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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.
Intrauterine growth restriction (IUGR) is associated with asthma. Murine models of IUGR have altered airway responsiveness in the absence of any inflammatory exposure. Given that a primary feature of asthma is airway inflammation, IUGR-affected individuals may develop more substantial respiratory impairment if subsequently exposed to an allergen. This study used a maternal hypoxia-induced mouse model of IUGR to determine the combined effects of IUGR and allergy on airway responsiveness.
Alexander Anthony Dr Katherine Larcombe Kicic Landwehr BScEnv (Hons) PhD BSc (Hons) PhD BSc(Hons) Honorary Research Fellow Rothwell Family Fellow;
Alexander Anthony Larcombe Kicic BScEnv (Hons) PhD BSc (Hons) PhD Honorary Research Fellow Rothwell Family Fellow; Head, Airway Epithelial Research
Heated-tobacco-products (HTPs) are electronic devices that "heat" a processed tobacco/chemical mixture to produce an inhalable emission. They are advertised as a reduced-risk alternative to cigarette smoking. The aim of our research was to assess their potential health impacts using a 3D human airway model.
Electronic cigarettes (e-cigarettes) lack regulatory status as therapeutic products in all jurisdictions worldwide. They are potentially unsafe consumer products, with significant evidence they pose a risk to human health. Therefore, developing rapid, economical test methods to assess the chemical composition of e-liquids in heated and unheated forms and the aerosols produced by e-cigarettes is crucial.
Treatment options for viral lung infections are currently limited. We aimed to explore the safety and efficacy of inhaled ethanol in an influenza-infection mouse model.
Mucopolysaccharidosis type IIIA (MPS IIIA) is characterized by neurological and skeletal pathologies caused by reduced activity of the lysosomal hydrolase, sulfamidase, and the subsequent primary accumulation of undegraded heparan sulfate (HS). Respiratory pathology is considered secondary in MPS IIIA and the mechanisms are not well understood.
Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids
Emerging data suggest that air pollution is a persistent source of neuroinflammation, reactive oxygen species, and neuropathology that contributes to central nervous system disorders. Previous research using animal models has shown that exposure to diesel exhaust causes considerable disruption of the blood-brain barrier, leading to marked neuroinflammation.