Author |
Rigonato-Oliveira, Nicole Cristine
![]() MacKenzie, BreAnne ![]() Lacerda Bachi, Andre Luis ![]() Oliveira-Junior, Manoel Carneiro ![]() Santos-Dias, Alana ![]() Rodrigues Brandao-Rangel, Maysa Alves ![]() ![]() Delle, Humberto ![]() Costa-Guimaraes, Tamara ![]() Damaceno-Rodrigues, Nilsa Regina ![]() Dulley, Larissa Hilario ![]() Benetti, Marcela Anhesini ![]() Malfitano, Christiane ![]() de Angelis, Katia ![]() ![]() Albertini, Regiane ![]() ![]() Ligeiro Oliveira, Ana Paula ![]() Abbasi, Asghar ![]() Northoff, Hinnak ![]() Vieira, Rodolfo Paula ![]() ![]() |
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 cytokines |
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] CAPES |
Grant number |
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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 |
Origin |
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Access rights | Open access ![]() |
Type | Article |
Web of Science ID | WOS:000428135000005 |
URI | https://repositorio.unifesp.br/handle/11600/53814 |
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