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Our data illustrate that rhinovirus infection is capable of infecting upper and lower airway epithelial cells, driving cell death and inflammation
Several lipid biomarkers of early cystic fibrosis lung disease were identified, which point toward potential disease monitoring and therapeutic approaches
Early viral infections were associated with greater neutrophilic inflammation and bacterial pathogens
Genome sequencing and phylogenetic analysis of a quorum sensing positive Psychrobacter isolate identified several quorum sensing associated systems
Allergic diseases are rising worldwide, especially in childhood, and their clinical diversity increasingly exposes the limits of traditional phenotype-based classifications. Genetic susceptibility, environmental exposures, epithelial barrier biology, and immune pathways interact to shape highly variable disease trajectories and treatment responses. In this context, precision medicine is no longer only an aspirational concept, but a practical effort to define meaningful endotypes, identify clinically useful biomarkers, and connect biological insight to prevention and care.
The airway epithelium is the primary structural and functional airway barrier and orchestrates innate immunity. Some children may have underlying epithelial vulnerabilities that contribute to the pathogenesis of acute wheeze and asthma.
Type 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.
Apically located tight junctions in airway epithelium perform a fundamental role in controlling macromolecule migration through paracellular spaces.
This study assessed an alternative approach, using a small scale halide assay that can be adapted for a personalized high throughput setting to analyze CFTR function of pAEC.
We aimed to delineate the effects of LPS and AMP on airway inflammation, and potential contribution to airway disease by measuring airway inflammatory responses