dc.creatorNogueira-Neto, Joes
dc.creatorCardoso, Andre S. C.
dc.creatorMonteiro, Hugo P.
dc.creatorFonseca, Fernando L. A.
dc.creatorRamos, Luiz Roberto
dc.creatorJunqueira, Virginia B. C.
dc.creatorSimon, Karin A.
dc.date.accessioned2020-08-14T13:44:29Z
dc.date.accessioned2022-10-07T21:30:41Z
dc.date.available2020-08-14T13:44:29Z
dc.date.available2022-10-07T21:30:41Z
dc.date.created2020-08-14T13:44:29Z
dc.date.issued2016
dc.identifierCell Biology International. Hoboken, v. 40, n. 7, p. 796-802, 2016.
dc.identifier1065-6995
dc.identifierhttps://repositorio.unifesp.br/handle/11600/57697
dc.identifier10.1002/cbin.10618
dc.identifierWOS:000377892100008
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/4029710
dc.description.abstractMuch attention has been drawn to the pro-inflammatory condition that accompanies aging. This study compared parameters from non-stimulated neutrophils, obtained from young (18-30 years old [y.o.]) and elderly (65-80 y.o.) human volunteers. Measured as an inflammatory marker, plasmatic concentration of hs-CRP was found higher in elderly individuals. Non-stimulated neutrophil production of ROS and NO was, respectively, 38 and 29% higher for the aged group. From the adhesion molecules evaluated, only CD11b expression was elevated in neutrophils from the aged group, whereas no differences were found for CD11a, CD18, or CD62. A 69% higher non-stimulated in vitro neutrophil/endothelial cell adhesion was observed for neutrophils isolated from elderly donors. Our results suggest that with aging, neutrophils may be constitutively producing more reactive species in closer proximity to endothelial cells of vessel walls, which may both contribute to vascular damage and reflect a neutrophil intracellular disrupted redox balance, altering neutrophil function in aging.
dc.languageeng
dc.publisherWiley-Blackwell
dc.relationCell Biology International
dc.rightsAcesso restrito
dc.subjectaging
dc.subjectcell function
dc.subjectendothelial implications
dc.titleBasal neutrophil function in human aging: Implications in endothelial cell adhesion
dc.typeArtigo


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