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

Nicklas Brustad (), Tingting Wang, Shizhen He, Casper-Emil Tingskov Pedersen, Olena Gruzieva, Liang Chen, Göran Pershagen, Mina Ali, Julie Nyholm Kyvsgaard, Marie Pedersen, Matthias Ketzel, Heikki Hyöty, Daniel Agardh, Erik Melén, Jonathan Thorsen, Jakob Stokholm, Klaus Bønnelykke and Bo Chawes
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Nicklas Brustad: Copenhagen University Hospital - Herlev and Gentofte
Tingting Wang: Copenhagen University Hospital - Herlev and Gentofte
Shizhen He: Karolinska Institutet
Casper-Emil Tingskov Pedersen: Copenhagen University Hospital - Herlev and Gentofte
Olena Gruzieva: Karolinska Institutet
Liang Chen: Copenhagen University Hospital - Herlev and Gentofte
Göran Pershagen: Karolinska Institutet
Mina Ali: Copenhagen University Hospital - Herlev and Gentofte
Julie Nyholm Kyvsgaard: Copenhagen University Hospital - Herlev and Gentofte
Marie Pedersen: University of Copenhagen
Matthias Ketzel: Aarhus University
Heikki Hyöty: and Fimlab Laboratories
Daniel Agardh: Lund University
Erik Melén: Karolinska Institutet
Jonathan Thorsen: Copenhagen University Hospital - Herlev and Gentofte
Jakob Stokholm: Copenhagen University Hospital - Herlev and Gentofte
Klaus Bønnelykke: Copenhagen University Hospital - Herlev and Gentofte
Bo Chawes: Copenhagen University Hospital - Herlev and Gentofte

Nature Communications, 2025, vol. 16, issue 1, 1-10

Abstract: 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 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.

Date: 2025
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DOI: 10.1038/s41467-025-61392-y

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