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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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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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Macrophage PD-1 associates with neutrophilia and reduced bacterial killing in early cystic fibrosis airway diseaseMacrophages are the major resident immune cells in human airways coordinating responses to infection and injury. In cystic fibrosis, neutrophils are recruited to the airways shortly after birth, and actively exocytose damaging enzymes prior to chronic infection, suggesting a potential defect in macrophage immunomodulatory function.
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Bacteriophage: A new therapeutic player to combat neutrophilic inflammation in chronic airway diseasesPersistent respiratory bacterial infections are a clinical burden in several chronic inflammatory airway diseases and are often associated with neutrophil infiltration into the lungs. Following recruitment, dysregulated neutrophil effector functions such as increased granule release and formation of neutrophil extracellular traps (NETs) result in damage to airway tissue, contributing to the progression of lung disease.
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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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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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Accumulation mode particles and LPS exposure induce TLR-4 dependent and independent inflammatory responses in the lungWe aimed to delineate the effects of LPS and AMP on airway inflammation, and potential contribution to airway disease by measuring airway inflammatory responses
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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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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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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...