Absence of peripheral blood mononuclear cells priming in hemodialysis patients

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dc.contributor.author Santos, B.c. [UNIFESP]
dc.contributor.author Starobinas, N.
dc.contributor.author Barbuto, J.a.m.
dc.contributor.author Russo, M.
dc.contributor.author Schor, Nestor [UNIFESP]
dc.date.accessioned 2015-06-14T13:29:56Z
dc.date.available 2015-06-14T13:29:56Z
dc.date.issued 2003-02-01
dc.identifier http://dx.doi.org/10.1590/S0100-879X2003000200009
dc.identifier.citation Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 36, n. 2, p. 219-225, 2003.
dc.identifier.issn 0100-879X
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/1656
dc.description.abstract As a consequence of the proinflammatory environment occurring in dialytic patients, cytokine overproduction has been implicated in hemodialysis co-morbidity. However, there are discrepancies among the various studies that have analyzed TNF-alpha synthesis and the presence of peripheral blood mononuclear cell (PBMC) priming in this clinical setting. We measured bioactive cytokine by the L929 cell bioassay, and evaluated PBMC TNF-alpha production by 32 hemodialysis patients (HP) and 51 controls. No difference in TNF-alpha secretion was observed between controls and HP (859 ± 141 vs 697 ± 130 U/10(6) cells). Lipopolysaccharide (5 µg/ml) did not induce any further TNF-alpha release, showing no PBMC priming. Paraformaldehyde-fixed HP PBMC were not cytotoxic to L929 cells, suggesting the absence of membrane-anchored TNF-alpha. Cycloheximide inhibited PBMC cytotoxicity in HP and controls, indicating lack of a PBMC TNF-alpha pool, and dependence on de novo cytokine synthesis. Actinomycin D reduced TNF-alpha production in HP, but had no effect on controls. Therefore, our data imply that TNF-alpha production is an intrinsic activity of normal PBMC and is not altered in HP. Moreover, TNF-alpha is a product of de novo synthesis by PBMC and is not constitutively expressed on HP cell membranes. The effect of actinomycin D suggests a putative tighter control of TNF-alpha mRNA turnover in HP. This increased dependence on TNF-alpha RNA transcription in HP may reflect an adaptive response to hemodialysis stimuli. en
dc.format.extent 219-225
dc.language.iso eng
dc.publisher Associação Brasileira de Divulgação Científica
dc.relation.ispartof Brazilian Journal of Medical and Biological Research
dc.rights Acesso aberto
dc.subject Cytokine en
dc.subject Stress response en
dc.subject Translational control en
dc.subject Transcriptional blockage en
dc.subject Priming en
dc.subject Membrane-anchored tumor necrosis factor en
dc.title Absence of peripheral blood mononuclear cells priming in hemodialysis patients en
dc.type Artigo
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Instituto Butantan Laboratório de Imunogenética
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade de São Paulo Instituto de Ciências Biomédicas Departamento de Imunologia
dc.description.affiliation Instituto Butantan Laboratório de Imunogenética
dc.description.affiliation Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de Medicina
dc.description.affiliationUnifesp UNIFESP, EPM, Depto. de Medicina
dc.identifier.file S0100-879X2003000200009.pdf
dc.identifier.scielo S0100-879X2003000200009
dc.identifier.doi 10.1590/S0100-879X2003000200009
dc.description.source SciELO
dc.identifier.wos WOS:000181135700009



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