Extracellular vesicles are key intercellular mediators in the development of immune dysfunction to allergens in the airways

Allergy. 2010 Oct;65(10):1256-65. doi: 10.1111/j.1398-9995.2010.02359.x. Epub 2010 Mar 7.

Abstract

Background: Previous evidence indicates that inhalation of lipopolysaccharide (LPS)-containing with allergens induced mixed Th1 and Th17 cell responses in the airways. Extracellular vesicles (EVs) are nanometer-sized spherical, lipid-bilayered structures and are recently in the public eye as an intercellular communicator in immune responses.

Objective: To evaluate the role of EVs secreted by LPS inhalation in the development of airway immune dysfunction in response to allergens.

Methods: Extracellular vesicles in bronchoalveolar lavage fluids of BALB/c mice were isolated and characterized 24 h after applications to the airway of 10 μg of LPS for 3 days. To evaluate the role of LPS-induced EVs on the development of airway immune dysfunction, in vivo and in vitro experiments were performed using the isolated LPS-induced EVs.

Results: The inhalation of LPS enhanced EVs release into the BAL fluid, when compared to the application of PBS. Airway sensitization with allergens and LPS-induced EVs resulted in a mixed Th1 and Th17 cell responses, although that with allergens and PBS-induced EVs induced immune tolerance. In addition, LPS-induced EVs enhanced the production of Th1- and Th17-polarizing cytokines (IL-12p70 and IL-6, respectively) by lung dendritic cells. Moreover, the immune responses induced by the LPS-induced EVs were blocked by denaturation of the EV-bearing proteins.

Conclusion: These data suggest that EVs (especially, the protein components) secreted by LPS inhalation are a key intercellular communicator in the development of airway immune dysfunction to inhaled LPS-containing allergens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / pharmacology*
  • Animals
  • Bronchoalveolar Lavage Fluid / immunology
  • Cell-Derived Microparticles / immunology*
  • Interleukin-12 / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lipopolysaccharides / pharmacology
  • Mice
  • Mice, Inbred BALB C
  • Respiratory System / immunology*
  • Th1 Cells / immunology
  • Th17 Cells / immunology

Substances

  • Allergens
  • Interleukin-6
  • Lipopolysaccharides
  • Interleukin-12