Cell activation state influences the modulation of HLA-DR surface expression on human monocytes/macrophages by parenteral fish oil lipid emulsion

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorTORRINHAS, R. S.
dc.contributor.authorJACINTHO, T.
dc.contributor.authorGOTO, H.
dc.contributor.authorGIDLUND, M.
dc.contributor.authorSALES, M. M.
dc.contributor.authorOLIVEIRA, P. A.
dc.contributor.authorWAITZBERG, D. L.
dc.date.accessioned2017-11-27T16:34:02Z
dc.date.available2017-11-27T16:34:02Z
dc.date.issued2011
dc.description.abstractAbnormal surface expression of HLA-DR by leukocytes is associated with a poor prognosis in critical care patients. Critical care patients often receive total parenteral nutrition with lipid emulsion (LE). In this study we evaluated the influence of fish oil LE (FO) on human monocyte/macrophage (M phi) expression of surface HLA-DR under distinct activation states. Mononuclear leukocytes from the peripheral blood of healthy volunteers (n=18) were cultured for 24 hours without LE (control) or with 3 different concentrations (0.1, 0.25, and 0.5%) of the follow LE: a) pure FO b) FO in association (1:1-v/v) with LE composed of 50% medium-chain trygliceride and 50% soybean oil (MCTSO), and c) pure MCTSO. The leukocytes were also submitted to different cell activation states, as determinate by INF-g addition time: no INF-gamma addition, 18 hours before, or at the time of LE addition. HLA-DR expression on MO surface was evaluated by flow cytometry using specific monoclonal antibodies. In relation to controls (for 0.1%, 0.25%, and 05%: 100) FO decreased the expression of HLA-DR when added alone in simultaneously-activated M., for 0.1%: 70 (59 +/- 73); for 0.25%: 51 (48 +/- 56); and for 05%: 52.5 (50 +/- 58)1 or in association with MCTSO [in simultaneously-activated MO, for 0.1%: 50.5 (47 +/- 61); for 25%: 49 (45 +/- 52); and for 0.5%: 51 (44 54) and in previously-activated Mf, for 1.0%: 63 (44 +/- 88); for 0.25%: 70 (41 +/- 88); and for 0.5%: 59.5 (39 +/- 79)1 in culture medium (Friedman p < 0.05). In relation to controls (for 0.1%, 0.25%, and 0.5%: 100), FO did not influence the expression of these molecules on non-activated M phi [for 0.1%: 87.5(75 +/- 93); for 0.25%: 111 (98 +/- 118); and for 0.5%: 101.5 (84 +/- 113)]. Results show that parenteral FO modulates the expression of HLA-DR on human MO surface accordingly to leukocyte activation state. Further clinical studies evaluating the ideal moment of fish oil LE infusion to modulate leukocyte functions may contribute to a better understanding of its immune modulatory properties.
dc.description.abstractLa expresión anómala del HLA-DR sobre la superficie de los leucocitos se asocia con un pronóstico sombrío en pacientes críticos. A menudo, estos pacientes reciben nutrición parenteral total con una emulsión lipídica (EL). En este estudio, evaluamos la influencia de una EL de aceite de pescado (AP) en la expresión del HLA-DR en la superficie de monocitos/macrófagos humanos (MΦ) bajo diferentes estados de activación. Se cultivaron leucocitos mononucleares de sangre periférica de voluntarios sanos (n = 18) durante 24 horas sin la EL (control) o con 3 concentraciones distintas (0,1, 0,25 y 0,5%) de la siguiente EL: a) AP puro b) AP en asociación con EL (1:1 v/v) compuesta de 50% de triglicéridos de cadena media y 50% de aceite de soja (TCMAS), y c) TCMAS puro. También sometimos a los