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http://dx.doi.org/10.1111/vcp.12677 | DOI Listing |
J Allergy Clin Immunol
January 2025
Division of Allergy, Pulmonary and Critical Care Medicine, University of Wisconsin-Madison, Madison, Wis. Electronic address:
Background: Airway inflammation has a critical role in asthma pathogenesis and pathophysiology. Yet, the molecular pathways contributing to airway inflammation are not fully known, particularly Type-2 (T2) inflammation characterized by both eosinophilia and higher FeNO levels.
Objective: To identify genes whose level of expression in epithelial brushing samples were associated with both bronchoalveolar lavage (BAL) eosinophilia and generation of FeNO.
J Allergy Clin Immunol
January 2025
Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI.
Background: Determining why some upper respiratory illnesses provoke asthma exacerbations remains an unmet need.
Objective: To identify transcriptome-wide gene expression changes associated with colds that progress to exacerbation.
Methods: 208 urban children (6-17 years) with exacerbation-prone asthma were prospectively monitored for up to two cold illnesses.
Int J Mol Sci
December 2024
Research Unit of Biomedicine and Internal Medicine, University of Oulu, 902 20 Oulu, Finland.
Mucins 5AC (MUC5AC) and 5B (MUC5B) are the major mucins providing the organizing framework for the airway's mucus gel. We retrieved bronchial mucosal biopsies and bronchial wash (BW) samples through bronchoscopy from patients with chronic obstructive pulmonary disease ( = 38), healthy never-smokers ( = 40), and smokers with normal lung function ( = 40). The expression of MUC5AC and MUC5B was assessed immunohistochemically.
View Article and Find Full Text PDFPLoS One
December 2024
Curriculum in Toxicology and Environmental Medicine, University of North Carolina, Chapel Hill, NC, United States of America.
Imbalance of airway proteases and antiproteases has been implicated in diseases such as COPD and environmental exposures including cigarette smoke and ozone. To initiate infection, endogenous proteases are commandeered by respiratory viruses upon encountering the airway epithelium. The airway proteolytic environment likely contains redundant antiproteases and proteases with diverse catalytic mechanisms, however a proteomic profile of these enzymes and inhibitors in airway samples has not been reported.
View Article and Find Full Text PDFPart Fibre Toxicol
December 2024
Department of Public Health and Clinical Medicine, Umeå University, SE-901 87, Umeå, Sweden.
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