Catecholamine-induced leukocytosis: early observations, current research, and future directions

Brain Behav Immun. 1996 Jun;10(2):77-91. doi: 10.1006/brbi.1996.0009.

Abstract

Recent studies demonstrate that acute psychological stress in man affects lymphocyte circulation. It has been suggested that catecholamines are responsible for these changes. The present review summarizes findings regarding catecholamine-induced lympho- and leukocytosis, starting with observations dating back to the beginning of this century. Particular attention is given to the mechanisms of this phenomenon and the potential site of origin of newly appearing leukocytes. Characteristically, two phases are recognized after catecholamine administration: a quick (<30 min) mobilization of lymphocytes, followed by an increase in granulocyte numbers with decreasing lymphocyte numbers. Many studies have shown that catecholamines predominantly affect natural killer (NK) cell and granulocyte circulation, whereas T- and B-cell numbers remain relatively unaffected. The changes in lymphocyte circulation seem to be mainly mediated via activation of beta2-adrenoceptors, whereas granulocyte increases involve alpha-adrenoceptor stimulation. Results further indicate that the marginal pool and the spleen are the major sources for freshly recruited lymphocytes, whereas granulocytes are predominantly released from the marginal pool and the lung. Results from acute psychological stress or physical exercise models corroborate the results obtained with catecholamine administration. Together, the data demonstrate that components of the innate immune system participate in the classical fight/flight response.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Disease
  • Adrenal Cortex / physiopathology
  • Chemotaxis, Leukocyte / drug effects
  • Emotions
  • Epinephrine / pharmacology*
  • Epinephrine / physiology
  • Female
  • Granulocytes / drug effects
  • Humans
  • Killer Cells, Natural / drug effects
  • Leukocyte Count / drug effects
  • Leukocytosis / etiology
  • Leukocytosis / physiopathology*
  • Lymphocytosis / chemically induced
  • Lymphocytosis / physiopathology
  • Lymphoid Tissue / immunology
  • Lymphoid Tissue / physiopathology
  • Male
  • Norepinephrine / pharmacology*
  • Norepinephrine / physiology
  • Psychoneuroimmunology
  • Receptors, Adrenergic, beta-2 / drug effects
  • Receptors, Adrenergic, beta-2 / physiology
  • Stress, Psychological / immunology
  • Stress, Psychological / physiopathology*

Substances

  • Receptors, Adrenergic, beta-2
  • Norepinephrine
  • Epinephrine