Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma. (26th August 2014)
- Record Type:
- Journal Article
- Title:
- Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma. (26th August 2014)
- Main Title:
- Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma
- Authors:
- Cho, Kyu-Sup
Park, Mi-Kyung
Kang, Shin-Ae
Park, Hee-Young
Hong, Sung-Lyong
Park, Hye-Kyung
Yu, Hak-Sun
Roh, Hwan-Jung - Other Names:
- Kleinjan Alex Academic Editor.
- Abstract:
- Abstract : Although several studies have demonstrated that mesenchymal stem cells derived from adipose tissue (ASCs) can ameliorate allergic airway inflammation, the immunomodulatory mechanism of ASCs remains unclear. In this study, we investigated whether regulatory T cells (Tregs) induction is a potential mechanism in immunomodulatory effects of ASCs on allergic airway disease and how these induced Tregs orchestrate allergic inflammation. Intravenous administration of ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation. Airway hyperresponsiveness, total immune cell and eosinophils in the bronchoalveolar lavage fluid, mucus production, and serum allergen-specific IgE and IgG1 were significantly reduced after ASCs administration. ASCs significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN- γ ) and regulatory cytokines (IL-10 and TGF- β ) in the bronchoalveolar lavage fluid and lung draining lymph nodes. Furthermore, levels of IDO, TGF- β, and PGE2 were significantly increased after ASCs administration. Interestingly, this upregulation was accompanied by increased Treg populations. In conclusion, ASCs ameliorated allergic airway inflammation and improved lung function through the induction of Treg expansion. The induction of Treg by ASCs involves the secretion of soluble factors such as IDO, TGF- β, and PGE2 and Treg might be involved in the downregulation of Th2 cytokines and upregulation of Th1 cytokinesAbstract : Although several studies have demonstrated that mesenchymal stem cells derived from adipose tissue (ASCs) can ameliorate allergic airway inflammation, the immunomodulatory mechanism of ASCs remains unclear. In this study, we investigated whether regulatory T cells (Tregs) induction is a potential mechanism in immunomodulatory effects of ASCs on allergic airway disease and how these induced Tregs orchestrate allergic inflammation. Intravenous administration of ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation. Airway hyperresponsiveness, total immune cell and eosinophils in the bronchoalveolar lavage fluid, mucus production, and serum allergen-specific IgE and IgG1 were significantly reduced after ASCs administration. ASCs significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN- γ ) and regulatory cytokines (IL-10 and TGF- β ) in the bronchoalveolar lavage fluid and lung draining lymph nodes. Furthermore, levels of IDO, TGF- β, and PGE2 were significantly increased after ASCs administration. Interestingly, this upregulation was accompanied by increased Treg populations. In conclusion, ASCs ameliorated allergic airway inflammation and improved lung function through the induction of Treg expansion. The induction of Treg by ASCs involves the secretion of soluble factors such as IDO, TGF- β, and PGE2 and Treg might be involved in the downregulation of Th2 cytokines and upregulation of Th1 cytokines production. … (more)
- Is Part Of:
- Mediators of inflammation. Volume 2014(2014)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 2014(2014)
- Issue Display:
- Volume 2014, Issue 2014 (2014)
- Year:
- 2014
- Volume:
- 2014
- Issue:
- 2014
- Issue Sort Value:
- 2014-2014-2014-0000
- Page Start:
- Page End:
- Publication Date:
- 2014-08-26
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1155/2014/436476 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 23451.xml