Modulation of granuloma formation in vitro by endogenous mediators

Immunopharmacology. 1991 Mar-Apr;21(2):73-82. doi: 10.1016/0162-3109(91)90010-v.

Abstract

We have reported previously that in vitro granulomas are inducible by culturing murine spleen cells in the presence of artificial microparticles, dextran beads, and that macrophages and macrophage-derived cytokines (monokines) including interleukin 1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) play a critical role in the initiation of bead-induced granulomas in vitro. To investigate regulatory mechanisms of granuloma formation, we examined the modulatory effects of various mediators such as IL-1, TNF-alpha, interferon-gamma (IFN-gamma), IL-4, IL-6, transforming growth factor-beta (TGF-beta), dexamethasone and prostaglandin E2 (PGE2) on the development of lesions, because these mediators are known to play a pivotal role in inflammatory responses. The lesions were suppressed by the addition of dexamethasone, PGE2 or certain T cell-derived lymphokines such as IL-4 and IFN-gamma. These results suggest that suppressive signals are different from granulomatogenic cytokines including IL-1 and TNF-alpha and that granulomas are regulated by multi-factor dependent mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / pharmacology
  • Dexamethasone / pharmacology
  • Dextrans
  • Dinoprostone / pharmacology
  • Female
  • Granuloma / etiology*
  • Granuloma / pathology
  • Granuloma / prevention & control
  • In Vitro Techniques
  • Lymphokines / pharmacology
  • Mice
  • Mice, Inbred BALB C
  • Microspheres
  • Splenic Diseases / etiology
  • Splenic Diseases / pathology
  • Splenic Diseases / prevention & control

Substances

  • Cytokines
  • Dextrans
  • Lymphokines
  • Dexamethasone
  • Dinoprostone