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Unique twin study reveals clues to childhood allergies

A study published in Science Advances has revealed that while genetics play a significant role in shaping children's immune systems, environmental factors also influence key immune responses, offering opportunity for preventing allergic diseases.

A mission to make home safer for kids with cystic fibrosis

Dr Kak-Ming Ling, a Wal-yan Respiratory researcher at the Kids Research Institute Australia, has been awarded a $25,000 Illuminate Award for her work to change that. Supported by Conquer Cystic Fibrosis, the award was presented at the 2026 Illuminate PitchFest hosted by The Kids.

Our team

Meet the team at Phage WA, who are working to tackle antimicrobial resistance (AMR) through phage therapy. 

Phage WA Artificial Intelligence Team

Our team uses AI to quickly analyse large amounts of genetic data to help discover alternate medications and improve existing treatments.

Community Involvement

As part of our research development and planning we invite members of the community to work with us. Click here to find out how.

Contact Information

If you have any questions or would like more information about the Western Australian Epithelial Research Program (WAERP), please click here to access our contact details.

An infant nasal microbial gene atlas uncovers intervention-driven microbiome shifts and salt-resistant pathogen expansion

Functional studies of how early-life interventions shape the airway microbiome remain scarce. Here, we performed metagenomic sequencing of 704 longitudinal nasal swabs from infants with and without cystic fibrosis (CF) to construct and characterize a non-redundant gene atlas of the infant nasal microbiome. We aimed to determine how the nasal microbiome is perturbed by early therapies, as CF is commonly treated with inhaled hypertonic saline to improve mucociliary clearance.

What goes up must come down: dynamics of type 1 interferon signaling across the lifespan

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.