leucocitos a diferentes estados de activación celular, determinado por INF-γ tiempo de adición: no INF-γ adición 18 horas antes, o en el momento de añadir la EL. La expresión del HLA-DR sobre la superficie de los MΦ se evaluó mediante citometría de flujo utilizando anticuerpos monoclonales específicos. En relación con los controles (para 0,1%, 0,25% y 0,5%: 100) el AP disminuyó la expresión de HLA-DR cuando se añadía solo [en MΦ activados simultáneamente, para 0,1%: 70 (59 ± 73); para 0,25%: 51 (48 ± 56); y para 0,5%: 52.5 (50 ± 58)] o en asociación con TCMAS [en MΦ activados simultáneamente para 0,1%: 50,5 (47 ± 61); para 0,25%:(45 ± 52); y para 0,5%: 51 (44 ± 54) y en MΦ previamente activados para 0,1%: 63 (44 ± 88); para 0,25%: 70 (41 ± 88); y para 0,5%: 59,5 (39 ± 79)] en el medio de cultivo (Friedman p < 0,05). Con respecto a los controles, (para 0,1%, 0,25% y 0,5%: 100), el AP no influyó en la expresión de estas moléculas en MΦ no activados [para 0,1%: 87,5 (75 ± 93); para 0,25%: 111 (98 ± 118); y para 0,5%: 101,5 (84 ± 113)]. Los resultados muestran que el AP parenteral modula la expresión del HLA-DR sobre la superficie de los MΦ humanos en función del estado de activación leucocitaria. Estudios clínicos adicionales que evalúen el momento idóneo de añadir la infusión de EL con aceite de pescado para modular las funciones leucocitarias podrían contribuir a entender mejor sus propiedades inmunomoduladoras.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo [FAPESP-98/11379-9, 99/08332-3]
dc.identifier.citationNUTRICION HOSPITALARIA, v.26, n.2, p.311-316, 2011
dc.identifier.doi10.3305/nh.2011.26.2.4648
dc.identifier.issn0212-1611
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/23354
dc.language.isoeng
dc.publisherAULA MEDICA EDICIONES
dc.relation.ispartofNutricion Hospitalaria
dc.rightsopenAccess
dc.rights.holderCopyright AULA MEDICA EDICIONES
dc.subjectparenteral fata emulsions
dc.subjectHLA-DR
dc.subjectFish oil
dc.subjectEmulsión lipídica parenteral
dc.subjectHLA-DR
dc.subjectAceite de pescado
dc.subject.othern-3 fatty-acids
dc.subject.otherhuman monocytes
dc.subject.othernutrition
dc.subject.otheromega-3-fatty-acids
dc.subject.othermacrophages
dc.subject.othersepsis
dc.subject.otherimpact
dc.subject.otheratherosclerosis
dc.subject.othersupplementation
dc.subject.otherinflammation
dc.subject.wosNutrition & Dietetics
dc.titleCell activation state influences the modulation of HLA-DR surface expression on human monocytes/macrophages by parenteral fish oil lipid emulsion
dc.title.alternativeEl estado de activación celular influye en la modulación de la expresión del HLA-DR sobre la superficie de monocitos/macrófagos humanos por una emulsión lipídica parenteral de aceite de pescado
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalGIDLUND, M.:Univ Sao Paulo, Sch Med, Sao Paulo, Brazil
hcfmusp.citation.scopus2
hcfmusp.contributor.author-fmusphcRAQUEL SUSANA MATOS DE MIRANDA TORRINHAS
hcfmusp.contributor.author-fmusphcMONICA NASCIMENTO JACINTHO
hcfmusp.contributor.author-fmusphcHIRO GOTO
hcfmusp.contributor.author-fmusphcMARIA MIRTES SALES
hcfmusp.contributor.author-fmusphcPATRICIA APARECIDA FERREIRA DE OLIVEIRA
hcfmusp.contributor.author-fmusphcDAN LINETZKY WAITZBERG
hcfmusp.description.beginpage311
hcfmusp.description.endpage316
hcfmusp.description.issue2
hcfmusp.description.volume26
hcfmusp.origemWOS
hcfmusp.origem.pubmed21666968
