Search
This review summarises the phage-microbe-human lung interactions in CF that must be addressed to successfully develop and deliver phage to CF airways
In 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.
PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation
Human rhinovirus infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children
HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15
Understanding early triggers of Cystic Fibrosis Lung Disease
Genetic factors in airway epithelial cells that are functionally associated with asthma pathogenesis
Patients with congenital heart disease (CHD) are identified in 1% of live births. Improved surgical intervention means many patients now survive to adulthood, the corollary of which is increased mortality in the over-65-year-old congenital heart disease population. In the clinic, genetic sequencing increasingly identifies novel genetic variants in genes related to CHD.
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.