and avidity state of adhesion molecules. These adhes ion molecules are involved in all steps of the leukocyte's adhesion pr ocess. Selectins, molecules of the immunoglobulin superfamily, and int egrins are necessary for an initial tethering, triggering, firm attach ment, and transendothelial migration of leukocytes. Hormones, cytokine s, other pro-inflammatory agents, and shedded receptors like the LPS-r eceptor significantly alter the adhesion process. Infectious and nonin fectious inflammatory processes are capable of inducing an altered adh esion of leukocytes to endothelial cells. The result is a preferential homing of leukocytes to sites of inflammation. Acute bouts of exercis e may induce a release or secretion of many of the aforementioned subs tances involved in the adhesion process. The acute immune response to exercise is strongly influenced by the activation of the sympathetic n ervous system and the hypothalamo-pituitary-adrenal axis. During the f irst 10-30 min of exercise an almost maximal increase of T and B lymph ocytes, monocytes, and NK cells from the marginal pool into the blood circulation is induced. This demargination of cells is likely an effec t mediated by beta(2) adrenergic receptors and probably due to a chang e of the avidity state of adhesion molecules. Strenuous exercise is as sociated with an increase of serum cortisol resulting in a delayed neu trocytosis and lymphocytopenia. Both phenomena are due to altered circ ulation patterns. It will be discussed how far adhesion molecules migh t contribute to this effect. Furthermore an evaluation of contradictin g experimental results about surface expression of selectins and integ rins will be provided.