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Changes in airway inflammation with pseudomonas eradication in early cystic fibrosisNeutrophil elastase is a significant risk factor for structural lung disease in cystic fibrosis, and Pseudomonas aeruginosa airway infection is linked with neutrophilic inflammation and substantial respiratory morbidity. We aimed to evaluate how neutrophil elastase (NE) activity changes after P. aeruginosa eradication and influences early disease outcomes. We assessed participants in the AREST CF cohort between 2000 and 2018 who had P. aeruginosa cultured from their routine annual bronchoalveolar lavage (BAL) fluid and who underwent eradication treatment and a post eradication BAL. Factors associated with persistent P. aeruginosa infection, persistent neutrophilic inflammation following eradication and worse structural lung disease one year post-eradication were evaluated.
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Epithelial Mesenchymal Transition in Respiratory Disease: Fact or FictionIn this translational review, the mechanisms, roles, and impact of epithelial-mesenchymal transition in chronic lung diseases are discussed
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Progress in Model Systems of Cystic Fibrosis Mucosal Inflammation to Understand Aberrant Neutrophil ActivityHere we examine the latest findings of neutrophils in pediatric CF lung disease and proposed mechanisms of their pathogenicity
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Ground zero—the airway epitheliumNew PageThis chapter will discuss the structure of the airway highlighting the now broad number of cell types that comprise it
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Interleukin-1 is associated with inflammation and structural lung disease in young children with cystic fibrosisOur data associates IL-1α with early structural lung damage in CF and suggests this pathway as a novel anti-inflammatory target
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Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmaticsOur findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatic with natural aeroallergen exposure
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Pulmonary microRNA profiles identify involvement of Creb1 and Sec14l3 in bronchial epithelial changes in allergic asthmaIn this study, we aimed to use microRNAs-which are critical regulators of signaling cascades-to identify so far uncharacterized asthma pathogenesis pathways
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Airway epithelial repair in health and disease: Orchestrator or simply a player?This review attempts to highlight migration-specific and cell-extracellular matrix (ECM) aspects of repair used by epithelial cells
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Rhinovirus exacerbates house-dust-mite induced lung disease in adult miceIn this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to...
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What goes up must come down: dynamics of type 1 interferon signaling across the lifespanType 1 interferons (T1IFNs) are typically expressed in low concentrations under homeostatic conditions, but upon pathogenic insult or perturbation of the pathway, these critical immune signaling molecules can become either protectors from or drivers of pathology. While essential for initiating antiviral defense and modulating inflammation, dysregulation of T1IFN signaling can contribute to immunopathology, making it and its associated pathways prime targets for immune evasion and disruption by pathogens.