γ-Secretase Inhibitor Alleviates Acute Airway Inflammation of Allergic Asthma in Mice by Downregulating Th17 Cell Differentiation

Mediators Inflamm. 2015:2015:258168. doi: 10.1155/2015/258168. Epub 2015 Aug 3.

Abstract

T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid Precursor Protein Secretases / antagonists & inhibitors*
  • Animals
  • Asthma / drug therapy*
  • Asthma / immunology*
  • Asthma / metabolism
  • Cell Differentiation / drug effects
  • Enzyme Inhibitors / therapeutic use*
  • Inflammation / drug therapy*
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Th17 Cells / cytology*
  • Th17 Cells / drug effects*
  • Th17 Cells / metabolism

Substances

  • Enzyme Inhibitors
  • Amyloid Precursor Protein Secretases