hcfmusp.origem.scopus2-s2.0-79955542624
hcfmusp.origem.wosWOS:000289226000011
hcfmusp.publisher.cityMADRID
hcfmusp.publisher.countrySPAIN
hcfmusp.relation.referenceCalder PC, 2003, BRAZ J MED BIOL RES, V36, P433, DOI 10.1590/S0100-879X2003000400004
hcfmusp.relation.referenceSiddiqui RA, 2007, NUTR CLIN PRACT, V22, P74, DOI 10.1177/011542650702200174
hcfmusp.relation.referenceSpittler A, 2003, INTENS CARE MED, V29, P1211, DOI 10.1007/s00134-003-1820-1
hcfmusp.relation.referenceFurst P, 2000, CLIN NUTR, V19, P7, DOI 10.1054/clnu.1999.0072
hcfmusp.relation.referenceWeiss G, 2002, BRIT J NUTR, V87, pS89, DOI 10.1079/BJN2001461
hcfmusp.relation.referenceDECATERINA R, 1994, ARTERIOSCLER THROMB, V14, P1829
hcfmusp.relation.referenceMorlion BJ, 1996, METABOLISM, V45, P1208, DOI 10.1016/S0026-0495(96)90237-1
hcfmusp.relation.referenceSchauder P, 2002, BRIT J NUTR, V87, pS103, DOI 10.1079/BJN2001463
hcfmusp.relation.referenceBASHAM TY, 1983, J IMMUNOL, V130, P1492
hcfmusp.relation.referenceKELLEY VE, 1985, J IMMUNOL, V134, P1914
hcfmusp.relation.referenceWaitzberg DL, 2006, JPEN-PARENTER ENTER, V30, P351, DOI 10.1177/0148607106030004351
hcfmusp.relation.referenceROSS R, 1993, NATURE, V362, P801, DOI 10.1038/362801a0
hcfmusp.relation.referenceWanten GJA, 2007, AM J CLIN NUTR, V85, P1171
hcfmusp.relation.referenceMayer K, 2003, AM J RESP CRIT CARE, V167, P1321, DOI 10.1164/rccm.200207-674OC
hcfmusp.relation.referenceMayer K, 2003, INTENS CARE MED, V29, P1472, DOI 10.1007/s00134-003-1900-2
hcfmusp.relation.referenceBACH FH, 1985, IMMUNOL TODAY, V6, P89, DOI 10.1016/0167-5699(85)90023-4
hcfmusp.relation.referenceBOYUM A, 1968, SCAND J CLIN LAB INV, VS 21, P77
hcfmusp.relation.referenceCampos FG, 2002, BRIT J NUTR, V87, pS83, DOI 10.1079/BJN2001460
hcfmusp.relation.referenceCarpentier YA, 2006, PROSTAG LEUKOTR ESS, V75, P145, DOI 10.1016/j.plefa.2006.05.004
hcfmusp.relation.referenceCLINE MJ, 1968, J EXP MED, V128, P1309, DOI 10.1084/jem.128.6.1309
hcfmusp.relation.referenceDas Undurti, 2002, Med Sci Monit, V8, pRA79
hcfmusp.relation.referenceDe Caterina Raffaele, 2004, Curr Atheroscler Rep, V6, P485, DOI 10.1007/s11883-004-0090-x
hcfmusp.relation.referenceDeckelbaum RJ, 2006, AM J CLIN NUTR, V83, p1520S
hcfmusp.relation.referenceDe Nardi L, 2008, CLIN NUTR, V27, P283, DOI 10.1016/j.clnu.2007.12.005
hcfmusp.relation.referenceFIRESTEIN GS, 1987, ARTHRITIS RHEUM, V30, P857, DOI 10.1002/art.1780300803
hcfmusp.relation.referenceHUANG SC, 1992, J NUTR, V122, P1219
hcfmusp.relation.referenceHughes DA, 1997, CLIN EXP IMMUNOL, V110, P516, DOI 10.1046/j.1365-2249.1997.4351455.x
hcfmusp.relation.referenceJACINTHO TM, 2005, ABCD ARQUIVOS BRASIL, V18, P13
hcfmusp.relation.referenceKINSELLA JE, 1990, JPEN-PARENTER ENTER, V14, pS200
hcfmusp.relation.referenceMOSQUERA J, 1990, CLIN IMMUNOL IMMUNOP, V56, P124, DOI 10.1016/0090-1229(90)90176-Q
hcfmusp.relation.referenceMULLER CP, 1983, J IMMUNOL, V131, P1356
hcfmusp.relation.referenceRoss R, 1999, NEW ENGL J MED, V340, P115
hcfmusp.relation.referenceSenkal M, 2007, JPEN-PARENTER ENTER, V31, P12, DOI 10.1177/014860710703100112
hcfmusp.relation.referenceThomas R, 1998, SPRINGER SEMIN IMMUN, V20, P53, DOI 10.1007/BF00831999
hcfmusp.relation.referenceVolk HD, 1996, INTENS CARE MED, V22, pS474, DOI 10.1007/BF01743727
hcfmusp.relation.referenceWallace FA, 2000, CYTOKINE, V12, P1374, DOI 10.1006/cyto.2000.0735
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