Please use this identifier to cite or link to this item: https://observatorio.fm.usp.br/handle/OPI/30903
Title: Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model
Authors: ITO, Juliana TiyakiCERVILHA, Daniela Aparecida de BritoLOURENCO, Juliana DiasGONCALVES, Natalia GomesVOLPINI, Rildo AparecidoCALDINI, Elia GarciaLANDMAN, GillesLIN, Chin JiaVELOSA, Ana Paula PereiraTEODORO, Walcy Paganelli RosoliaTIBERIO, Iolanda de Fatima Lopes CalvoMAUAD, ThaisMARTINS, Milton de ArrudaMACCHIONE, MariangelaLOPES, Fernanda Degobbi Tenorio Quirino dos Santos
Citation: PLOS ONE, v.14, n.1, article ID e0209351, 19p, 2019
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.
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