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Articles by Dennis K. Ninaber
Farm Dust Exposure Reduces Cytokine‐ and Rhinovirus‐Induced IL‐33 Expression in Bronchial Epithelial Cells
Farm dust reduces expression of IL-33 in rhinovirus-infected and in TNF-α/IFN-γ-exposed airway epithelial cells. This effect is in part mediated through interference with the interferon-gamma receptor-JAK–STAT1 signalling pathway. To the Editor, Pre-school wheeze, attributed to respiratory viral infections, with rhinovirus (RV) being the most important risk factor, may contribute to early-onset asthma development [1, 2].
Farm dust reduces mucin production in rhinovirus‐infected primary bronchial epithelial cells
To the Editor, Growing up on traditional farms is associated with protection against the development of wheezing, respiratory allergies, and asthma.1 Rhinovirus (RV) infections in early life are a substantial risk factor for asthma development and are linked to mucus hypersecretion in the lungs.2, 3 This results in impaired mucociliary clearance, which contributes to obstruction of (small) airways, processes implicated in asthma pathogenesis.4 Interestingly, the protective farm-effect against...
Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures
Skip to main page content Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Save citation to file Format: Add to My Bibliography Your saved search Name of saved search: Search terms: Frequency: Which day? Which day? Report format: Send at most: Send even when there aren't any new results Optional text in email: Create a file for external citation management software doi: 10.3791/65102.
Farm dust reduces viral load in human bronchial epithelial cells by increasing barrier function and antiviral responses
Publication HistoryPublished online: February 07, 2018Accepted: January 8, 2018; Received in revised form: December 11, 2017; Received: May 5, 2017;
Cigarette smoke differentially affects IL‐13‐induced gene expression in human airway epithelial cells
AbstractAllergic airways inflammation in asthma is characterized by an airway epithelial gene signature composed of POSTN, CLCA1, and SERPINB2. This Th2 gene signature is proposed as a tool to classify patients with asthma into Th2?high and Th2?low phenotypes. However, many asthmatics smoke and the effects of cigarette smoke exposure on the epithelial Th2 gene signature are largely unknown.
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