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Robert M. Powell

Researcher at University of Southampton

Publications -  28
Citations -  3361

Robert M. Powell is an academic researcher from University of Southampton. The author has contributed to research in topics: ADAM33 & Bronchial hyperresponsiveness. The author has an hindex of 19, co-authored 28 publications receiving 3198 citations. Previous affiliations of Robert M. Powell include Southampton General Hospital.

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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.
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Airway remodeling in asthma: New insights

TL;DR: An alternative view of asthma pathogenesis is discussed by emphasizing the importance of the airway microenvironment (the epithelial mesenchymal trophic unit) in the origins of the disease by supporting the recent identification of ADAM33 as an asthma susceptibility gene.
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Inflammatory processes have differential effects on claudins 2, 3 and 4 in colonic epithelial cells

TL;DR: It is suggested that INFγ/TNFα and IL-13 have differential effects on CL 2, 3 and 4 in tight junctions, which may lead to increased permeability via different mechanisms.
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Invariant Natural Killer T Cells in Asthma and Chronic Obstructive Pulmonary Disease

TL;DR: Investigating the frequency of invariant natural killer T cells in the airways of subjects with mild or moderately severe asthma and whether an increased number of these cells is a feature of chronic obstructive pulmonary disease (COPD) found them in low numbers.
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Autocrine ligands for the epidermal growth factor receptor mediate interleukin-8 release from bronchial epithelial cells in response to cigarette smoke.

TL;DR: The data indicate that secretion of IL-8 in response to CSE is dependent on EGFR activation and that autocrine production of TGF-alpha makes a substantial contribution to this response.