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Immune Development in Early Life (IDEaL) longitudinal cohort study protocol: Identifying biomarkers of vaccine responsiveness, respiratory infection, and asthma

Early-life immune development is a critical factor in predicting the risk of childhood respiratory infections, asthma, and poor vaccine responses. Identifying immune endotypes that predispose children to these conditions could lead to the development of predictive biomarkers and early interventions, potentially improving long-term health outcomes. 

Who gets asthma, and why?

Citation: Evans DJ, D Sly PD, Foster P, Donovan C. Who gets asthma, and why? Med J Aust. 2025;223(S10):S19-S23. Keywords: Asthma; Lung diseases;

Viral Induced Effects on a Vulnerable Epithelium; Lessons Learned From Paediatric Asthma and Eosinophilic Oesophagitis

The epithelium is integral to the protection of many different biological systems and for the maintenance of biochemical homeostasis. Emerging evidence suggests that particular children have epithelial vulnerabilities leading to dysregulated barrier function and integrity, that resultantly contributes to disease pathogenesis.

Dysregulated Notch Signaling in the Airway Epithelium of Children with Wheeze

The airway epithelium of children with wheeze is characterized by defective repair that contributes to disease pathobiology. Dysregulation of developmental processes controlled by Notch has been identified in chronic asthma. However, its role in airway epithelial cells of young children with wheeze, particularly during repair, is yet to be determined.

IRF7-Associated Immunophenotypes Have Dichotomous Responses to Virus/Allergen Coexposure and OM-85-Induced Reprogramming

High risk for virus-induced asthma exacerbations in children is associated with an IRF7lo immunophenotype, but the underlying mechanisms are unclear. Here, we applied a Systems Biology approach to an animal model comprising rat strains manifesting high versus low susceptibility to experimental asthma, induced by virus/allergen coexposure, to elucidate the mechanism(s)-of-action of the high-risk asthma immunophenotype.

The National Paediatric Applied Research Translation Initiative (N-PARTI): using implementation science to improve primary care for Australian children with asthma, type 1 diabetes

General practice-based care for Australian children is facing low levels of clinical guideline adherence particularly in three key areas: asthma, type 1 diabetes and antibiotic use. We offer an implementation science-informed position paper, providing a broad overview of how we aim to address this issue.

A health inequality analysis of childhood asthma prevalence in urban Australia

Long-standing health inequalities in Australian society that were exposed by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic were described as "fault lines" in a recent call to action by a consortium of philanthropic organizations. With asthma a major contributor to childhood disease burden, studies of its spatial epidemiology can provide valuable insights into the emergence of health inequalities early in life.

Identifying the asthma research priorities of people with asthma, their carers and other stakeholders

People living with asthma, their carers, clinicians and policymakers are the end-users of research and need research that address their individual healthcare needs. We aimed to understand the research priorities of end-users of asthma research.

Quantifying airway remodelling for research or clinical purposes: How should we normalize for airway size?

Citation: Donovan GM, Wang KCW, Elliot JG, James AL, Noble PB. Quantifying airway remodelling for research or clinical purposes: How should we

Maternal diet modulates the infant microbiome and intestinal Flt3L necessary for dendritic cell development and immunity to respiratory infection

Poor maternal diet during pregnancy is a risk factor for severe lower respiratory infections in the offspring, but the underlying mechanisms remain elusive. Here, we demonstrate that in mice a maternal low-fiber diet led to enhanced LRI severity in infants because of delayed plasmacytoid dendritic cell recruitment and perturbation of regulatory T cell expansion in the lungs.