Data/hora: 09/06/2024 06:40:02

Provedor de dados: | 56
País: | Brazil
Título: | Absence of peripheral blood mononuclear cells priming in hemodialysis patients
Autores: | Santos,B.C.; Starobinas,N.; Barbuto,J.A.M.; Russo,M.; Schor,N.
Data: | 2003-02-01
Ano: | 2003
Palavras-chave: | Cytokine; Stress response; Translational control; Transcriptional blockage; Priming; Membrane-anchored tumor necrosis factor.
Resumo: | 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.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000200009
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2003000200009
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.36 n.2 2003
Fonte: | info:eu-repo/semantics/openAccess