Document Detail

Exercise-induced stimulation of murine macrophage chemotaxis: role of corticosterone and prolactin as mediators.
MedLine Citation:
PMID:  9051584     Owner:  NLM     Status:  MEDLINE    
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.
E Ortega; M A Forner; C Barriga
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  498 ( Pt 3)     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1997 Feb 
Date Detail:
Created Date:  1997-05-15     Completed Date:  1997-05-15     Revised Date:  2010-09-13    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  729-34     Citation Subset:  IM    
Department of Physiology (Animal Physiology), Faculty of Science, University of Extremadura, Badajoz, Spain.
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MeSH Terms
Anti-Inflammatory Agents / metabolism,  pharmacology
Chemotaxis, Leukocyte / drug effects,  physiology*
Corticosterone / metabolism,  pharmacology,  physiology*
Exudates and Transudates / cytology
Macrophages, Peritoneal / drug effects,  metabolism,  physiology*
Mice, Inbred BALB C
Physical Exertion / physiology*
Prolactin / metabolism,  pharmacology,  physiology*
Reg. No./Substance:
0/Anti-Inflammatory Agents; 50-22-6/Corticosterone; 9002-62-4/Prolactin

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