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Air pollution-induced proteomic alterations increase the risk of child respiratory infections

Brustad, Nicklas ; Wang, Tingting ; He, Shizhen ; Pedersen, Casper Emil Tingskov ; Gruzieva, Olena ; Chen, Liang ; Pershagen, Göran ; Ali, Mina ; Kyvsgaard, Julie Nyholm and Pedersen, Marie , et al. (2025) In Nature Communications 16(1).
Abstract

Early life air pollution exposure may play a role in development of respiratory infections, but underlying mechanisms are still not understood. We utilized data from two independent prospective birth cohorts to investigate the influence of prenatal and postnatal ambient air pollution exposure of PM2.5, PM10 and NO2 on maternal and child proteomic profiles and the risk of daily diary-registered common infections age 0-3 years in the Danish COPSAC2010 (n = 613) and pneumonia, croup and bronchitis age 1-2 years in the Swedish EMIL (n = 101). A supervised sparse partial least square model generated proteomic fingerprints of air pollution analyzed against infection outcomes using Quasi-Poisson and... (More)

Early life air pollution exposure may play a role in development of respiratory infections, but underlying mechanisms are still not understood. We utilized data from two independent prospective birth cohorts to investigate the influence of prenatal and postnatal ambient air pollution exposure of PM2.5, PM10 and NO2 on maternal and child proteomic profiles and the risk of daily diary-registered common infections age 0-3 years in the Danish COPSAC2010 (n = 613) and pneumonia, croup and bronchitis age 1-2 years in the Swedish EMIL (n = 101). A supervised sparse partial least square model generated proteomic fingerprints of air pollution analyzed against infection outcomes using Quasi-Poisson and logistic regression models, respectively. Here we demonstrated that prenatal ambient air pollution exposure was associated with altered maternal proteomic profile with significant downregulation of the AXIN1 protein. The prenatal air pollution proteomic fingerprints related to a significantly higher risk of total number of infections, cold, pneumonia and fever episodes in COPSAC2010 and similar postnatal air pollution proteomic fingerprints related to a significantly higher risk of respiratory infections in EMIL. Higher AXIN1 protein levels associated with significantly decreased risks of total number of infections, cold, pneumonia, tonsillitis and fever episodes, and asthma risk in COPSAC2010 and a significantly decreased risk of respiratory infections in EMIL suggesting a protective effect of this specific protein in both cohorts. This study of two prospective birth cohorts demonstrates ambient air pollution alterations in the maternal and child’s proteomic profiles that associates with respiratory infection risk suggesting the AXIN1 protein as a potential target for respiratory infection and asthma prevention in childhood.

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organization
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type
Contribution to journal
publication status
published
subject
in
Nature Communications
volume
16
issue
1
article number
5930
publisher
Nature Publishing Group
external identifiers
  • pmid:40595623
  • scopus:105009702968
ISSN
2041-1723
DOI
10.1038/s41467-025-61392-y
language
English
LU publication?
yes
id
834fc721-f230-4927-be9a-cd554fca703c
date added to LUP
2025-10-29 15:27:17
date last changed
2025-10-30 03:00:03
@article{834fc721-f230-4927-be9a-cd554fca703c,
  abstract     = {{<p>Early life air pollution exposure may play a role in development of respiratory infections, but underlying mechanisms are still not understood. We utilized data from two independent prospective birth cohorts to investigate the influence of prenatal and postnatal ambient air pollution exposure of PM<sub>2.5</sub>, PM<sub>10</sub> and NO<sub>2</sub> on maternal and child proteomic profiles and the risk of daily diary-registered common infections age 0-3 years in the Danish COPSAC<sub>2010</sub> (n = 613) and pneumonia, croup and bronchitis age 1-2 years in the Swedish EMIL (n = 101). A supervised sparse partial least square model generated proteomic fingerprints of air pollution analyzed against infection outcomes using Quasi-Poisson and logistic regression models, respectively. Here we demonstrated that prenatal ambient air pollution exposure was associated with altered maternal proteomic profile with significant downregulation of the AXIN1 protein. The prenatal air pollution proteomic fingerprints related to a significantly higher risk of total number of infections, cold, pneumonia and fever episodes in COPSAC<sub>2010</sub> and similar postnatal air pollution proteomic fingerprints related to a significantly higher risk of respiratory infections in EMIL. Higher AXIN1 protein levels associated with significantly decreased risks of total number of infections, cold, pneumonia, tonsillitis and fever episodes, and asthma risk in COPSAC<sub>2010</sub> and a significantly decreased risk of respiratory infections in EMIL suggesting a protective effect of this specific protein in both cohorts. This study of two prospective birth cohorts demonstrates ambient air pollution alterations in the maternal and child’s proteomic profiles that associates with respiratory infection risk suggesting the AXIN1 protein as a potential target for respiratory infection and asthma prevention in childhood.</p>}},
  author       = {{Brustad, Nicklas and Wang, Tingting and He, Shizhen and Pedersen, Casper Emil Tingskov and Gruzieva, Olena and Chen, Liang and Pershagen, Göran and Ali, Mina and Kyvsgaard, Julie Nyholm and Pedersen, Marie and Ketzel, Matthias and Hyöty, Heikki and Agardh, Daniel and Melén, Erik and Thorsen, Jonathan and Stokholm, Jakob and Bønnelykke, Klaus and Chawes, Bo}},
  issn         = {{2041-1723}},
  language     = {{eng}},
  number       = {{1}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Communications}},
  title        = {{Air pollution-induced proteomic alterations increase the risk of child respiratory infections}},
  url          = {{http://dx.doi.org/10.1038/s41467-025-61392-y}},
  doi          = {{10.1038/s41467-025-61392-y}},
  volume       = {{16}},
  year         = {{2025}},
}