Rapamycin attenuates pulmonary allergic vasculitis in murine model by reducing TGF-β production in the lung

Allergol Int. 2014 Sep;63(3):457-66. doi: 10.2332/allergolint.13-OA-0679. Epub 2014 May 25.

Abstract

Background: Rapamycin has been reported to inhibit mesenchymal cell proliferation in a murine model of pulmonary fibrosis. In the present study, we examined the effects of rapamycin on vascular remodeling including intraluminal myofibroblast proliferation in a murine model of allergic vasculitis with eosinophil infiltration.

Methods: C57BL/6 mice were sensitized with ovalbumin (OVA) and alum. The positive controls were exposed to aerosolized OVA daily for 7 days. The other group of mice was administered with rapamycin (1mg/kg) intraperitoneally, in parallel with daily exposure to aerosolized OVA for 7 days. On the 3rd and 7th day, bronchoalveolar lavage (BAL) was performed and the lungs were excised for pathological analysis. Cell differentials were determined and concentrations of IL-4, IL-5, IL-13 and TGF-β in the BAL fluid (BALF) were measured. Semi-quantitative analysis of pathological changes in the pulmonary arteries was evaluated according to the severity of vasculitis.

Results: The number of eosinophils in BALF was reduced significantly in the mice treated with rapamycin compared to the positive control. There was a significant decrease in the TGF-β concentration of the BALF in the rapamycin-treated group compared to that of the positive control. The pathological scores were reduced significantly in the rapamycin-treated group compared to the positive control group. Intraluminal myofibroblasts in pulmonary arteries were reduced dramatically in the rapamycin-treated group compared to the positive control group.

Conclusions: Rapamycin suppressed pulmonary vascular remodeling in a murine model of allergic vasculitis with eosinophil infiltration through reducing eosinophil infiltration and TGF-β production in the lung and inhibition against biological action of TGF-β.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Proliferation / drug effects
  • Disease Models, Animal
  • Disease Progression
  • Eosinophils / drug effects
  • Eosinophils / pathology
  • Female
  • Humans
  • Hypersensitivity / drug therapy*
  • Hypersensitivity / immunology
  • Immunosuppressive Agents / administration & dosage*
  • Lung Diseases / drug therapy*
  • Lung Diseases / immunology
  • Mice
  • Mice, Inbred C57BL
  • Myofibroblasts / drug effects
  • Myofibroblasts / physiology
  • Pulmonary Artery / drug effects*
  • Pulmonary Artery / pathology
  • Sirolimus / administration & dosage*
  • Transforming Growth Factor beta / metabolism*
  • Vascular Remodeling / drug effects*
  • Vasculitis / drug therapy*
  • Vasculitis / immunology

Substances

  • Immunosuppressive Agents
  • Transforming Growth Factor beta
  • Sirolimus