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Identification of epithelial phospholipase A2 receptor 1 as a potential target in asthmaPLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation
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Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeabilityHRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15
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The genetic and epigenetic landscapes of the epithelium in asthmaGenetic factors in airway epithelial cells that are functionally associated with asthma pathogenesis
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Productive infection of human embryonic stem cell-derived nkx2.1+ respiratory progenitors with human rhinovirus.Our experiments provide proof of principle for the use of PSC-derived respiratory epithelial cells in the study of cell-virus interactions.
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The airway epithelium is a direct source of matrix degrading enzymes in bronchiolitis obliterans syndromeLong-term survival after lung transplantation is hindered by the development of bronchiolitis obliterans syndrome (BOS).
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Transcription factor p63 regulates key genes and wound repair in human airway epithelial Basal cellsThe airway epithelium in asthma displays altered repair and incomplete barrier formation.
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Persistent induction of goblet cell differentiation in the airways: Therapeutic approachesHere we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation
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Suppression of adrenomedullin contributes to vascular leakage and altered epithelial repair during asthmaThe anti-inflammatory peptide, adrenomedullin (AM), and its cognate receptor are expressed in lung tissue, but its pathophysiological significance in airway...
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Vulnerable from the first breath - epithelial dysfunction and respiratory outcomes in childrenWe have been studying the importance of the epithelial cells lining the airways in the nose and lungs.
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ACE2 expression is elevated in airway epithelial cells from older and male healthy individuals but reduced in asthmaCOVID-19 is complicated by acute lung injury, and death in some individuals. It is caused by SARS-CoV-2 that requires the ACE2 receptor and serine proteases to enter AEC. We determined what factors are associated with ACE2 expression particularly in patients with asthma and COPD. We obtained lower AEC from 145 people from two independent cohorts, aged 2-89 years, Newcastle (n = 115) and Perth (n = 30), Australia. The Newcastle cohort was enriched with people with asthma (n = 37) and COPD (n = 38). Gene expression for ACE2 and other genes potentially associated with SARS-CoV-2 cell entry was assessed by qPCR, and protein expression was confirmed with immunohistochemistry on endobronchial biopsies and cultured AEC.