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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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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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Conditionally reprogrammed primary airway epithelial cells maintain morphology, lineage and disease specific functional characteristicsHere, we show that conditionally reprogrammed airway epithelial cells (CRAECs) can be established from both healthy and diseased phenotypes.
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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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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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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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tesG expression as a potential clinical biomarker for chronic Pseudomonas aeruginosa pulmonary biofilm infectionsPseudomonas aeruginosa infections in the lungs affect millions of children and adults worldwide. To our knowledge, no clinically validated prognostic biomarkers for chronic pulmonary P. aeruginosa infections exist. Therefore, this study aims to identify potential prognostic markers for chronic P. aeruginosa biofilm lung infections.
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A complete genome of an obligately lytic Pseudomonas aeruginosa bacteriophage, Minga-mokiny 4We report the isolation of a bacteriophage with obligately lytic activity against Pseudomonas aeruginosa from wastewater. The reported phage, Minga-mokiny 4, appears to belong to the Schitoviridae family, is of the Litunavirus genus, and has a 72,362-bp genome. No known genes associated with lysogeny, bacterial resistance, or virulence were predicted.
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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.