Please use this identifier to cite or link to this item: https://observatorio.fm.usp.br/handle/OPI/33566
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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.authorSILVA, Johnatas D.
dc.contributor.authorLOPES-PACHECO, Miqueias
dc.contributor.authorCASTRO, Ligia L. de
dc.contributor.authorKITOKO, Jamil Z.
dc.contributor.authorTRIVELIN, Stefano A.
dc.contributor.authorAMORIM, Natalia R.
dc.contributor.authorCAPELOZZI, Vera L.
dc.contributor.authorMORALES, Marcelo M.
dc.contributor.authorGUTFILEN, Bianca
dc.contributor.authorSOUZA, Sergio A. L. de
dc.contributor.authorWEISS, Daniel J.
dc.contributor.authorDIAZ, Bruno L.
dc.contributor.authorROCCO, Patricia R. M.
dc.date.accessioned2019-09-23T14:20:31Z-
dc.date.available2019-09-23T14:20:31Z-
dc.date.issued2019
dc.identifier.citationSTEM CELL RESEARCH & THERAPY, v.10, n.1, article ID 264, 16p, 2019
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/33566-
dc.description.abstractBackground Even though mesenchymal stromal cells (MSCs) mitigate lung and distal organ damage in experimental polymicrobial sepsis, mortality remains high. We investigated whether preconditioning with eicosapentaenoic acid (EPA) would potentiate MSC actions in experimental sepsis by further decreasing lung and distal organ injury, thereby improving survival. Methods In C57BL/6 mice, sepsis was induced by cecal hligation and puncture (CLP); sham-operated animals were used as control. Twenty-four hours after surgery, CLP mice were further randomized to receive saline, adipose tissue-derived (AD)-MSCs (10(5), nonpreconditioned), or AD-MSCs preconditioned with EPA for 6 h (10(5), EPA-preconditioned MSCs) intravenously. After 24 h, survival rate, sepsis severity score, lung mechanics and histology, protein level of selected biomarkers in lung tissue, cellularity in blood, distal organ damage, and MSC distribution (by technetium-99m tagging) were analyzed. Additionally, the effects of EPA on the secretion of resolvin-D-1 (RvD(1)), prostaglandin E-2 (PGE(2)), interleukin (IL)-10, and transforming growth factor (TGF)-beta 1 by MSCs were evaluated in vitro. Results Nonpreconditioned and EPA-preconditioned AD-MSCs exhibited similar viability and differentiation capacity, accumulated mainly in the lungs and kidneys following systemic administration. Compared to nonpreconditioned AD-MSCs, EPA-preconditioned AD-MSCs further reduced static lung elastance, alveolar collapse, interstitial edema, alveolar septal inflammation, collagen fiber content, neutrophil cell count as well as protein levels of interleukin-1 beta and keratinocyte chemoattractant in lung tissue, and morphological abnormalities in the heart (cardiac myocyte architecture), liver (hepatocyte disarrangement and Kupffer cell hyperplasia), kidney (acute tubular necrosis), spleen (increased number of megakaryocytes and lymphocytes), and small bowel (villi architecture disorganization). EPA preconditioning of MSCs resulted in increased secretion of pro-resolution and anti-inflammatory mediators (RvD(1), PGE(2), IL-10, and TGF-beta). Conclusions Compared to nonpreconditioned cells, EPA-preconditioned AD-MSCs yielded further reductions in the lung and distal organ injury, resulting in greater improvement in sepsis severity score and higher survival rate in CLP-induced experimental sepsis. This may be a promising therapeutic approach to improve outcome in septic patients.eng
dc.description.sponsorshipBrazilian Council for Scientific and Technological Development (CNPq)
dc.description.sponsorshipRio de Janeiro State Research Foundation (FAPERJ)
dc.description.sponsorshipCoordination for the Improvement of Higher Education Personnel (CAPES)
dc.description.sponsorshipNational Institute of Science and Technology for Regenerative Medicine/CNPq
dc.description.sponsorshipDepartment of Science and Technology-Brazilian Ministry of Health (DECIT/MS)
dc.language.isoeng
dc.publisherBMCeng
dc.relation.ispartofStem Cell Research & Therapy
dc.rightsopenAccesseng
dc.subjectSepsiseng
dc.subjectMesenchymal stromal cellseng
dc.subjectPreconditioningeng
dc.subjectEicosapentaenoic acideng
dc.subjectInflammationeng
dc.subjectMacrophageseng
dc.subject.otherstem-cellseng
dc.subject.otherbone-marroweng
dc.subject.otherpulmonaryeng
dc.subject.otherinflammationeng
dc.subject.othermacrophageseng
dc.titleEicosapentaenoic acid potentiates the therapeutic effects of adipose tissue-derived mesenchymal stromal cells on lung and distal organ injury in experimental sepsiseng
dc.typearticleeng
dc.rights.holderCopyright BMCeng
dc.identifier.doi10.1186/s13287-019-1365-z
dc.identifier.pmid31443678
dc.subject.wosCell & Tissue Engineeringeng
dc.subject.wosCell Biologyeng
dc.subject.wosMedicine, Research & Experimentaleng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
hcfmusp.author.externalSILVA, Johnatas D.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil
hcfmusp.author.externalLOPES-PACHECO, Miqueias:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil; Natl Inst Sci & Technol Regenerat Med, Rio De Janeiro, Brazil
hcfmusp.author.externalCASTRO, Ligia L. de:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil
hcfmusp.author.externalKITOKO, Jamil Z.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil
hcfmusp.author.externalTRIVELIN, Stefano A.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil
hcfmusp.author.externalAMORIM, Natalia R.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Biophys Inst, Lab Inflammat, Rio De Janeiro, Brazil
hcfmusp.author.externalMORALES, Marcelo M.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Biophys Inst, Lab Cellular & Mol Physiol, Rio De Janeiro, Brazil; Natl Inst Sci & Technol Regenerat Med, Rio De Janeiro, Brazil
hcfmusp.author.externalGUTFILEN, Bianca:Univ Fed Rio de Janeiro, Sch Med, Dept Radiol, Rio De Janeiro, Brazil
hcfmusp.author.externalSOUZA, Sergio A. L. de:Univ Fed Rio de Janeiro, Sch Med, Dept Radiol, Rio De Janeiro, Brazil
hcfmusp.author.externalWEISS, Daniel J.:Univ Vermont, Coll Med, Dept Med, Burlington, VT 05405 USA
hcfmusp.author.externalDIAZ, Bruno L.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Biophys Inst, Lab Inflammat, Rio De Janeiro, Brazil
hcfmusp.author.externalROCCO, Patricia R. M.:Univ Fed Rio de Janeiro, Carlos Chagas Filho Inst Biophys, Ctr Ciencias Saude, Lab Pulm Invest, Ave Carlos Chagas Filho S-N,Bloco G-014, BR-21941902 Rio De Janeiro, RJ, Brazil; Natl Inst Sci & Technol Regenerat Med, Rio De Janeiro, Brazil
hcfmusp.description.articlenumber264
hcfmusp.description.issue1
hcfmusp.description.volume10
hcfmusp.origemWOS
hcfmusp.origem.idWOS:000482955000006
hcfmusp.origem.id2-s2.0-85071427763
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
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dc.description.indexMEDLINEeng
dc.identifier.eissn1757-6512
hcfmusp.citation.scopus16-
hcfmusp.scopus.lastupdate2022-06-10-
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