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Azithromycin improves symptomology in various chronic airway diseases exacerbated by viral infections. However, the mechanisms underlying the apparent antiviral effects of azithromycin remain unclear.
A population of neutrophils recruited into cystic fibrosis (CF) airways is associated with proteolytic lung damage, exhibiting high expression of primary granule exocytosis marker CD63 and reduced phagocytic receptor CD16. Causative factors for this population are unknown, limiting intervention. Here we present a laboratory model to characterize responses of differentiated airway epithelium and neutrophils following respiratory infection.
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Investigators: Andrew Gill External collaborators: Assoc Prof David Tingay (Murdoch Children's Research Institute) The POLAR trial is an MRFF-funded
Antimicrobial resistance poses a significant threat to modern healthcare as it limits treatment options for bacterial infections, particularly impacting those with chronic conditions such as cystic fibrosis (CF). Viscous mucus accumulation in the lungs of individuals genetically predisposed to CF leads to recurrent bacterial infections, necessitating prolonged antimicrobial chemotherapy. Pseudomonas aeruginosa infections are the predominant driver of CF lung disease, and airway isolates are frequently resistant to multiple antimicrobials.
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.
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In adults, respiratory movements, such as tidal and deep breaths, reduce airway smooth muscle force and cause bronchodilation.
Vancomycin is first-line treatment for methicillin-resistant Staphylococcus aureus infections. However, despite guideline recommendations, there is no evidence that targeting vancomycin trough concentrations of ≥15 mg/L in children confers clinical benefit and is associated with vancomycin-associated nephrotoxicity.