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Biodiesel exhaust-induced cytotoxicity and proinflammatory mediator production in human airway epithelial cellsCanola biodiesel exhaust exposure elicits inflammation and reduces viability of human epithelial cell cultures in vitro when compared with ULSD exhaust exposure
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Defective cell migration as a mechanism of dysregulated asthmatic airway repairThe findings from this study show that in children with asthma this protective barrier is different from children without asthma.
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Ancestral SARS-CoV-2, but not Omicron, replicates less efficiently in primary pediatric nasal epithelial cellsChildren typically experience more mild symptoms of Coronavirus Disease 2019 (COVID-19) when compared to adults. There is a strong body of evidence that children are also less susceptible to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection with the ancestral viral isolate.
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Toxicity of different biodiesel exhausts in primary human airway epithelial cells grown at air-liquid interfaceBiodiesel is created through the transesterification of fats/oils and its usage is increasing worldwide as global warming concerns increase. Biodiesel fuel properties change depending on the feedstock used to create it.
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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.
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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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Vitamin D supplementation of initially vitamin D-deficient mice diminishes lung inflammation with limited effects on pulmonary epithelial integrityIn disease settings, vitamin D may be important for maintaining optimal lung epithelial integrity and suppressing inflammation, but less is known of its effects prior to disease onset.
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Impaired airway epithelial cell responses from children with asthma to rhinoviral infectionHuman rhinovirus infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children
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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