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Extracellular vesicles are key intercellular mediators in the development of immune dysfunction to allergens in the airways
Author(s) -
Shin T.S.,
Kim J. H.,
Kim Y.S.,
Jeon S. G.,
Zhu Z.,
Gho Y. S.,
Kim Y.K.
Publication year - 2010
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2010.02359.x
Subject(s) - extracellular vesicles , immune system , extracellular , intracellular , immunology , immune dysfunction , medicine , microbiology and biotechnology , biology
To cite this article: Shin T‐S, Kim JH, Kim Y‐S, Jeon SG, Zhu Z, Gho YS, Kim Y‐K. Extracellular vesicles are key intercellular mediators in the development of immune dysfunction to allergens in the airways. Allergy 2010; 65 : 1256–1265. 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.