Exercise-induced modulation of macrophage function

Woods, J. A.; Lu, Qin; Lowder, Thomas

doi:10.1046/j.1440-1711.2000.00960.x

Cited by 23 publications

(21 citation statements)

References 50 publications

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“…These seemingly contrasting results between our studies may be explained, in part, by the differences in the length of the exercise protocols. The effects of exercise on physiologic responses are dependent upon several variables, including the total duration of the exercise protocol (21)(22)(23)(24)(25)(26). The mechanism that underlies such a disparity likely involves changes in the levels of circulating hormones, including catecholamines, that are released from the hypothalamic-pituitaryadrenal axis (HPA) upon exercise.…”

Section: Discussionmentioning

confidence: 99%

Repeated Bouts of Moderate-Intensity Aerobic Exercise Reduce Airway Reactivity in a Murine Asthma Model

Hewitt

Estell²,

Davis³

et al. 2010

Am J Respir Cell Mol Biol

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We have reported that moderate-intensity aerobic exercise training attenuates airway inflammation in mice sensitized/challenged with ovalbumin (OVA). The current study determined the effects of repeated bouts of aerobic exercise at a moderate intensity on airway hyperresponsiveness (AHR) in these mice. Mice were sensitized/ challenged with OVA or saline and exercised at a moderate intensity 3 times/week for 4 weeks. At protocol completion, mice were analyzed for changes in AHR via mechanical ventilation. Results show that exercise decreased total lung resistance 60% in OVAtreated mice as compared with controls; exercise also decreased airway smooth muscle (ASM) thickness. In contrast, exercise increased circulating epinephrine levels 3-fold in saline-and OVAtreated mice. Because epinephrine binds b 2 -adrenergic receptors (AR), which facilitate bronchodilatation, the role of b 2 -AR in exercise-mediated improvements in AHR was examined. Application of the b 2 -AR antagonist butoxamine HCl blocked the effects of exercise on lung resistance in OVA-treated mice. In parallel, ASM cells were examined for changes in the protein expression of b 2 -AR and G-protein receptor kinase-2 (GRK-2); GRK-2 promotes b 2 -AR desensitization. Exercise had no effect on b 2 -AR expression in ASM cells of OVA-treated mice; however, exercise decreased GRK-2 expression by 50% as compared with controls. Exercise also decreased prostaglandin E 2 (PGE 2 ) production 5-fold, but had no effect on E prostanoid-1 (EP1) receptor expression within the lungs of OVA-treated mice; both PGE 2 and the EP1 receptor have been implicated in b 2 -AR desensitization. Together, these data indicate that moderate-intensity aerobic exercise training attenuates AHR via a mechanism that involves b 2 -AR.Keywords: asthma; airway hyperresponsiveness; exercise; b 2 -adrenergic receptor Allergic or atopic asthma, the most common form of asthma, is identified by the presence of characteristic clinical symptoms of wheezing, chest tightness, dyspnea and cough, and by the presence of reversible airway narrowing and/or airway hyperresponsiveness (AHR) to a variety of inhaled bronchoconstrictor stimuli. For the treatment of asthma-associated AHR, patients are typically administered inhaled, long-acting b 2 -agonists. b 2 -agonists bind to and activate b 2 -adrenergic receptors (b 2 -AR), which are expressed on a variety of cell types, including airway smooth muscle (ASM) cells, airway epithelial cells, and mast cells (1).Several clinical studies suggest that continued aerobic exercise training improves the overall physical fitness and health of individuals with asthma and reduces their disease-related hospital admissions (2-4); these studies also observed improvements in exercise-induced bronchoconstriction after physical training. We have reported previously that moderate intensity aerobic exercise training reduces lung inflammatory responses in an ovalbumin (OVA)-driven mouse model of pulmonary inflammation (5, 6).Repetitive exercise increases the levels of circulating...

