Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis

Autores
González, Daniel; Infante, Alexis; López, Liliana; Ceschin, Danilo Guillermo; Fernández Sanchez, María José; Cañas, Alejandra; Zafra-Mejía, Carlos; Rojas, Adriana
Año de publicación
2025
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fine particulate matter (PM2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.
Fil: González, Daniel. Pontificia Universidad Javeriana; Colombia
Fil: Infante, Alexis. Universidad Nacional de Colombia; Colombia
Fil: López, Liliana. Universidad Nacional de Colombia; Colombia
Fil: Ceschin, Danilo Guillermo. Instituto Universitario de Ciencias Biomédicas de Córdoba; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Fernández Sanchez, María José. Pontificia Universidad Javeriana; Colombia
Fil: Cañas, Alejandra. Pontificia Universidad Javeriana; Colombia
Fil: Zafra-Mejía, Carlos. Pontificia Universidad Javeriana; Colombia
Fil: Rojas, Adriana. Pontificia Universidad Javeriana; Colombia
Materia
environment
epigenetics
transcriptome
air pollution;
asthma
risk factor
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/269331
Acceder
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network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysisGonzález, DanielInfante, AlexisLópez, LilianaCeschin, Danilo GuillermoFernández Sanchez, María JoséCañas, AlejandraZafra-Mejía, CarlosRojas, Adrianaenvironmentepigeneticstranscriptomeair pollution;asthmarisk factorhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Fine particulate matter (PM2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.Fil: González, Daniel. Pontificia Universidad Javeriana; ColombiaFil: Infante, Alexis. Universidad Nacional de Colombia; ColombiaFil: López, Liliana. Universidad Nacional de Colombia; ColombiaFil: Ceschin, Danilo Guillermo. Instituto Universitario de Ciencias Biomédicas de Córdoba; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Fernández Sanchez, María José. Pontificia Universidad Javeriana; ColombiaFil: Cañas, Alejandra. Pontificia Universidad Javeriana; ColombiaFil: Zafra-Mejía, Carlos. Pontificia Universidad Javeriana; ColombiaFil: Rojas, Adriana. Pontificia Universidad Javeriana; ColombiaOxford University Press2025-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/269331González, Daniel; Infante, Alexis; López, Liliana; Ceschin, Danilo Guillermo; Fernández Sanchez, María José; et al.; Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis; Oxford University Press; Environmental Epigenetics; 11; 1; 2-2025; 1-172058-5888CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/eep/article/doi/10.1093/eep/dvae026/7941693info:eu-repo/semantics/altIdentifier/doi/10.1093/eep/dvae026info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:06:17Zoai:ri.conicet.gov.ar:11336/269331instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:06:17.915CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
title Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
spellingShingle Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
González, Daniel
environment
epigenetics
transcriptome
air pollution;
asthma
risk factor
title_short Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
title_full Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
title_fullStr Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
title_full_unstemmed Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
title_sort Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis
dc.creator.none.fl_str_mv González, Daniel
Infante, Alexis
López, Liliana
Ceschin, Danilo Guillermo
Fernández Sanchez, María José
Cañas, Alejandra
Zafra-Mejía, Carlos
Rojas, Adriana
author González, Daniel
author_facet González, Daniel
Infante, Alexis
López, Liliana
Ceschin, Danilo Guillermo
Fernández Sanchez, María José
Cañas, Alejandra
Zafra-Mejía, Carlos
Rojas, Adriana
author_role author
author2 Infante, Alexis
López, Liliana
Ceschin, Danilo Guillermo
Fernández Sanchez, María José
Cañas, Alejandra
Zafra-Mejía, Carlos
Rojas, Adriana
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv environment
epigenetics
transcriptome
air pollution;
asthma
risk factor
topic environment
epigenetics
transcriptome
air pollution;
asthma
risk factor
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Fine particulate matter (PM2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.
Fil: González, Daniel. Pontificia Universidad Javeriana; Colombia
Fil: Infante, Alexis. Universidad Nacional de Colombia; Colombia
Fil: López, Liliana. Universidad Nacional de Colombia; Colombia
Fil: Ceschin, Danilo Guillermo. Instituto Universitario de Ciencias Biomédicas de Córdoba; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Fernández Sanchez, María José. Pontificia Universidad Javeriana; Colombia
Fil: Cañas, Alejandra. Pontificia Universidad Javeriana; Colombia
Fil: Zafra-Mejía, Carlos. Pontificia Universidad Javeriana; Colombia
Fil: Rojas, Adriana. Pontificia Universidad Javeriana; Colombia
description Fine particulate matter (PM2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.
publishDate 2025
dc.date.none.fl_str_mv 2025-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/269331
González, Daniel; Infante, Alexis; López, Liliana; Ceschin, Danilo Guillermo; Fernández Sanchez, María José; et al.; Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis; Oxford University Press; Environmental Epigenetics; 11; 1; 2-2025; 1-17
2058-5888
CONICET Digital
CONICET
url http://hdl.handle.net/11336/269331
identifier_str_mv González, Daniel; Infante, Alexis; López, Liliana; Ceschin, Danilo Guillermo; Fernández Sanchez, María José; et al.; Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis; Oxford University Press; Environmental Epigenetics; 11; 1; 2-2025; 1-17
2058-5888
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/eep/article/doi/10.1093/eep/dvae026/7941693
info:eu-repo/semantics/altIdentifier/doi/10.1093/eep/dvae026
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Oxford University Press
publisher.none.fl_str_mv Oxford University Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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