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Title: | Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells |
Authors: | 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 Hilario; BENETTI, Marcela Anhesini; MALFITANO, Christiane; ANGELIS, Katia de; ALBERTINI, Regiane; OLIVEIRA, Ana Paula Ligeiro; ABBASI, Asghar; NORTHOFF, Hinnak; VIEIRA, Rodolfo Paula |
Citation: | EXERCISE IMMUNOLOGY REVIEW, v.24, p.48-56, 2018 |
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. |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - LIM/59 Artigos e Materiais de Revistas Científicas - ODS/03 |
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