25-vitamin D reduces inflammation in uremic environment

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorBRITO, Rodrigo Barbosa de Oliveira
dc.contributor.authorREBELLO, Jacqueline Ferritto
dc.contributor.authorGRABULOSA, Caren Cristina
dc.contributor.authorPINTO, Walter
dc.contributor.authorJR, Armando Morales
dc.contributor.authorELIAS, Rosilene Motta
dc.contributor.authorMOYSES, Rosa Maria Affonso
dc.contributor.authorDALBONI, Maria Aparecida
dc.date.accessioned2020-08-20T13:27:46Z
dc.date.available2020-08-20T13:27:46Z
dc.date.issued2020
dc.description.abstractChronic kidney disease (CKD) is characterized by loss of renal function and a consequent increase of serum uremic toxins, which contribute to inflammation status. Deficiency of 25-vitamin D, often found in patients with CKD, has been included as an inflammatory factor since it might modulate the immune system. The aim of this study was to investigate the role of 25-vitamin D on inflammatory pathways in healthy and uremic environment. Toll-like receptor 4 (TLR4), oxidative stress (ROS), vitamin D receptor (VDR), 1-alpha hydroxylase (CYP27), 24 hydroxylase, cathelicidin, and MCP-1 were evaluated in monocytes exposed to a uremic serum pool compared with healthy pool. The human monocytes lineage (U937) was incubated with or without 25-vitamin D (50 ng/ml for 24 hours). TRL4, VDR, CYP27, CYP24, and ROS were evaluated by flow cytometry. We used ELISA to measure IL-6, TNF-alpha, IL-10, cathelicidin, and MCP-1 in the cell culture supernatant. We observed a higher expression of TRL-4, IL-6, TNF-alpha, IL-10, cathelicidin and MCP-1 in monocytes incubated with uremic serum when compared with serum from healthy individuals. Supplementation of 25-vitamin D was able to reduce the expression of TRL4, cathelicidin, and MCP-1 in the uremic environment. There was no difference in the expression of VDR, CYP27 and CYP24 intracellular enzymes. This in vitro study showed that the uremic pool activates inflammatory response in monocytes, which was reversed by 25-vitamin D supplementation; this finding suggests that 25-vitamin D has an anti-inflammatory role in the uremic environment.eng
dc.description.indexMEDLINEeng
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo, FAPESPFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2014-14192-1]
dc.identifier.citationSCIENTIFIC REPORTS, v.10, n.1, article ID 128, 8p, 2020
dc.identifier.doi10.1038/s41598-019-56874-1
dc.identifier.issn2045-2322
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/37188
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUPeng
dc.relation.ispartofScientific Reports
dc.rightsopenAccesseng
dc.rights.holderCopyright NATURE PUBLISHING GROUPeng
dc.subject.otherchronic kidney-diseaseeng
dc.subject.othernf-kappa-beng
dc.subject.othercardiorenal syndromeeng
dc.subject.othervitamineng
dc.subject.otheractivationeng
dc.subject.otherexpressioneng
dc.subject.othertoxinseng
dc.subject.other1,25-dihydroxyvitamin-d3eng
dc.subject.othercathelicidinseng
dc.subject.otherphagocytosiseng
dc.subject.wosMultidisciplinary Scienceseng
dc.title25-vitamin D reduces inflammation in uremic environmenteng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.author.externalBRITO, Rodrigo Barbosa de Oliveira:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.author.externalREBELLO, Jacqueline Ferritto:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.author.externalGRABULOSA, Caren Cristina:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.author.externalPINTO, Walter:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.author.externalJR, Armando Morales:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.author.externalDALBONI, Maria Aparecida:Univ Nove Julho, UNINOVE, Sao Paulo, Brazil
hcfmusp.citation.scopus15
hcfmusp.contributor.author-fmusphcROSILENE MOTTA ELIAS
hcfmusp.contributor.author-fmusphcROSA MARIA AFFONSO MOYSES
hcfmusp.description.articlenumber128
hcfmusp.description.issue1
hcfmusp.description.volume10
hcfmusp.origemWOS
hcfmusp.origem.pubmed31924826
hcfmusp.origem.scopus2-s2.0-85077683524
hcfmusp.origem.wosWOS:000551344800021
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
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