scispace - formally typeset
D

Donna E. Davies

Researcher at University of Southampton

Publications -  265
Citations -  19127

Donna E. Davies is an academic researcher from University of Southampton. The author has contributed to research in topics: Asthma & Epidermal growth factor. The author has an hindex of 67, co-authored 253 publications receiving 17322 citations. Previous affiliations of Donna E. Davies include National Oceanography Centre, Southampton & École normale supérieure de Lyon.

Papers
More filters
Journal ArticleDOI

Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

TL;DR: A causal link between deficient interferon-β, impaired apoptosis and increased virus replication is demonstrated, suggesting a novel use for type I interferons in the treatment or prevention of virus-induced asthma exacerbations.
Journal ArticleDOI

Role of deficient type III interferon-λ production in asthma exacerbations

TL;DR: In this paper, the authors show deficient induction of interferon-λs by rhinovirus in primary bronchial epithelial cells and alveolar macrophages, which was highly correlated with severity of rhinovirus induced asthma exacerbation and virus load in experimentally infected human volunteers.
Journal ArticleDOI

Involvement of the epidermal growth factor receptor in epithelial repair in asthma

TL;DR: It is found that EGF accelerated repair of scrape‐wounded monolayers and that the EGFR‐selective inhibitor, tyrphostin AG1478, inhibited both EGF‐stimulated and basal wound closure whereas dexamethasone was without effect.
Journal ArticleDOI

Defective epithelial barrier function in asthma.

TL;DR: The results show that the bronchial epithelial barrier in asthma is compromised, which may facilitate the passage of allergens and other agents into the airway tissue, leading to immune activation and may thus contribute to the end organ expression of asthma.
Journal ArticleDOI

Epithelial-mesenchymal interactions in the pathogenesis of asthma.

TL;DR: It is proposed that impaired epithelial repair cooperates with the TH2 environment to shift the set point for communication within the trophic unit and leads to myofibroblast activation, excessive matrix deposition, and production of mediators that propagate and amplify the remodeling responses throughout the airway wall.