Competition of sodium salt of 9-oxo-10-acridineacetic acid with analogs during induction of interferon in the mouse bone marrow-derived macrophages

Arch Immunol Ther Exp (Warsz). 1985;33(2):287-97.

Abstract

Analogs of 9-oxo-10-acridineacetic acid (CMA) including new synthetic compounds, were found to be valuable tools for investigating the mechanism of interferon (IFN) induction. Experiments were performed on the long-term cultures of mouse bone marrow-derived macrophages which are unusually susceptible to IFN induction by CMA. CMA in the optimal nontoxic concentration of 600 micrograms/ml may induce in the macrophages up to 3.500 units of IFN/ml. The response was found to be dose related. The analogs of CMA, compounds 3, 7-16, were found to be inactive as IFN inducers. However, the analogs 3, and 8-16 administered together with the suboptimal doses of CMA enhanced by 10 to 40-fold the interferon response to CMA. On the other hand, the compound 7 was shown to inhibit completely the induction of interferon by CMA. L-tryptophan was inactive as either enhancer or inhibitor of CMA. The mode of action of CMA is explained in terms of the hormonal concept of IFN induction.

Publication types

  • Comparative Study

MeSH terms

  • Acridines / pharmacology*
  • Animals
  • Bone Marrow / immunology
  • Cells, Cultured
  • Female
  • Interferon Inducers / pharmacology*
  • Interferon Type I / biosynthesis*
  • Kinetics
  • Macrophages / drug effects
  • Macrophages / immunology*
  • Male
  • Mice
  • Mice, Inbred AKR
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Species Specificity
  • Structure-Activity Relationship
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology

Substances

  • Acridines
  • Interferon Inducers
  • Interferon Type I
  • 10-carboxymethyl-9-acridanone