Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution

Vieira, Rodolfo Paula; Toledo, Alessandra Choqueta de; Silva, Lucas Bogaz; Almeida, Francine Maria de; Damaceno-Rodrigues, Nilsa Regina; Caldini, Élia Garcia; Santos, Ângela Batista Gomes dos; Rivero, Dolores Helena Rodriguez Ferreira; Hizume, Deborah C.; Lopes, Fernanda D.T.Q.S.; Olivo, Clarice Rosa; Castro‐Faria‐Neto, Hugo C.; Martins, Mílton A.; Saldiva, Paulo Hilário Nascimento; Dolhnikoff, Marisa

doi:10.1249/mss.0b013e31824b2877

Cited by 72 publications

(85 citation statements)

References 16 publications

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“…Frozen lung tissue sections were cut and stained with H&E. The density of neutrophils in the lung parenchyma was obtained as previously described (32–35). In brief, 20 photomicrographs of lung parenchyma (excluding areas of pulmonary vessels) were randomly obtained at ×400 magnification.…”

Section: Methodsmentioning

confidence: 99%

C1P Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Preventing NF-κB Activation in Neutrophils

Baudiß

Vieira

Cicko

et al. 2016

The Journal of Immunology

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Recently, ceramide-1-phosphate (C1P) has been shown to modulate acute inflammatory events. Acute lung injury (Arnalich et al. 2000. Infect. Immun. 68: 1942–1945) is characterized by rapid alveolar injury, lung inflammation, induced cytokine production, neutrophil accumulation, and vascular leakage leading to lung edema. The aim of this study was to investigate the role of C1P during LPS-induced acute lung injury in mice. To evaluate the effect of C1P, we used a prophylactic and therapeutic LPS-induced ALI model in C57BL/6 male mice. Our studies revealed that intrapulmonary application of C1P before (prophylactic) or 24 h after (therapeutic) LPS instillation decreased neutrophil trafficking to the lung, proinflammatory cytokine levels in bronchoalveolar lavage, and alveolar capillary leakage. Mechanistically, C1P inhibited the LPS-triggered NF-κB levels in lung tissue in vivo. In addition, ex vivo experiments revealed that C1P also attenuates LPS-induced NF-κB phosphorylation and IL-8 production in human neutrophils. These results indicate C1P playing a role in dampening LPS-induced acute lung inflammation and suggest that C1P could be a valuable candidate for treatment of ALI.

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Section: Methodsmentioning

confidence: 99%

C1P Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Preventing NF-κB Activation in Neutrophils

Baudiß

Vieira

Cicko

et al. 2016

The Journal of Immunology

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“…The lung slices were silanized and evaluated for the expression of IL‐5, eotaxin, RANTES, ICAM‐1, VCAM‐1, VEGF, TGF‐β, and OPN using antibodies from Santa Cruz (Santa Cruz, California, USA), and their expression was quantified using a morphometric technique. The slides were coded, and the researcher who performed the measurements was blinded to the study groups, as previously described (Olivo et al., ; Toledo et al., ; Vieira et al., ).…”

Section: Methodsmentioning

confidence: 99%

Airway remodeling is reversed by aerobic training in a murine model of chronic asthma

Silva

Almeida

Olivo

et al. 2014

Scandinavian Med Sci Sports

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The aim of this study was to investigate if the aerobic training (AT) reverses airway remodeling (AR) in an asthma model. BALB/c were divided into four groups: control (unsensitized and untrained); ovalbumin (OVA: sensitized and untrained); AT (unsensitized and trained) and OVA + AT. Allergic inflammation was induced with intraperitoneal and OVA inhalation. AT (low intensity; 5×/week; 60 min/session) was performed at 7, 15, and 30 days. Leukocyte counting in the bronchoalveolar lavage fluid; the expression of IL-5, eotaxin, RANTES, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1); AR features (airway smooth muscle, epithelium thickness, collagen and elastic fibers, mucus production); and AR inducers (transforming growing factor-beta, osteopontin, vascular endothelial growth factor). OVA induced an increase in leukocyte airway migration and increased AR features (P < 0.05). After 7 days, AT reversed the OVA-induced eosinophil and macrophage airway migration, the expression of IL-5, eotaxin, RANTES, ICAM-1, VCAM-1, and all AR inducers. However, total reversion of the AR features and inducers and airway inflammation occurred only after 15 days of AT compared with the OVA groups (P < 0.05) and the effects were maintained until the 30th day. AT reverses AR after 15 days and this effect is preceded by the inhibition of leukocyte migration and occurs simultaneously with the reduction in the expression of inflammatory mediators and AR inducers.

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“…Aerobic exercise also seems to reduce airway remodeling, with reduced airway smooth muscle hypertrophy and hyperplasia [4, 30] (even if effects on remodeling were a matter of debate in another animal study [31]), a reduction in leukocyte infiltration, proinflammatory cytokine production, adhesion molecules expression [32], and enhanced regulatory T-cell (Treg) responses [16]. Aerobic exercise also shows an anti-inflammatory effect in mice exposed to air pollution [33]. A single session of moderate aerobic exercise can decrease airway inflammation (but not responsiveness) in mice, with a downregulation of inflammatory mediators' genes expression and Th-2 derived cytokines production [15].…”

Section: Discussionmentioning

confidence: 99%

Exercise Training, Lymphocyte Subsets and Their Cytokines Production: Experience of an Italian Professional Football Team and Their Impact on Allergy

Giacco

Scorcu²,

Argiolas³

et al. 2014

BioMed Research International

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Background. In recent years, numerous articles have attempted to shed light on our understanding of the pathophysiological mechanisms of exercise-induced immunologic changes and their impact on allergy and asthma. It is known that lymphocyte subclasses, cytokines, and chemokines show modifications after exercise, but outcomes can be affected by the type of exercise as well as by its intensity and duration. Interesting data have been presented in many recent studies on mouse models, but few studies on humans have been performed to check the long-term effects of exercise over a whole championship season. Methods. This study evaluated lymphocyte subsets and their intracellular IL-2, IL-4, TNF-α, and IFN-γ production in professional football (soccer) players, at three stages of the season, to evaluate if alterations occur, particularly in relation to their allergic status. Results and Conclusion. Despite significant mid-season alterations, no significant lymphocyte subclasses count modifications, except for NKs that were significantly higher, were observed at the end. IL-2 and IL-4 producing cells showed a significant decrease (P = 0.018 and P = 0.001, but in a steady fashion for IL-4), confirming the murine data about the potential beneficial effects of aerobic exercise for allergic asthma.

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Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution

Abstract: We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.

Cited by 72 publications

References 16 publications

C1P Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Preventing NF-κB Activation in Neutrophils

C1P Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Preventing NF-κB Activation in Neutrophils

Airway remodeling is reversed by aerobic training in a murine model of chronic asthma

Exercise Training, Lymphocyte Subsets and Their Cytokines Production: Experience of an Italian Professional Football Team and Their Impact on Allergy

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