Cytokine regulation of TNF-alpha mRNA and protein production by unprimed macrophages from C57Bl/6 and NZW mice

Détails

ID Serval
serval:BIB_1B4FC08FD88B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Cytokine regulation of TNF-alpha mRNA and protein production by unprimed macrophages from C57Bl/6 and NZW mice
Périodique
Journal of Leukocyte Biology
Auteur(s)
Schook  L. B., Albrecht  H., Gallay  P., Jongeneel  C. V.
ISSN
0741-5400 (Print)
Statut éditorial
Publié
Date de publication
10/1994
Volume
56
Numéro
4
Pages
514-20
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Oct
Résumé
It is well known that bacterial lipopolysaccharide (LPS) induces the synthesis of tumor necrosis factor alpha (TNF-alpha) and other inflammatory cytokines by primary monocytes and macrophages and that the Th1 lymphokines, interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), augment this response. We investigated the ability of IL-2 and IFN-gamma to induce the production of TNF-alpha mRNA and protein independently of LPS and the modulation of this response by macrophage colony-stimulating factor (M-CSF) and IL-10. We found that IL-2 and IFN-gamma were both able to induce the accumulation of TNF-alpha mRNA, albeit with slower kinetics than LPS, and that they acted synergistically. However, very little TNF bioactivity was secreted by lymphokine-stimulated macrophages unless LPS was also added. This finding underscores the importance of translational effects in the control of TNF production. M-CSF and IL-10 strongly inhibited TNF production at the level of both mRNA and bioactivity but had no effect on the production of IL-6. Bone marrow-derived or thioglycollate-elicited macrophages from the NZW mouse strain, which have been reported to be deficient in their ability to produce TNF, were at least as responsive to LPS or lymphokines as those taken from the C57Bl/6 strain and were similarly affected by M-CSF and IL-10. Therefore, the genetic defect of NZW mice is not a primary deficiency in TNF production.
Mots-clé
Animals Cytokines/*pharmacology Gene Expression/drug effects Interleukin-10/pharmacology Interleukin-2/pharmacology Interleukin-6/metabolism Lipopolysaccharides/pharmacology Macrophage Colony-Stimulating Factor/pharmacology Macrophages/*metabolism Mice Mice, Inbred C3H Mice, Inbred C57BL Mice, Inbred NOD RNA, Messenger/genetics Tumor Necrosis Factor-alpha/*metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 15:39
Dernière modification de la notice
20/08/2019 12:52
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