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Section: Discussionmentioning

confidence: 99%

Repeated Bouts of Moderate-Intensity Aerobic Exercise Reduce Airway Reactivity in a Murine Asthma Model

Hewitt

Estell²,

Davis³

et al. 2010

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…In particular, the disparity in exercise-mediated effects on airway remodeling is likely due to the difference in the number of bouts of exercise. The effects of exercise on physiologic responses are dependent upon several variables, including the frequency of each bout and the total duration of the exercise protocol (40)(41)(42)(43)(44)(45); the mechanism that underlies this disparity may involve changes in the levels of circulating hormones (e.g., glucocorticoids, catecholamines) that are released from the hypothalamic-pituitary axis during exercise. With regard to differences in the extent of airway eosinophilia between these studies, we hypothesize that the extended OVA exposure may Figure 7.…”

Section: Discussionmentioning

confidence: 99%

Acute Exercise Decreases Airway Inflammation, but Not Responsiveness, in an Allergic Asthma Model

Hewitt

Creel²,

Estell³

et al. 2009

Am J Respir Cell Mol Biol

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Previous studies have suggested that the asthmatic responses of airway inflammation, remodeling, and hyperresponsiveness (AHR) are interrelated; in this study, we used exercise to examine the nature of this interrelationship. Mice were sensitized and challenged with ovalbumin (OVA); mice were then exercised via running on a motorized treadmill at a moderate intensity. Data indicate that, within the lungs of OVA-treated mice, exercise attenuated the production of inflammatory mediators, including chemokines KC, RANTES, and MCP-1 and IL-12p40/p80. Coordinately, OVA-treated and exercised mice displayed decreases in leukocyte infiltration, including eosinophils, as compared with sedentary controls. Results also show that a single bout of exercise significantly decreased phosphorylation of the NFkB p65 subunit, which regulates the gene expression of a wide variety of inflammatory mediators. In addition, OVA-treated and exercised mice exhibited decreases in the levels of Th2-derived cytokines IL-5 and IL-13 and the prostaglandin PGE 2 , as compared with sedentary controls. In contrast, results show that a single bout of exercise had no effect on AHR in OVA-treated mice challenged with increasing doses of aerosolized methacholine (0-50 mg/ml) as compared with sedentary mice. Exercise also had no effect on epithelial cell hypertrophy, mucus production, or airway wall thickening in OVA-treated mice as compared with sedentary controls. These findings suggest that a single bout of aerobic exercise at a moderate intensity attenuates airway inflammation but not AHR or airway remodeling in OVA-treated mice. The implication of these findings for the interrelationship between airway inflammation, airway remodeling, and AHR is discussed.

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“…The capacity of the macrophage to efficiently degrade the phagocytosed microorganisms has been shown repeatedly (20,21,76). Vacuolar ATPases involved in the acidification of the phagosome accumulate in the phagosomal membrane during maturation (40,71).…”

Section: Discussionmentioning

confidence: 99%

Phagocytosis and Intracellular Fate ofAspergillus fumigatusConidia in Alveolar Macrophages

et al. 2003

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Aspergillus fumigatus is the most prevalent airborne fungal pathogen responsible for fatal invasive aspergillosis in immunocompromised patients. Upon arrival in the lung alveolus, conidia of A. fumigatus are phagocytosed by alveolar macrophages, the major phagocytic cells of the lung. Engulfment and intracellular trafficking of A. fumigatus conidia in alveolar macrophages of two different origins, the murine cell line MH-S and human pulmonary alveolar macrophages, were analyzed by electron microscopy and immunofluorescence. Phagocytosis of A. fumigatus conidia required actin polymerization and phosphatidylinositol 3-kinase activity. Fusion of A. fumigatus phagosomes with early and late endosomes was shown by immunolabeling with specific markers for the transferrin receptor, early endosome antigen, and Rab7. Maturation of A. fumigatus phagolysosomes was monitored by using a fixable acidotropic probe, LysoTracker Red DND-99, and an anti-cathepsin D antibody. Bafilomycin A-induced inhibition of lysosomal acidification abolished the conidial killing by the macrophages. These data suggest that the maturation of A. fumigatus phagosomes results from fusion with the compartments of the endocytic pathway and that the killing of conidia depends on phagolysosome acidification. A model for the phagocytosis of A. fumigatus conidia by alveolar macrophages is proposed on the basis of these results.

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Exercise-induced modulation of macrophage function

Cited by 23 publications

References 50 publications

Repeated Bouts of Moderate-Intensity Aerobic Exercise Reduce Airway Reactivity in a Murine Asthma Model

Repeated Bouts of Moderate-Intensity Aerobic Exercise Reduce Airway Reactivity in a Murine Asthma Model

Acute Exercise Decreases Airway Inflammation, but Not Responsiveness, in an Allergic Asthma Model

Phagocytosis and Intracellular Fate ofAspergillus fumigatusConidia in Alveolar Macrophages

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