The ability of macrophages to secrete cytokines is important in host responses to infections inflammatory stimuli, both of which are altered with aging. In this study, age-associated changes in the release of TNF-alpha from LPS-stimulated rat alveolar macrophages were determined and correlated with a decrease in the level of RACK1, the anchoring protein involved in protein kinase C translocation and activation, Macrophages from aged rats produced similar to 50% less TNF-alpha than those from young rats. This effect was observed independently from the concentration of LPS used and the time considered, The decrease observed was associated with a defective PRC translocation, due to a reduction in the expression of RACK1, whereas no differences were detected in the expression of LPS receptor (CD14) or total PRC isoforms (alpha and beta(II)) in old and young rats. Use of RACK1 antisense oligonucleotide reduced the ability of young macrophages to respond to LPS, further supporting the idea that a deficit in RACK1 contributes to the functional impairment in aged macrophages and that age-induced macrophage immuno-deficiencies are associated with alteration in signal transduction pathways.

Corsini, E., Battaini, F.m., Lucchi, L., Marinovich, M., Racchi, M., Govoni, S., et al. (1999). A defective protein kinase C anchoring system underlying age-associated impairment in TNF-alpha production in rat macrophages. JOURNAL OF IMMUNOLOGY, 163(6), 3468-3473.

A defective protein kinase C anchoring system underlying age-associated impairment in TNF-alpha production in rat macrophages

BATTAINI, FIORENZO MARIA;
1999-01-01

Abstract

The ability of macrophages to secrete cytokines is important in host responses to infections inflammatory stimuli, both of which are altered with aging. In this study, age-associated changes in the release of TNF-alpha from LPS-stimulated rat alveolar macrophages were determined and correlated with a decrease in the level of RACK1, the anchoring protein involved in protein kinase C translocation and activation, Macrophages from aged rats produced similar to 50% less TNF-alpha than those from young rats. This effect was observed independently from the concentration of LPS used and the time considered, The decrease observed was associated with a defective PRC translocation, due to a reduction in the expression of RACK1, whereas no differences were detected in the expression of LPS receptor (CD14) or total PRC isoforms (alpha and beta(II)) in old and young rats. Use of RACK1 antisense oligonucleotide reduced the ability of young macrophages to respond to LPS, further supporting the idea that a deficit in RACK1 contributes to the functional impairment in aged macrophages and that age-induced macrophage immuno-deficiencies are associated with alteration in signal transduction pathways.
1999
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/14 - FARMACOLOGIA
English
Con Impact Factor ISI
antisense oligonucleotide; cd14 antigen; lipopolysaccharide; protein kinase c; tumor necrosis factor alpha; aged; aging; animal cell; animal experiment; animal tissue; article; controlled study; cytokine production; cytokine release; enzyme activation; immune deficiency; lung alveolus macrophage; male; nonhuman; priority journal; protein expression; rat; signal transduction; Aging; Animals; Antigens, CD14; Cell Aging; Down-Regulation; Isoenzymes; Lipopolysaccharides; Macrophages, Alveolar; Male; Peptides; Protein Kinase C; Rats; Rats, Sprague-Dawley; Receptors, Cell Surface; Time Factors; Tumor Necrosis Factor-alpha
Corsini, E., Battaini, F.m., Lucchi, L., Marinovich, M., Racchi, M., Govoni, S., et al. (1999). A defective protein kinase C anchoring system underlying age-associated impairment in TNF-alpha production in rat macrophages. JOURNAL OF IMMUNOLOGY, 163(6), 3468-3473.
Corsini, E; Battaini, Fm; Lucchi, L; Marinovich, M; Racchi, M; Govoni, S; Galli, Cl
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/51449
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