This project investigates how early-life respiratory infection predisposes to a allergic Th2-biased immunological response, which is a prerequisite for the development of allergic asthma, and how airway inflammation is sustained as asthma develops and progresses. Using a novel mouse model developed in our laboratories, which combines recovery from neonatal infection with a pneumovirus and subsequent inhalational sensitisation/challenge, we are examining the molecular mechanisms involved in disease. In particular, we are studying the role of interleukin-25 in initiating a Th2-biased response; the role of transcriptional regulation via epigenetic mechanisms in determining commitment of CD4+ cells to Th2 differentiation; and the contribution of post-transcriptional regulation via microRNA in the maintenance of asthmatic inflammation.
National Health & Medical Research Council - Project Grant
Project ID: 630501