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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.

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Double-stranded RNA induces disproportionate expression of thymic stromal lymphopoietin versus interferon-beta in bronchial epithelial cells from donors with asthma.

TL;DR: BECs from subjects with asthma are biased towards higher TSLP and lower IFNβ production in response to dsRNA, suggesting that viral infection in asthma may lead to an altered mediator profile that biases towards a Th2 immune response.
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Expression of ErbB receptors and mucins in the airways of long term current smokers

TL;DR: It is suggested that long term current smoking induces enhanced epidermal growth factor receptor, ErbB3, and MUC5AC expression in vivo; these increases are not associated with the presence of neutrophilic inflammation.
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Local genetic and environmental factors in asthma disease pathogenesis: chronicity and persistence mechanisms

TL;DR: This type of research will not only identify biomarkers of different types of asthma across the full range of phenotypic expression, but will also identify novel therapeutic targets that could influence the natural history of the heterogenes lung disease.
Journal Article

Eosinophil recruitment following allergen challenge is associated with the release of the chemokine RANTES into asthmatic airways.

TL;DR: The presence of eosinophil chemotactic activity in bronchoalveolar lavage fluid obtained from allergic asthmatics 4 h after endobronchial allergen challenge suggests that RANTES in involved in the recruitment of eOSinophils into the asthmatic airways after allergenic challenge.
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Expression of c-erbB receptors and ligands in the bronchial epithelium of asthmatic subjects

TL;DR: Because bronchial epithelial cells respond to physical damage through activation of several c-erbB family members, the shift in favor of increased EGFR levels in asthma may lead to altered epithelial function by influencing the number and type of heterodimeric signaling complexes, assuming sufficient ligand availability.