ArticleNature communications2025
Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Progenitor T cells drive chronic pulmonary type 2 inflammation.Nature immunology · 2026Article
- Article
- Altered expression of Toll-like receptor 9 in the lung tissue of adult mice generated by in vitro embryo culture and embryo transfer.Histochemistry and cell biology · 2026Article
- Dynamic Regulation of Collagens, Proteases, Their Inhibitors, and Cell Death in Experimental Asthma in Mice.Allergy · 2026Article
- The epigenetic-immune-microbiome axis in early life: reprogramming the origins and endotypes of pediatric asthma.Frontiers in immunology · 2026Review
- Glucocorticoid Insensitivity: Is It a Question of Time and Place?Biomedicines · 2025Review
- Maternal IgE Influence on Fetal and Infant Health.Immunological reviews · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
The root of asthma can be linked to early life, with prenatal environments influencing risk. We investigate the effects of maternal asthma on the offspring's lungs during fetal and adult life. Adult offspring of asthmatic mothers show an increase in lung group 2 innate lymphoid cell (ILC2) number and function with allergen-induced lung inflammation. Offspring of asthmatic mothers show phenotypic alteration of their lung ILC2s during fetal life, with increased expression of genes related to activation and glucocorticoid signaling. Furthermore, these offspring carry overlapping chromatin-accessible altered regions, including glucocorticoid receptor-binding regions in their lung ILC2s both at the fetal stage and adulthood, suggesting persistent prenatal epigenetic changes. Moreover, maternal exposure to glucocorticoids has similar effects on fetal lung ILC2s and contributes to allergen-induced lung inflammation during adulthood. Thus, asthma during pregnancy may have long-term effects on lung ILC2s in the offspring from the embryonic period, contributing to an increased risk of developing asthma.
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Registered trials
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