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

• Autor(a) principal: Rigonato-Oliveira, Nicole Cristine
• Data de Publicação: 2018
• Outros Autores: MacKenzie, BreAnne, Bachi, Andre Luis Lacerda, Oliveira-Junior, Manoel Carneiro, Dias, Alana dos Santos, Rodrigues Brandao-Rangel, Maysa Alves [UNIFESP], Delle, Humberto, Costa-Guimaraes, Tamara, Damaceno-Rodrigues, Nilsa Regina, Dulley, Larissa Hilario, Benetti, Marcela Anhesini, Malfitano, Christiane, De Angelis, Kátia [UNIFESP], Albertini, Regiane [UNIFESP], Oliveira, Ana Paula Ligeiro, Abbasi, Asghar, Northoff, Hinnak, Vieira, Rodolfo de Paula [UNIFESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: https://repositorio.unifesp.br/handle/11600/53814; https://eir-isei.de/2018/eir-2018-036-article.pdf
• topic: Exercise immunology; Lung inflammation; Immune response; Acute lung injury; Cytokines

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.