Corticosterone, Prolactin and Thyroid Hormones as Hormonal Mediators of the Stimulated Phagocytic Capacity of Peritoneal Macrophages After High-Intensity Exercise

Abstract

The aim of this study was to evaluate the effect of high-intensity physical activity (swimming until exhaustion) with or without previous training on the phagocytosis and destruction of inert particle capacities of macrophages, and the role of corticosterone, prolactin and thyroid hormones as possible hormonal mediators. The results indicated that high-intensity exercise provokes a stimulation of both phagocytosis and destruction of inert particles when performed in absence of previous training. However, swimming until exhaustion after a one month training program (25 min/day) induced an increase in phagocytosis but not in the destruction of latex beads. Corticosterone, prolactin and thyroid hormones can be considered as hormonal mediators of the exercise-induced stimulation of phagocytosis, since these hormones increased plasma concentration, and the in vitro incubation of macrophages with the same higher physiological plasma concentrations of each hormone, as after exercise, also induced phagocytic stimulation of these cells.

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

“…Induction of phagocytosis in murine macrophages is positively influenced by thyroid hormones through a glutamine mechanism [55]. Exercise (swimming) increases phagocytosis and thyroid hormones are responsible for it [56]. Triiodothyronine (T3) stimulated granulocytes' phagocytic activity [57,58].…”

“…Prolactin increases the in vitro phagocytic capacity of macrophages [63] and helps to stimulate the exercise (swimming) induced phagocytosis [56]. Folliclestimulating hormone (FSH) negatively influences phagocytic activity of Sertoli cells in tissue cultures [64].…”

Exercise-induced modulation of macrophage function

“…Aside from one study that found that acute exercise increased tissue macrophage chemotaxis and phagocytosis in humans, 28 most studies of exercise or stress on macrophage function have been performed using animal models obtaining macrophages from the spleen, peritoneum or alveoli. [32][33][34][35][36][37] and antitumour 11,38 activity. Our group has shown that both moderate and exhaustive treadmill running over periods of 3-7 days increases the antitumour activity of thioglycolate (TG)-elicited or P. acnes-activated peritoneal macrophages in young mice.…”

“…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.…”

“…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.…”