Severe asthma in children is characterised by severe and multiple aeroallergen sensitisation, food allergy, eosinophilic airway inflammation and airway remodelling. However, it is a heterogeneous disease with considerable variability in the manifestation of each of these characteristics between patients. Recent data from mechanistic studies that have used translational approaches including neonatal mouse models and airway bronchoscopic samples, have shown specific molecular mediators that drive remodelling and steroid resistance in paediatric severe asthma will be discussed. The importance of undertaking studies using age appropriate models and primary cells from children to identify novel therapeutic targets will be highlighted.