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dc.contributor.authorRigonato-Oliveira, Nicole Cristine
dc.contributor.authorMacKenzie, BreAnne
dc.contributor.authorLacerda Bachi, Andre Luis
dc.contributor.authorOliveira-Junior, Manoel Carneiro
dc.contributor.authorSantos-Dias, Alana
dc.contributor.authorRodrigues Brandao-Rangel, Maysa Alves [UNIFESP]
dc.contributor.authorDelle, Humberto
dc.contributor.authorCosta-Guimaraes, Tamara
dc.contributor.authorDamaceno-Rodrigues, Nilsa Regina
dc.contributor.authorDulley, Larissa Hilario
dc.contributor.authorBenetti, Marcela Anhesini
dc.contributor.authorMalfitano, Christiane
dc.contributor.authorde Angelis, Katia [UNIFESP]
dc.contributor.authorAlbertini, Regiane [UNIFESP]
dc.contributor.authorLigeiro Oliveira, Ana Paula
dc.contributor.authorAbbasi, Asghar
dc.contributor.authorNorthoff, Hinnak
dc.contributor.authorVieira, Rodolfo Paula [UNIFESP]
dc.date.accessioned2020-07-02T18:52:00Z
dc.date.available2020-07-02T18:52:00Z
dc.date.issued2018
dc.identifierhttp://eir-isei.de/2018/eir-2018-036-article.pdf
dc.identifier.citationExercise Immunology Review. Greven, v. 24, p. 48-56, 2018.
dc.identifier.issn1077-5552
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/53814
dc.description.abstractAcute 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.en
dc.description.sponsorshipSao Paulo Research Foundation (FAPESP) [2012/15165-2]
dc.description.sponsorshipConselho Nacional de Pesquisa e Desenvolvimento (CNPq) [311335-2015-2]
dc.description.sponsorshipComissao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [12804/13-4, 1303/13-9]
dc.description.sponsorshipFAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]
dc.description.sponsorshipCAPES
dc.format.extent48-56
dc.language.isoeng
dc.publisherW W F Verlagsgesellschaft Gmbh
dc.relation.ispartofExercise Immunology Review
dc.rightsAcesso aberto
dc.subjectexercise immunologyen
dc.subjectlung inflammationen
dc.subjectimmune responseen
dc.subjectacute lung injuryen
dc.subjectcytokinesen
dc.titleAerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cellsen
dc.typeArtigo
dc.description.affiliationNove Julho Univ, Sao Paulo, SP, Brazil
dc.description.affiliationBrazilian Inst Teaching & Res Pulm & Exercise Imm, Sao Jose Dos Campos, SP, Brazil
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, Brazil
dc.description.affiliationUniv Brasil, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Sch Med, Dept Pathol LIM 59, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Fed Lavras UFLA, Sci Dept Hlth, Lavras, MG, Brazil
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Campus Sao Paulo, Sao Paulo, SP, Brazil
dc.description.affiliationHarbor UCLA Med Ctr, Div Resp & Crit Care Physiol & Med, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA
dc.description.affiliationUniv Tubingen, Inst Clin & Expt Transfus Med IKET, Tubingen, Germany
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, Brazil
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Campus Sao Paulo, Sao Paulo, SP, Brazil
dc.description.sponsorshipIDFAPESP [2012/15165-2]
dc.description.sponsorshipIDCNPq [311335-2015-2]
dc.description.sponsorshipIDCAPES [12804/13-4, 1303/13-9]
dc.description.sponsorshipIDFAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]
dc.identifier.fileWOS000428135000005.pdf
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000428135000005
dc.coverageGreven
dc.citation.volume24


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