Acute stress evokes selective mobilization of T cells that differ in chemokine receptor expression: A potential pathway linking immunologic reactivity to cardiovascular disease

Jos A. Bosch, Gary G. Berntson, John T. Cacioppo, Firdaus Dhabhar, Phillip T. Marucha

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

T lymphocytes and monocytes/macrophages are the most abundant cells found in the atherosclerotic plaque. These cells can migrate towards the activated endothelium through the local release of chemotactic cytokines, or chemokines. Given the important role of leukocyte migration in atherosclerosis and the role of stress in mediating leukocyte trafficking, the present study examined the effects of an acute stressor on the redistribution of T cells (CD3+) and monocytes that express the chemokine receptors CCR5, CCR6, CXCR1, CXCR2, CXCR3, and CXCR4. Forty-four undergraduate students underwent a public speaking task. The acute stressor induced sympathetic cardiac activation, parasympathetic cardiac withdrawal, lymphocytosis, and monocytosis (all p<.001). Although the total number of T lymphocytes did not change, there was a selective increase in the number of circulating T cells expressing CXCR2, CXCR3, and CCR5. The ligands of these receptors are chemokines known to be secreted by activated endothelial cells. Analyses of individual differences in stress-induced responses demonstrated a positive relationship between sympathetic cardiac reactivity and mobilization of the various T cell subsets (.35<r<.56;p<.05). For the monocytes, all sub-populations increased in parallel with total monocyte numbers, with no relation to changes in sympathetic cardiac drive. These results indicate that acute stress induces a mobilization of T cells that are primed to respond to inflamed endothelium. Acute stressors may thus promote the recruitment of circulating immune cells into the sub-endothelia, and therefore accelerate atherosclerotic plaque formation and potentially contribute to the complications that follow acute stressful events. This mechanism may help explain the link between stress, reactivity, and cardiovascular disease.

Original languageEnglish (US)
Pages (from-to)251-259
Number of pages9
JournalBrain, Behavior, and Immunity
Volume17
Issue number4
DOIs
StatePublished - Jan 1 2003
Externally publishedYes

Fingerprint

Chemokine Receptors
Cardiovascular Diseases
Monocytes
T-Lymphocytes
Endothelium
Atherosclerotic Plaques
Chemokines
Leukocytes
Lymphocytosis
T-Lymphocyte Subsets
Individuality
Atherosclerosis
Endothelial Cells
Macrophages
Students
Ligands
Population

Keywords

  • Acute psychological stressor
  • Autonomic balance
  • Cardiovascular disease
  • Cardiovascular reactivity
  • Chemokines
  • Lymphocyte redistribution
  • Psychoneuroimmunology

ASJC Scopus subject areas

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience

Cite this

Acute stress evokes selective mobilization of T cells that differ in chemokine receptor expression : A potential pathway linking immunologic reactivity to cardiovascular disease. / Bosch, Jos A.; Berntson, Gary G.; Cacioppo, John T.; Dhabhar, Firdaus; Marucha, Phillip T.

In: Brain, Behavior, and Immunity, Vol. 17, No. 4, 01.01.2003, p. 251-259.

Research output: Contribution to journalArticle

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