دورية أكاديمية
Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.
العنوان: | Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model. |
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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. |
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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 |
تدمد: | 1932-6203 |
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DOI: | 10.1371/journal.pone.0209351 |