OBJECTIVE: Activation of a psychological stress response increases autonomic activity and enhances immune function by inducing a significant increase in numbers of leukocytes at sites of inflammation. Chemotaxis and cellular adhesion are thought to mediate leukocyte trafficking. In this study, we examine the effects of an acute psychological stress on chemotactic responses of PBMCs and on CAM expression in relation to measures of sympathetic activation. METHODS: Subjects underwent either a public speaking task (N = 24) or a control condition (N = 13). Blood was drawn before the task, immediately after, and 20 minutes after, the task for changes in percentage of cells expressing cellular adhesion molecules, chemotaxis to chemokines, HR, blood pressure, and E and NE levels. RESULTS: In response to the laboratory stressor, increases of PBMC chemotaxis to FMLP and SDF-1 were found, which were coupled with increases in the percentages of lymphocytes expressing the integrin Mac-1. Autonomic activity, including blood pressure and circulating levels of catecholamines, increased after administration of the stressor, and correlated with increases of Mac-1. CONCLUSIONS: These data show that acute stress induces increase of chemotaxis and expression of CAM expression, which may contribute to increased migration and recruitment of immune cells to sites of infection and/or inflammation.
OBJECTIVE: Activation of a psychological stress response increases autonomic activity and enhances immune function by inducing a significant increase in numbers of leukocytes at sites of inflammation. Chemotaxis and cellular adhesion are thought to mediate leukocyte trafficking. In this study, we examine the effects of an acute psychological stress on chemotactic responses of PBMCs and on CAM expression in relation to measures of sympathetic activation. METHODS: Subjects underwent either a public speaking task (N = 24) or a control condition (N = 13). Blood was drawn before the task, immediately after, and 20 minutes after, the task for changes in percentage of cells expressing cellular adhesion molecules, chemotaxis to chemokines, HR, blood pressure, and E and NE levels. RESULTS: In response to the laboratory stressor, increases of PBMC chemotaxis to FMLP and SDF-1 were found, which were coupled with increases in the percentages of lymphocytes expressing the integrin Mac-1. Autonomic activity, including blood pressure and circulating levels of catecholamines, increased after administration of the stressor, and correlated with increases of Mac-1. CONCLUSIONS: These data show that acute stress induces increase of chemotaxis and expression of CAM expression, which may contribute to increased migration and recruitment of immune cells to sites of infection and/or inflammation.
Authors: Laura S Redwine; Petra H Wirtz; Suzi Hong; Jos A Bosch; Jos Bosch; Michael G Ziegler; Barry Greenberg; Paul J Mills Journal: J Am Coll Cardiol Date: 2010-11-16 Impact factor: 24.094
Authors: Frieda A Koopman; Susanne P Stoof; Rainer H Straub; Marjolein A Van Maanen; Margriet J Vervoordeldonk; Paul P Tak Journal: Mol Med Date: 2011-05-20 Impact factor: 6.354
Authors: Jennifer M Curry; Mark L Hanke; Melissa G Piper; Michael T Bailey; Benjamin D Bringardner; John F Sheridan; Clay B Marsh Journal: Brain Behav Immun Date: 2009-11-10 Impact factor: 7.217
Authors: R Barzilay; F Ventorp; H Segal-Gavish; I Aharony; A Bieber; S Dar; M Vescan; R Globus; A Weizman; D Naor; J Lipton; S Janelidze; L Brundin; D Offen Journal: J Mol Neurosci Date: 2016-09-13 Impact factor: 3.444