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Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice

In 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...

Defective cell migration as a mechanism of dysregulated asthmatic airway repair

The findings from this study show that in children with asthma this protective barrier is different from children without asthma.

Cultures of HRV-C for investigations of pathogenesis in children

Anthony Belinda Ingrid Kicic Hales Laing BSc (Hons) PhD BSc (Hons) PhD BSc PhD Rothwell Family Fellow; Head, Airway Epithelial Research Senior

Improved diagnosis, treatment and prevention of recurrent tonsillitis

Strep A causes over 775 million infections each year world-wide, including over 615 million cases of tonsil infection (Strep throat).

Vulnerable from the first breath - epithelial dysfunction and respiratory outcomes in children

We have been studying the importance of the epithelial cells lining the airways in the nose and lungs.

Regional Differences in Susceptibiity of Bronchial Epithelium to Mesenchymal Transition and Inhibition by the Macrolide Antibiotic Azithromycin

Dysregulated repair following epithelial injury is a key forerunner of disease in many organs, and the acquisition of a mesenchymal phenotype by the injured...

DNA Methylation Profiles of Airway Epithelial Cells and PBMCs from Healthy, Atopic and Asthmatic Children

Allergic inflammation is commonly observed in a number of conditions that are associated with atopy including asthma, eczema and rhinitis.

Innate inflammatory responses of pediatric cystic fibrosis airway epithelial cells: Effects of nonviral and viral stimulation

There is controversy regarding whether cystic fibrosis (CF) airway epithelial cells (AECs) are intrinsically proinflammatory.

Primary Nasal Epithelial Cells as a Surrogate Cell Culture Model for Type-II Alveolar Cells to Study ABCA-3 Deficiency

ATP Binding Cassette Subfamily A Member 3 (ABCA-3) is a lipid transporter protein highly expressed in type-II alveolar (AT-II) cells. Mutations in ABCA3 can result in severe respiratory disease in infants and children. To study ABCA-3 deficiency in vitro, primary AT-II cells would be the cell culture of choice although sample accessibility is limited. Our aim was to investigate the suitability of primary nasal epithelial cells, as a surrogate culture model for AT-II cells, to study ABCA-3 deficiency.