Acute psychological stress: effects on chemotaxis and cellular adhesion molecule expression.

TitleAcute psychological stress: effects on chemotaxis and cellular adhesion molecule expression.
Publication TypeJournal Article
Year of Publication2003
AuthorsRedwine L, Snow S, Mills P, Irwin M
JournalPsychosom Med
Volume65
Issue4
Pagination598-603
Date Published2003 Jul-Aug
ISSN1534-7796
KeywordsAcute Disease, Adult, African Americans, Catecholamines, Cell Adhesion Molecules, Chemokines, Chemotaxis, Female, Gene Expression Regulation, Hemodynamics, Humans, L-Selectin, Leukocytes, Mononuclear, Macrophage-1 Antigen, Male, Middle Aged, N-Formylmethionine Leucyl-Phenylalanine, Speech, Stress, Psychological
Abstract

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.

Alternate JournalPsychosom Med
PubMed ID12883110
Grant ListAA10215 / AA / NIAAA NIH HHS / United States
AA13239 / AA / NIAAA NIH HHS / United States
AG18267 / AG / NIA NIH HHS / United States
M01 RR00827 / RR / NCRR NIH HHS / United States
MH55253 / MH / NIMH NIH HHS / United States
MHI8399 / MH / NIMH NIH HHS / United States