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Endogenous IFN-alpha beta suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-alpha.
J Immunol. 1996 Apr 01; 156(7):2553-7.JI

Abstract

Murine bone marrow-derived macrophages (BMM) are widely used as a suitable model to study the proliferative response to macrophage-CSF or CSF-1. We report here that the amount of DNA synthesis observed in BMM cultures in response to CSF-1 can be masked quite significantly by low levels of IFN-alpha beta produced in the cultures. It was found that Ab to IFN-alpha beta could enhance the proliferative response in CSF-treated BMM that were able to respond to endogenous IFN-alpha beta; however, BMM from mice lacking a component of the type I IFN receptor did not show any enhancement of CSF-1-dependent DNA synthesis on addition of the Ab. While DNA synthesis in CSF-1-stimulated BMM from normal mice was also very sensitive to the inhibitory actions of very low concentrations of added IFN-alpha beta, DNA synthesis in BMM from the "knockout" mice was not, indicating that the type I IFN receptor component containing the null mutation was essential for signal transduction. Previously it was shown that bacterial LPS, TNF-alpha, IFN-gamma, and cAMP could all inhibit CSF-1-stimulated BMM DNA synthesis and proliferation. Using the combined approach of blocking IFN-alpha beta Ab and the IFN receptor "knockout" mice, it was found here that the growth-inhibitory effects of LPS and TNF-alpha are due, to a significant extent, to endogenous IFN-alpha beta, whereas those of IFN-gamma and cAMP occur by a different mechanism. it is proposed that the type I IFN receptor (IFNAR 1) "knockout" mice may be useful in delineating some of the in vivo actions of CSF-1, LPS, TNF-alpha, and possibly other agents.

Authors+Show Affiliations

Department of Medicine, University of Melbourne, The Royal Melbourne Hospital, Victoria, Australia.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

8786318

Citation

Hamilton, J A., et al. "Endogenous IFN-alpha Beta Suppresses Colony-stimulating Factor (CSF)-1-stimulated Macrophage DNA Synthesis and Mediates Inhibitory Effects of Lipopolysaccharide and TNF-alpha." Journal of Immunology (Baltimore, Md. : 1950), vol. 156, no. 7, 1996, pp. 2553-7.
Hamilton JA, Whitty GA, Kola I, et al. Endogenous IFN-alpha beta suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-alpha. J Immunol. 1996;156(7):2553-7.
Hamilton, J. A., Whitty, G. A., Kola, I., & Hertzog, P. J. (1996). Endogenous IFN-alpha beta suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-alpha. Journal of Immunology (Baltimore, Md. : 1950), 156(7), 2553-7.
Hamilton JA, et al. Endogenous IFN-alpha Beta Suppresses Colony-stimulating Factor (CSF)-1-stimulated Macrophage DNA Synthesis and Mediates Inhibitory Effects of Lipopolysaccharide and TNF-alpha. J Immunol. 1996 Apr 1;156(7):2553-7. PubMed PMID: 8786318.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endogenous IFN-alpha beta suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-alpha. AU - Hamilton,J A, AU - Whitty,G A, AU - Kola,I, AU - Hertzog,P J, PY - 1996/4/1/pubmed PY - 1996/4/1/medline PY - 1996/4/1/entrez SP - 2553 EP - 7 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 156 IS - 7 N2 - Murine bone marrow-derived macrophages (BMM) are widely used as a suitable model to study the proliferative response to macrophage-CSF or CSF-1. We report here that the amount of DNA synthesis observed in BMM cultures in response to CSF-1 can be masked quite significantly by low levels of IFN-alpha beta produced in the cultures. It was found that Ab to IFN-alpha beta could enhance the proliferative response in CSF-treated BMM that were able to respond to endogenous IFN-alpha beta; however, BMM from mice lacking a component of the type I IFN receptor did not show any enhancement of CSF-1-dependent DNA synthesis on addition of the Ab. While DNA synthesis in CSF-1-stimulated BMM from normal mice was also very sensitive to the inhibitory actions of very low concentrations of added IFN-alpha beta, DNA synthesis in BMM from the "knockout" mice was not, indicating that the type I IFN receptor component containing the null mutation was essential for signal transduction. Previously it was shown that bacterial LPS, TNF-alpha, IFN-gamma, and cAMP could all inhibit CSF-1-stimulated BMM DNA synthesis and proliferation. Using the combined approach of blocking IFN-alpha beta Ab and the IFN receptor "knockout" mice, it was found here that the growth-inhibitory effects of LPS and TNF-alpha are due, to a significant extent, to endogenous IFN-alpha beta, whereas those of IFN-gamma and cAMP occur by a different mechanism. it is proposed that the type I IFN receptor (IFNAR 1) "knockout" mice may be useful in delineating some of the in vivo actions of CSF-1, LPS, TNF-alpha, and possibly other agents. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/8786318/Endogenous_IFN_alpha_beta_suppresses_colony_stimulating_factor__CSF__1_stimulated_macrophage_DNA_synthesis_and_mediates_inhibitory_effects_of_lipopolysaccharide_and_TNF_alpha_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=8786318 DB - PRIME DP - Unbound Medicine ER -