Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells

Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells

Author Rigonato-Oliveira, Nicole Cristine Google Scholar
MacKenzie, BreAnne Google Scholar
Lacerda Bachi, Andre Luis Google Scholar
Oliveira-Junior, Manoel Carneiro Google Scholar
Santos-Dias, Alana Google Scholar
Rodrigues Brandao-Rangel, Maysa Alves Autor UNIFESP Google Scholar
Delle, Humberto Google Scholar
Costa-Guimaraes, Tamara Google Scholar
Damaceno-Rodrigues, Nilsa Regina Google Scholar
Dulley, Larissa Hilario Google Scholar
Benetti, Marcela Anhesini Google Scholar
Malfitano, Christiane Google Scholar
de Angelis, Katia Autor UNIFESP Google Scholar
Albertini, Regiane Autor UNIFESP Google Scholar
Ligeiro Oliveira, Ana Paula Google Scholar
Abbasi, Asghar Google Scholar
Northoff, Hinnak Google Scholar
Vieira, Rodolfo Paula Autor UNIFESP Google Scholar
Abstract Acute respiratory distress syndrome (ARDS) is defined as hypoxemic respiratory failure with intense pulmonary inflammation, involving hyperactivation of endothelial cells and neutrophils. Given the anti-inflammatory effects of aerobic exercise (AE), this study investigated whether AE performed daily for 5 weeks would inhibit extra-pulmonary LPS-induced ARDS. C57Bl/6 mice were distributed into Control, Exercise, LPS and Exercise+ LPS groups. AE was performed on a treadmill for 5x/week for four weeks before LPS administration. 24hours after the final AE physical test, animals received 100ug of LPS intra-peritoneally. In addition, whole blood cell culture, neutrophils and human endothelial cells were pre-incubated with IL-10, an anti-inflammatory cytokine induced by exercise. AE reduced total protein levels (p<0.01) and neutrophil accumulation in bronchoalveolar lavage (BAL) (p<0.01) and lung parenchyma (p<0.01). AE reduced BAL inflammatory cytokines IL-1 beta, IL-6 and GM-CSF (p<0.001), CXCL1/KC, IL-17, TNF-alpha and IGF-1 (p<0.01). Systemically, AE reduced IL-1 beta, IL-6 and IFN-gamma (p<0.001), CXCL1/KC (p<0.01) and TNF-alpha (p<0.05). AE increased IL-10 levels in serum (p<0.001) and BAL (p<0.001). Furthermore, AE increased superoxide dismutase SOD (p<0.01) and decreased superoxide anion accumulation in the lungs (p<0.01). Lastly, pre-incubation with IL-10 significantly reduced LPS-induced activation of whole blood cells, neutrophils and HUVECs, as observed by reduced production of IL-1 beta, IL-6, IL-8 and TNF-alpha. Our data suggest that AE inhibited LPS-induced lung inflammation by attenuating inflammatory cytokines and oxidative stress markers in mice and human cell culture via enhanced IL-10 production.
Keywords exercise immunology
lung inflammation
immune response
acute lung injury
xmlui.dri2xhtml.METS-1.0.item-coverage Greven
Language English
Sponsor Sao Paulo Research Foundation (FAPESP) [2012/15165-2]
Conselho Nacional de Pesquisa e Desenvolvimento (CNPq) [311335-2015-2]
Comissao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [12804/13-4, 1303/13-9]
FAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]
Grant number FAPESP [2012/15165-2]
CNPq [311335-2015-2]
CAPES [12804/13-4, 1303/13-9]
FAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]
Date 2018
Published in Exercise Immunology Review. Greven, v. 24, p. 48-56, 2018.
ISSN 1077-5552 (Sherpa/Romeo, impact factor)
Publisher W W F Verlagsgesellschaft Gmbh
Extent 48-56
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000428135000005

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