Intracellular mechanisms responsible for exercise-induced suppression of macrophage antigen presentation

被引:28
作者
Ceddia, MA
Voss, EW
Woods, JA
机构
[1] Univ Illinois, Dept Kinesiol, Phys Fitness Res Lab, Urbana, IL 61801 USA
[2] Univ Illinois, Dept Microbiol, Urbana, IL 61801 USA
关键词
antigenic peptide generation; immune; mice; stress;
D O I
10.1152/jappl.2000.88.2.804
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
In a previous study, we demonstrated that exhaustive exercise suppressed peritoneal macrophage antigen presentation (AP). In this study, we explored the intracellular mechanism(s) responsible for this suppression. Pathogen-free male BALB/c mice (8 +/- 2 wk) were randomly assigned to either home cage control (HCC) or exhaustive exercise stress (Exh, 18-30 m/min for 3 h/day) treatment groups. The mice underwent treatments for a period of 4 days during induced peritoneal thioglycollate inflammation. Elicited macrophages were harvested, purified, and incubated with chicken ovalbumin (C-Ova, 2.5 and 10 mg/ml) for 18 h. After macrophages were washed, they were cocultured with C-Ova-specific T cells for 48 h at which time the supernates were harvested and analyzed via ELISA for interleukin (IL)-2 as an indication of macrophage AP. There was no significant (P > 0.05) difference in macrophage AP between cells fixed with paraformaldehyde vs. those that remained unfixed, suggesting that Exh did not affect production of soluble factors influencing macrophage AP (i.e., IL-1, IL-4, PGE(2)). The ability of macrophages to generate C-Ova immunogenic peptides was analyzed using FITC-labeled C-Ova, which shows fluorescence only when degraded intracellularly. There was a significant (similar to 20%, P < 0.05) suppression in fluorescence in the Exh compared with HCC, indicating a possible defect in the ability of macrophages from Exh to degrade C-Ova into immunogenic peptides. Macrophages were also incubated with C-Ova immunogenic peptide in a manner identical to that for native C-Ova. We found a similar suppression (similar to 22-38%, P < 0.05) in macrophage AP using a C-Ova peptide when compared with native C-Ova in the Exh group, indicating reduced major histocompatibility complex (MHC) II loading and/or C-Ova-MHC II complex cell surface expression. In conclusion, these data indicate an intracellular defect in the macrophage antigen processing pathway induced by Exh.
引用
收藏
页码:804 / 810
页数:7
相关论文
共 34 条
[1]   THE CELL BIOLOGY OF MACROPHAGE ACTIVATION [J].
ADAMS, DO ;
HAMILTON, TA .
ANNUAL REVIEW OF IMMUNOLOGY, 1984, 2 :283-318
[2]   Trauma-induced suppression of antigen presentation and expression of major histocompatibility class II antigen complex in leukocytes [J].
Ayala, A ;
Ertel, W ;
Chaudry, IH .
SHOCK, 1996, 5 (02) :79-90
[3]   Bordetella pertussis infection of human monocytes inhibits antigen-dependent CD4 T cell proliferation [J].
Boschwitz, JS ;
Batanghari, JW ;
Kedem, H ;
Relman, DA .
JOURNAL OF INFECTIOUS DISEASES, 1997, 176 (03) :678-686
[4]  
BRISSEAU GF, 1994, SURGERY, V116, P268
[5]   Exercise suppresses macrophage antigen presentation [J].
Ceddia, MA ;
Woods, JA .
JOURNAL OF APPLIED PHYSIOLOGY, 1999, 87 (06) :2253-2258
[6]  
COZEN SD, 1988, IMMUNOLOGY, V63, P683
[7]   EFFECT OF PHYSICAL EXERCISE ON THE PHAGOCYTIC FUNCTION OF PERITONEAL-MACROPHAGES FROM SWISS MICE [J].
DELAFUENTE, M ;
MARTIN, I ;
ORTEGA, E .
COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES, 1993, 16 (01) :29-37
[8]   CHANGES IN THE PHAGOCYTIC FUNCTION OF PERITONEAL-MACROPHAGES FROM OLD MICE AFTER STRENUOUS PHYSICAL EXERCISE [J].
DELAFUENTE, M ;
MARTIN, MI ;
ORTEGA, E .
COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES, 1990, 13 (04) :189-198
[9]   CHEMICALLY-INDUCED HYPOTENSION INCREASES PGE(2) RELEASE AND DEPRESSES MACROPHAGE ANTIGEN PRESENTATION [J].
ERTEL, W ;
SINGH, G ;
MORRISON, MH ;
AYALA, A ;
CHAUDRY, IH .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (04) :R655-R660
[10]   THE INFLUENCE OF PHYSICAL EXERCISE ON PERITONEAL MACROPHAGE FUNCTIONS - HISTOCHEMICAL AND PHAGOCYTIC STUDIES [J].
FEHR, HG ;
LOTZERICH, H ;
MICHNA, H .
INTERNATIONAL JOURNAL OF SPORTS MEDICINE, 1988, 9 (01) :77-81