Maternal Influences on Allergic Airway Disease

Maternal factors during pregnancy have emerged as critical determinants of allergic airway disease susceptibility in offspring. These influences span maternal immune status, nutritional exposures, hormonal milieu and environmental contacts. Maternal asthma and atopy can prime the in utero environment through altered cytokine profiles, driving foetal immune cell programming and epigenetic modifications that persist postnatally. Nutritional inputs such as vitamins A and D modulate both maternal and foetal immune development, with imbalances linked to increased airway hyperresponsiveness and altered airway remodelling. Maternal microbiome composition and perinatal microbial exposures further shape neonatal immune tolerance, affecting regulatory T-cell induction and barrier function in the developing lung. Together, these prenatal and perinatal factors interact with genetic predisposition to establish the trajectory for allergic sensitisation, airway inflammation and asthma development, highlighting opportunities for early preventive interventions on a global scale.

Research from Nature Portfolio

Recent studies have demonstrated that maternal asthma during gestation imprints foetal lung group 2 innate lymphoid cells (ILC2s) via glucocorticoid-driven epigenetic programming. In murine models, offspring of asthmatic mothers exhibit persistent chromatin accessibility changes in ILC2s, enhanced type 2 cytokine production and exaggerated airway inflammation upon allergen challenge in adulthood. These findings underscore how hormonal and immune signals in utero can induce long-lasting alterations in innate immune populations, linking prenatal maternal disease to heightened offspring asthma risk.

Maternal Influences on Allergic Airway Disease publication trend

The graph below shows the total number of articles in maternal influences on allergic airway disease across all publications each year (not limited to Nature Index journals).

Technical terms

Group 2 innate lymphoid cells (ILC2s): Innate immune cells that produce type 2 cytokines and contribute to airway inflammation.

Epigenetic programming: Stable changes in gene expression patterns without alteration of DNA sequence, often via chromatin modifications.

Glucocorticoid signalling: Hormone-mediated pathways involving glucocorticoid receptors, influencing immune cell development and activity.

Retinoic acid: Active metabolite of vitamin A that regulates gene transcription and immune cell differentiation.

Regulatory T cells (Tregs): A subset of T lymphocytes that suppress excessive immune responses and maintain tolerance to self and benign antigens.

References

1. Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring. Nature Communications (2025).
2. Association between vitamin A and asthma: A meta-analysis with trial sequential analysis. Frontiers in Pharmacology (2023).
3. Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease. Allergo Journal International (2018).
4. Vitamin A and D intake in pregnancy, infant supplementation, and asthma development: the Norwegian Mother and Child Cohort. American Journal of Clinical Nutrition (2018).
5. Allergic diseases and asthma in the family predict the persistence and onset-age of asthma: a prospective cohort study. Respiratory Research (2014).