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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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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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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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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
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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