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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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Ito, Juliana Tiyaki [1] ; de Brito Cervilha, Daniela Aparecida [1] ; Lourenco, Juliana Dias [1] ; Goncalves, Natalia Gomes [2] ; Volpini, Rildo Aparecido [3] ; Caldini, Elia Garcia [4] ; Landman, Gilles [5] ; Lin, Chin Jia [2] ; Pereira Velosa, Ana Paula [6] ; Rosolia Teodoro, Walcy Paganelli [6] ; Lopes Calvo Tiberio, Iolanda de Fatima [1] ; Mauad, Thais [7] ; Martins, Milton de Arruda [1] ; Macchione, Mariangela [7] ; Quirino dos Santos Lopes, Fernanda Degobbi Tenorio [1]
Total Authors: 15
Affiliation:
[1] Univ Sao Paulo, Sch Med, Dept Clin Med, Lab Expt Therapeut, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Med, Dept Pathol, Lab Mol Pathol, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Med, Dept Clin Med, Basic Res Lab Kidney Dis, Sao Paulo - Brazil
[4] Univ Sao Paulo, Sch Med, Dept Pathol, Cell Biol Lab, Sao Paulo - Brazil
[5] Univ Fed Sao Paulo, Dept Pathol, Multipurpose Lab Mol Pathol, Sao Paulo - Brazil
[6] Univ Sao Paulo, Sch Med, Dept Clin Med, Lab Extracellular Matrix, Sao Paulo - Brazil
[7] Univ Sao Paulo, Sch Med, Dept Pathol, Expt Air Pollut Lab, Sao Paulo - Brazil
Total Affiliations: 7
Document type: Journal article
Source: PLoS One; v. 14, n. 1 JAN 10 2019.
Web of Science Citations: 3
Abstract

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-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-beta positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-kappa B and TNF in bronchiolar epithelial cells. Results Our CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-beta 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 cyto-kines during COPD progression lead to a Th17/Treg imbalance. (AU)

FAPESP's process: 14/15819-8 - The respiratory epithelium as a immune response mediator in COPD pathogenesis
Grantee:Fernanda Degobbi Tenorio Quirino dos Santos Lopes
Support Opportunities: Regular Research Grants