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Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation
Asthma is an allergic lung disease and, when associated to cigarette smoke exposition, some patients show controversial signs about lung function and other inflammatory mediators. Epidemiologic and experimental studies have shown both increasing and decreasing inflammation in lungs of subjects with...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472682/ https://www.ncbi.nlm.nih.gov/pubmed/28670318 http://dx.doi.org/10.3389/fimmu.2017.00718 |
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author | Brüggemann, Thayse Regina Fernandes, Paula Oliveira, Luana de Mendonça Sato, Maria Notomi Martins, Mílton de Arruda Arantes-Costa, Fernanda Magalhães |
author_facet | Brüggemann, Thayse Regina Fernandes, Paula Oliveira, Luana de Mendonça Sato, Maria Notomi Martins, Mílton de Arruda Arantes-Costa, Fernanda Magalhães |
author_sort | Brüggemann, Thayse Regina |
collection | PubMed |
description | Asthma is an allergic lung disease and, when associated to cigarette smoke exposition, some patients show controversial signs about lung function and other inflammatory mediators. Epidemiologic and experimental studies have shown both increasing and decreasing inflammation in lungs of subjects with asthma and exposed to cigarette smoke. Therefore, in this study, we analyzed how cigarette smoke affects pro-inflammatory and anti-inflammatory mediators in a murine model of allergic pulmonary inflammation. We sensitized Balb/c mice to ovalbumin (OVA) with two intraperitoneal injections. After sensitization, the animals were exposed to cigarette smoke twice a day, 30 min per exposition, for 12 consecutive days. In order to drive the cell to the lungs, four aerosol challenges were performed every 48 h with the same allergen of sensitization. OVA sensitization and challenge developed pulmonary Th2 characteristic response with increased airway responsiveness, remodeling, increased levels of IgE, interleukin (IL)-4, and IL-13. Cigarette smoke, unexpectedly, reduced the levels of IL-4 and IL-13 and simultaneously decreased anti-inflammatory cytokines as IL-10 and transforming growth factor (TGF)-β in sensitized and challenged animals. OVA combined with cigarette smoke exposition decreased the number of eosinophils in bronchoalveolar lavage and increased the number of neutrophils in lung. The combination of cigarette smoke and lung allergy increased recruitment of lymphoid dendritic cells (DCs) into lymph nodes, which may be the leading cause to an increase in number and activation of CD8(+) T cells in lungs. In addition, lung allergy and cigarette smoke exposure decreased an important regulatory subtype of DC such as plasmacytoid DC as well as its activation by expression of CD86, PDL2, and ICOSL, and it was sufficient to decrease T regs influx and anti-inflammatory cytokines release such as IL-10 and TGF-β but not enough to diminish the structural changes. In conclusion, we observed, in this model, that OVA sensitization and challenge combined with cigarette smoke exposure leads to mischaracterization of the Th2 response of asthma by decreasing the number of eosinophils, IL-4, and IL-13 and increasing number of neutrophils, which is related to the increased number of CD8ɑ(+) DCs and CD8(+) T cells as well as reduction of the regulatory cells and its released cytokines. |
format | Online Article Text |
id | pubmed-5472682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54726822017-06-30 Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation Brüggemann, Thayse Regina Fernandes, Paula Oliveira, Luana de Mendonça Sato, Maria Notomi Martins, Mílton de Arruda Arantes-Costa, Fernanda Magalhães Front Immunol Immunology Asthma is an allergic lung disease and, when associated to cigarette smoke exposition, some patients show controversial signs about lung function and other inflammatory mediators. Epidemiologic and experimental studies have shown both increasing and decreasing inflammation in lungs of subjects with asthma and exposed to cigarette smoke. Therefore, in this study, we analyzed how cigarette smoke affects pro-inflammatory and anti-inflammatory mediators in a murine model of allergic pulmonary inflammation. We sensitized Balb/c mice to ovalbumin (OVA) with two intraperitoneal injections. After sensitization, the animals were exposed to cigarette smoke twice a day, 30 min per exposition, for 12 consecutive days. In order to drive the cell to the lungs, four aerosol challenges were performed every 48 h with the same allergen of sensitization. OVA sensitization and challenge developed pulmonary Th2 characteristic response with increased airway responsiveness, remodeling, increased levels of IgE, interleukin (IL)-4, and IL-13. Cigarette smoke, unexpectedly, reduced the levels of IL-4 and IL-13 and simultaneously decreased anti-inflammatory cytokines as IL-10 and transforming growth factor (TGF)-β in sensitized and challenged animals. OVA combined with cigarette smoke exposition decreased the number of eosinophils in bronchoalveolar lavage and increased the number of neutrophils in lung. The combination of cigarette smoke and lung allergy increased recruitment of lymphoid dendritic cells (DCs) into lymph nodes, which may be the leading cause to an increase in number and activation of CD8(+) T cells in lungs. In addition, lung allergy and cigarette smoke exposure decreased an important regulatory subtype of DC such as plasmacytoid DC as well as its activation by expression of CD86, PDL2, and ICOSL, and it was sufficient to decrease T regs influx and anti-inflammatory cytokines release such as IL-10 and TGF-β but not enough to diminish the structural changes. In conclusion, we observed, in this model, that OVA sensitization and challenge combined with cigarette smoke exposure leads to mischaracterization of the Th2 response of asthma by decreasing the number of eosinophils, IL-4, and IL-13 and increasing number of neutrophils, which is related to the increased number of CD8ɑ(+) DCs and CD8(+) T cells as well as reduction of the regulatory cells and its released cytokines. Frontiers Media S.A. 2017-06-16 /pmc/articles/PMC5472682/ /pubmed/28670318 http://dx.doi.org/10.3389/fimmu.2017.00718 Text en Copyright © 2017 Brüggemann, Fernandes, Oliveira, Sato, Martins and Arantes-Costa. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Brüggemann, Thayse Regina Fernandes, Paula Oliveira, Luana de Mendonça Sato, Maria Notomi Martins, Mílton de Arruda Arantes-Costa, Fernanda Magalhães Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title | Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title_full | Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title_fullStr | Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title_full_unstemmed | Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title_short | Cigarette Smoke Increases CD8α(+) Dendritic Cells in an Ovalbumin-Induced Airway Inflammation |
title_sort | cigarette smoke increases cd8α(+) dendritic cells in an ovalbumin-induced airway inflammation |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472682/ https://www.ncbi.nlm.nih.gov/pubmed/28670318 http://dx.doi.org/10.3389/fimmu.2017.00718 |
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