Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice
The perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to al...
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Elsevier
2022-08-01
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Series: | Ecotoxicology and Environmental Safety |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651322006613 |
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author | Natália de Souza Xavier Costa Aila Mirtes Teles Jôse Mára de Brito Thaís de Barros Mendes Lopes Renata Calciolari Rossi Fernanda Magalhães Arantes Costa Beatriz Mangueira Saraiva-Romanholo Adenir Perini Tatiane Katsue Furuya Alexis Germán Murillo Carrasco Mariana Matera Veras Paulo Hilário Nascimento Saldiva Roger Chammas Thais Mauad |
author_facet | Natália de Souza Xavier Costa Aila Mirtes Teles Jôse Mára de Brito Thaís de Barros Mendes Lopes Renata Calciolari Rossi Fernanda Magalhães Arantes Costa Beatriz Mangueira Saraiva-Romanholo Adenir Perini Tatiane Katsue Furuya Alexis Germán Murillo Carrasco Mariana Matera Veras Paulo Hilário Nascimento Saldiva Roger Chammas Thais Mauad |
author_sort | Natália de Souza Xavier Costa |
collection | DOAJ |
description | The perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban-derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alterations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolarization by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM2.5 exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth. |
first_indexed | 2024-12-11T01:06:50Z |
format | Article |
id | doaj.art-8238763b7fb34eb2be12ccd5fa80ae77 |
institution | Directory Open Access Journal |
issn | 0147-6513 |
language | English |
last_indexed | 2024-12-11T01:06:50Z |
publishDate | 2022-08-01 |
publisher | Elsevier |
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series | Ecotoxicology and Environmental Safety |
spelling | doaj.art-8238763b7fb34eb2be12ccd5fa80ae772022-12-22T01:26:09ZengElsevierEcotoxicology and Environmental Safety0147-65132022-08-01241113821Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult miceNatália de Souza Xavier Costa0Aila Mirtes Teles1Jôse Mára de Brito2Thaís de Barros Mendes Lopes3Renata Calciolari Rossi4Fernanda Magalhães Arantes Costa5Beatriz Mangueira Saraiva-Romanholo6Adenir Perini7Tatiane Katsue Furuya8Alexis Germán Murillo Carrasco9Mariana Matera Veras10Paulo Hilário Nascimento Saldiva11Roger Chammas12Thais Mauad13Laboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilDepartment of Pathology, Universidade do Oeste Paulista UNOESTE, Presidente Prudente, SP, BrazilLaboratory of Experimental Therapeutics (LIM20), Department of Medicine, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratory of Experimental Therapeutics (LIM20), Department of Medicine, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratory of Experimental Therapeutics (LIM20), Department of Medicine, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilCenter of Translational Research in Oncology (LIM24), Instituto do Cancer do Estado de Sao Paulo (ICESP), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilCenter of Translational Research in Oncology (LIM24), Instituto do Cancer do Estado de Sao Paulo (ICESP), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilCenter of Translational Research in Oncology (LIM24), Instituto do Cancer do Estado de Sao Paulo (ICESP), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BrazilLaboratório de Patologia Ambiental e Experimental (LIM05), Departamento de Patologia, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, Brazil; Correspondence to: University of São Paulo School of Medicine, Department of Pathology, Av. Dr. Arnaldo, 455 – 1st floor – Room: 1155, Cerqueira Cesar, São Paulo 01246-903, SP, Brazil.The perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban-derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alterations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolarization by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM2.5 exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth.http://www.sciencedirect.com/science/article/pii/S0147651322006613Air pollutionParticulate matterAsthmaAllergic sensitizationAlveolarization |
spellingShingle | Natália de Souza Xavier Costa Aila Mirtes Teles Jôse Mára de Brito Thaís de Barros Mendes Lopes Renata Calciolari Rossi Fernanda Magalhães Arantes Costa Beatriz Mangueira Saraiva-Romanholo Adenir Perini Tatiane Katsue Furuya Alexis Germán Murillo Carrasco Mariana Matera Veras Paulo Hilário Nascimento Saldiva Roger Chammas Thais Mauad Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice Ecotoxicology and Environmental Safety Air pollution Particulate matter Asthma Allergic sensitization Alveolarization |
title | Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice |
title_full | Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice |
title_fullStr | Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice |
title_full_unstemmed | Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice |
title_short | Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice |
title_sort | allergic sensitization and exposure to ambient air pollution beginning early in life lead to a copd like phenotype in young adult mice |
topic | Air pollution Particulate matter Asthma Allergic sensitization Alveolarization |
url | http://www.sciencedirect.com/science/article/pii/S0147651322006613 |
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