Exercise‐induced stimulation of murine macrophage chemotaxis: role of corticosterone and prolactin as mediators.

Abstract

1. Exercise provokes changes in the immune system, including macrophage activity. Chemotaxis is a necessary function of macrophages if they are to reach the focus of infection and strenuous acute exercise may modulate chemotaxis. However, the precise mechanisms remain unknown. 2. Three experiments were performed in the present study. (1) The effect of strenuous acute exercise (swimming until exhaustion) on the chemotactic capacity of macrophages was evaluated. (2) Peritoneal macrophages from control mice were incubated with plasma from exercised mice or control (no exercise) mice. The differences in the resulting chemotactic capacity were measured. (3) Changes in the concentration of plasma corticosterone and prolactin after exercise were also measured, and the effect of incubation with the post‐exercise levels of plasma corticosterone and prolactin on the chemotactic capacity of the peritoneal macrophages was then studied in vitro. 3. Exercise induced an increase in the macrophage chemotaxis index (103 +/‐ 8 vs. 47 +/‐ 11 in controls). Incubation with plasma from exercised mice led to an increased level of chemotaxis (68 +/‐ 18 vs. 40 +/‐ 6 with plasma from controls). Incubation with concentrations of corticosterone and prolactin similar to those observed in plasma immediately after exercise (corticosterone, 0.72 mumol l‐1; prolactin, 88 pmol l‐1) raised the chemotactic capacity with respect to that following incubation with the basal concentrations of the hormones in control animals (90 +/‐ 9 vs. 37 +/‐ 4 for corticosterone; 72 +/‐ 9 vs. 41 +/‐ 4 for prolactin). 4. It is concluded that corticosterone and prolactin may mediate the increased chemotaxis of peritoneal macrophages induced by exercise.

Prolactin stimulates integrin-mediated adhesion of circulating mononuclear cells to endothelial cells

“…29 Also, PRL stimulates the expression of ICAM-1 in the corpus luteum, 29 and in vitro studies showed that PRL promotes the chemotactic capacity of macrophages. 43 Stimulation of cell adhesion by PRL may involve the activation of integrins LFA-1 and VLA-4, major molecular pathways that mediate firm attachment of leukocytes to vascular endothelium.…”

Inflammatory/Stress Feedback Dysregulation in Women with Fibromyalgia

“…Neutrophil chemotaxis was evaluated in a Boyden chamber with a modification [11] of the original technique [12], using an isopore polyvinylpyrrolidone-free polycarbonate filter with a pore diameter of 3 µm (Millipore) placed between the two compartments of the chamber. n -formyl-methionyl-leucyl-phenylalanine peptide (10 –8 m , Sigma) diluted in PBS was used as a chemoattractant in the lower compartment of the chamber.…”

Exercise-induced modulation of macrophage function

“…One group has attempted to delineate the mechanism responsible for the exercise-induced increases in chemotaxis 30 and phagocytosis. 37 Their circumstantial evidence points to a hormonal influence perhaps mediated by corticosterone or prolactin and thyroxine, in the case of chemotaxis and phagocytosis, respectively.…”

“…They have shown that incubation of macrophages from control animals with plasma from exercised animals stimulates chemotaxis and phagocytosis to similar levels seen in macrophages taken from exercised animals. 30,37 In addition, incubation of macrophages with physiological levels (i.e. plasma levels attained during exercise) of corticosterone, prolactin or thyroxine can stimulate chemotaxis or phagocytosis.…”