دورية أكاديمية

Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.

التفاصيل البيبلوغرافية
العنوان: Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.
المؤلفون: Ito JT; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Cervilha DAB; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Lourenço JD; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Gonçalves NG; Department of Pathology, Laboratory of Molecular Pathology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Volpini RA; Department of Clinical Medicine, Basic Research Laboratory on Kidney Diseases, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Caldini EG; Department of Pathology, Laboratory of Cell Biology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Landman G; Department of Pathology, Multi-purpose Laboratory of Molecular Pathology, Federal University of São Paulo, São Paulo, Brazil., Lin CJ; Department of Pathology, Laboratory of Molecular Pathology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Velosa APP; Department of Clinical Medicine, Laboratory of Extracellular Matrix, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Teodoro WPR; Department of Clinical Medicine, Laboratory of Extracellular Matrix, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Tibério IFLC; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Mauad T; Department of Pathology, Experimental Air Pollution Laboratory, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Martins MA; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Macchione M; Department of Pathology, Experimental Air Pollution Laboratory, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Lopes FDTQDS; Department of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
المصدر: PloS one [PLoS One] 2019 Jan 10; Vol. 14 (1), pp. e0209351. Date of Electronic Publication: 2019 Jan 10 (Print Publication: 2019).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Pulmonary Disease, Chronic Obstructive/*immunology , T-Lymphocytes, Regulatory/*immunology , Th17 Cells/*immunology, Animals ; Biomarkers/metabolism ; Cellular Microenvironment/immunology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Progression ; Inflammation Mediators/metabolism ; Lung/pathology ; Lung/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Respiratory Mechanics ; Smoking/adverse effects ; T-Lymphocytes, Regulatory/pathology ; Th17 Cells/pathology ; Time Factors
مستخلص: Background: The imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses.
Methods: C57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals. We then performed functional (respiratory mechanics) and structural (alveolar enlargement) analyses. We also quantified the NF-κB, TNF-α, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-β positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-κB and TNF in bronchiolar epithelial cells.
Results: Our CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-κB, TNF-α, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-β markers) compared with the control mice. These changes in the immune responses were associated with increased alveolar enlargement and impaired lung function starting on the first month and third month of CS exposure, respectively, compared with the control mice.
Conclusion: Our results showed that the microenvironmental stimuli produced by the release of cytokines during COPD progression lead to a Th17/Treg imbalance.
Competing Interests: The authors have declared that no competing interests exist.
References: Gerontology. 2013;59(6):481-9. (PMID: 24008598)
Respir Res. 2013 Jan 20;14:5. (PMID: 23331548)
Am J Respir Crit Care Med. 2010 Nov 1;182(9):1129-36. (PMID: 20622034)
Am J Respir Crit Care Med. 2006 Apr 1;173(7):751-8. (PMID: 16399994)
J Immunol. 2009 Mar 1;182(5):3270-7. (PMID: 19234225)
COPD. 2017 Oct;14(5):533-542. (PMID: 28745532)
J Immunol. 2013 Feb 1;190(3):1331-40. (PMID: 23264660)
Lab Invest. 1963 Feb;12:131-55. (PMID: 13999512)
PLoS One. 2011;6(5):e20333. (PMID: 21647421)
Clin Exp Immunol. 2009 Aug;157(2):316-24. (PMID: 19604272)
Eur Respir J. 2012 Feb;39(2):254-64. (PMID: 21700603)
Am J Med Sci. 2015 May;349(5):392-7. (PMID: 25782336)
J Immunol. 2011 May 15;186(10):5896-906. (PMID: 21490151)
Chest. 2007 Jul;132(1):156-63. (PMID: 17505034)
Curr Drug Targets. 2011 Apr;12(4):450-9. (PMID: 21194409)
Am Rev Respir Dis. 1991 Feb;143(2):391-400. (PMID: 1990959)
Nat Rev Immunol. 2009 Dec;9(12):883-9. (PMID: 19935807)
Am J Respir Crit Care Med. 2009 Oct 1;180(7):618-31. (PMID: 19608716)
Eur Respir J. 2015 Apr;45(4):1150-62. (PMID: 25700381)
Eur Respir J. 2008 Mar;31(3):555-62. (PMID: 18057064)
Thorax. 2010 Oct;65(10):930-6. (PMID: 20627907)
Respir Physiol Neurobiol. 2012 Apr 30;181(2):167-76. (PMID: 22446562)
Clin Immunol. 2005 Jun;115(3):268-76. (PMID: 15893694)
N Engl J Med. 2004 Jun 24;350(26):2645-53. (PMID: 15215480)
Int Immunopharmacol. 2012 Dec;14(4):504-12. (PMID: 23044435)
Eur Respir J. 2006 Jan;27(1):60-4. (PMID: 16387936)
J Allergy Clin Immunol. 2002 Aug;110(2):209-14. (PMID: 12170259)
J Appl Physiol (1985). 2000 Sep;89(3):908-16. (PMID: 10956333)
PLoS Med. 2006 Nov;3(11):e442. (PMID: 17132052)
Am J Respir Cell Mol Biol. 2004 Oct;31(4):405-12. (PMID: 15220136)
Int Immunopharmacol. 2011 Nov;11(11):1780-8. (PMID: 21791252)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
Am J Respir Crit Care Med. 2015 Aug 15;192(4):428-37. (PMID: 26039632)
Eur Respir J. 2017 Oct 12;50(4):. (PMID: 29025886)
Cytokine Growth Factor Rev. 2003 Apr;14(2):85-9. (PMID: 12651220)
Eur J Immunol. 2010 Jul;40(7):1830-5. (PMID: 20583029)
Inflammation. 2016 Aug;39(4):1334-44. (PMID: 27150336)
PLoS One. 2014 Oct 16;9(10):e111044. (PMID: 25329073)
Eur Respir J. 2008 Mar;31(3):486-8. (PMID: 18310394)
Clin Respir J. 2015 Jul;9(3):330-41. (PMID: 24720797)
J Appl Physiol (1985). 1992 Jan;72(1):168-78. (PMID: 1537711)
Lancet. 2011 Sep 10;378(9795):1015-26. (PMID: 21907865)
المشرفين على المادة: 0 (Biomarkers)
0 (Cytokines)
0 (Inflammation Mediators)
تواريخ الأحداث: Date Created: 20190111 Date Completed: 20190924 Latest Revision: 20200309
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC6328193
DOI: 10.1371/journal.pone.0209351
PMID: 30629626
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0209351