LSC 2013 abstract - Early sources of IL-13 in house dust mite-induced neonatal allergic airways disease

Innate immunity is important in neonatal immune defence. Innate lymphoid cells have been identified in the lung, and due to their ability to produce interlukin (IL)-13 they have been shown to be both necessary and sufficient in the induction of allergic airway inflammation. We aimed to investigate the source of IL-13 in a house dust mite (HDM)-induced neonatal model of allergic airways disease. Intranasal HDM was administered intermittently from day 3 of life for 2 weeks. Mice were culled at 1 and 2 weeks of age and flow cytometry used to assess cell populations in the lung. HDM-exposed neonatal mice show increased lung inflammation at weeks 1 and 2 and an associated increase in IL-13. IL-13 + innate lymphoid cells (ILCs) were significantly elevated in the lungs of HDM-exposed neonatal mice 1 week after allergen exposure compared to controls, however IL-13 + CD4 + T cells were more prevalent. IL-13 + CD4 + T cells were observed in non-allergic neonatal mice, with this population decreasing with age. Conversely, IL-13 + ILCs increased with age in non-allergic neonatal mice. In order to assess the relative contribution of IL-13 + CD4 + T cells and IL-13 + ILCs in disease development, neonatal SCID mice were administered HDM from day 3 of life for 2 weeks. In contrast to immunocompetent mice, HDM-exposed SCID mice did not develop airway hyperresponsiveness. Collectively, these data suggest an early Th2-skew in the lung during the early postnatal period which is critical for the development of neonatal allergic airways disease.