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

Autor(es):Mostrar menos -

Rigonato-Oliveira, Nicole Cristine ^[1] ; MacKenzie, BreAnne ^[2] ; Lacerda Bachi, Andre Luis ^[2] ; Oliveira-Junior, Manoel Carneiro ^[2] ; Santos-Dias, Alana ^[2] ; Rodrigues Brandao-Rangel, Maysa Alves ^{[2, 3]} ; Delle, Humberto ^[1] ; Costa-Guimaraes, Tamara ^{[4, 2]} ; Damaceno-Rodrigues, Nilsa Regina ^[5] ; Dulley, Larissa Hilario ^[2] ; Benetti, Marcela Anhesini ^[2] ; Malfitano, Christiane ^[6] ; de Angelis, Katia ^[7] ; Albertini, Regiane ^[3] ; Ligeiro Oliveira, Ana Paula ^[1] ; Abbasi, Asghar ^[8] ; Northoff, Hinnak ^[9] ; Vieira, Rodolfo Paula ^{[4, 2, 3]}

Afiliação do(s) autor(es)

^[1] Nove Julho Univ, Sao Paulo, SP - Brazil

^[2] Brazilian Inst Teaching & Res Pulm & Exercise Imm, Sao Jose Dos Campos, SP - Brazil

^[3] Fed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP - Brazil

^[4] Univ Brasil, Sao Paulo, SP - Brazil

^[5] Univ Sao Paulo, Sch Med, Dept Pathol LIM 59, Sao Paulo, SP - Brazil

^[6] Univ Fed Lavras UFLA, Sci Dept Hlth, Lavras, MG - Brazil

^[7] Fed Univ Sao Paulo UNIFESP, Campus Sao Paulo, Sao Paulo, SP - Brazil

^[8] Harbor UCLA Med Ctr, Div Resp & Crit Care Physiol & Med, Los Angeles Biomed Res Inst, Torrance, CA 90509 - USA

^[9] Univ Tubingen, Inst Clin & Expt Transfus Med IKET, Tubingen - Germany

• Tipo de documento: Artigo de Revisão
• Fonte: EXERCISE IMMUNOLOGY REVIEW; v. 24, p. 48-56, 2018.
• Citações Web of Science: 5

Resumo

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. (AU)

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