title: The role of stress hormones in exercise-induced suppression of alveolar macrophage antiviral function.
abstract: We hypothesized that a previously observed exercise-induced suppression of alveolar macrophage antiviral resistance results from increases in corticosterone and/or epinephrine. Mice (CD-1) were run to fatigue on a treadmill (exercise), or placed in Plexiglas lanes above the treadmill (control). The role of corticosterone was assessed by further dividing mice into groups receiving one of the following treatments; sham surgery, adrenalectomy, or adrenalectomy plus corticosterone replacement. Macrophage antiviral function was suppressed in the exercised mice compared to the control mice. However, macrophage antiviral function was not suppressed in the exercised mice that underwent adrenalectomy or adrenalectomy plus corticosterone replacement. We tested whether another adrenal factor (epinephrine) may be involved by dividing mice into exercise and control groups treated with either saline or propranolol. Macrophage antiviral function was again suppressed in the saline-treated exercised mice compared to saline-treated control mice, but no differences were found between the exercised mice receiving propranolol, control mice receiving propranolol, or saline-treated control mice. Isoproterenol, when added to alveolar macrophages in culture, also suppressed antiviral resistance. These findings suggest that decreased macrophage antiviral function following exercise may be due to increased release of adrenal catecholamines.
authors.affiliation: Department of Exercise Science, School of Public Health, University of South Carolina, Columbia 29208, USA.
authors.forename: M L
authors.initials: ML
authors.lastname: Kohut
authors.forename: J M
authors.initials: JM
authors.lastname: Davis
authors.forename: D A
authors.initials: DA
authors.lastname: Jackson
authors.forename: L H
authors.initials: LH
authors.lastname: Colbert
authors.forename: A
authors.initials: A
authors.lastname: Strasner
authors.forename: D A
authors.initials: DA
authors.lastname: Essig
authors.forename: R R
authors.initials: RR
authors.lastname: Pate
authors.forename: A
authors.initials: A
authors.lastname: Ghaffar
authors.forename: E P
authors.initials: EP
authors.lastname: Mayer
mesh_terms: D000309:Adrenal Insufficiency / Q000188:drug therapy / Q000503:physiopathology; D000315:Adrenalectomy; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000502:physiology* / Q000627:therapeutic use; D000242:Cyclic AMP / Q000502:physiology; D004837:Epinephrine / Q000502:physiology*; D005221:Fatigue; D006561:Herpes Simplex / Q000276:immunology*; D007108:Immune Tolerance; D007113:Immunity, Innate; D007545:Isoproterenol / Q000494:pharmacology; D008262:Macrophage Activation / Q000187:drug effects; D016676:Macrophages, Alveolar / Q000276:immunology*; D051379:Mice; D005082:Physical Exertion / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D012420:Running; D018139:Simplexvirus / Q000502:physiology*; D013312:Stress, Physiological / Q000276:immunology*
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D000242:Cyclic AMP; D007545:Isoproterenol; D003345:Corticosterone; D004837:Epinephrine