IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice

Int Arch Allergy Immunol. 1998 Sep:117 Suppl 1:24-7. doi: 10.1159/000053566.

Abstract

We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusion of IL-5-producing T cell clones. In this study, we investigated the effects of dexamethasone and cyclosporin A on the airway eosinophilic inflammation in mice transferred with T cell clones. An ovalbumin-reactive T cell clone, KW29, produced IL-5 as well as IL-2 and IL-4 upon stimulation with relevant antigen. Dexamethasone and cyclosporin A dose-dependently suppressed the production of these cytokines in vitro. The number of eosinophils recovered in the bronchoalveolar lavage fluid and the airway responsiveness to acetylcholine were increased in KW29-transferred mice after antigen provocation. Both responses were dose-dependently suppressed by the administration of dexamethasone or cyclosporin A in vivo. We concluded that airway eosinophilic inflammation can be controlled by agents capable of downregulating IL-5 production in T cells.

MeSH terms

  • Adoptive Transfer
  • Animals
  • Bronchial Hyperreactivity / etiology*
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / prevention & control
  • CD4-Positive T-Lymphocytes / drug effects*
  • CD4-Positive T-Lymphocytes / immunology*
  • Clone Cells
  • Cyclosporine / pharmacology*
  • Dexamethasone / pharmacology*
  • Eosinophilia / etiology*
  • Eosinophilia / immunology
  • Eosinophilia / prevention & control
  • Immunosuppressive Agents / pharmacology
  • Interleukin-5 / biosynthesis*
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / immunology
  • Respiratory Tract Diseases / etiology
  • Respiratory Tract Diseases / immunology
  • Respiratory Tract Diseases / prevention & control

Substances

  • Immunosuppressive Agents
  • Interleukin-5
  • Dexamethasone
  • Cyclosporine
  • Ovalbumin