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metadata.artigo.dc.title: Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells
metadata.artigo.dc.creator: Rigonato-Oliveira, Nicole Cristine
MacKenzie, BreAnne
Bachi, Andre Luis Lacerda
Oliveira Junior, Manoel Carneiro
Santos-Dias, Alana
Brandao-Rangel, Maysa Alves Rodrigues
Delle, Humberto
Costa-Guimaraes, Tamara
Damaceno-Rodrigues, Nilsa Regina
Dulley, Larissa Hilário
Benetti, Marcela Anhesini
Malfitano, Christiane
Angelis, Kátia de
Albertini, Regiane
Oliveira, Ana Paula Ligeiro
Abbasi, Asghar
Northoff, Hinnak
Vieira, Rodolfo Paula
metadata.artigo.dc.subject: Exercise immunology
Lung inflammation
Immune response
Acute lung injury
Imunologia do exercício
Inflamação pulmonar
Resposta imune
Lesão pulmonar aguda
metadata.artigo.dc.publisher: International Society of Exercise and Immunology 2018
metadata.artigo.dc.identifier.citation: RIGONATO-OLIVEIRA, N. C. et al. Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells. Exercise Immunology, [S. l.], v. 24, p. 36-44, 2018.
metadata.artigo.dc.description.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 preincubated 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-1β, IL-6 and GM-CSF (p<0.001), CXCL1/KC, IL-17, TNF-alpha and IGF-1 (p<0.01). Systemically, AE reduced IL-1β, 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-1β, 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.
metadata.artigo.dc.language: en_US
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