Nrf2−/− and Nrf2+/+ mice were used in both of BALB/c and C57BL/6 mice. Allergic airway inflammation was generated in the mice by intraperitoneal sensitization with OVA/alum on days 0, 6 and 7. The mice were challenged with OVA intranasally on day 21. After OVA challenge twenty-four hours, we examined the cell populations in bronchoalveolar lavage (BAL) fluid, and the IgE levels in the serum. Airway hyperresponsiveness (AHR) was assessed by whole-body plethysmography with a free-moving application.
The number of total cells, macrophages and eosinophils in BAL fluid was decreased in Nrf2-/- compared with Nrf2+/+ mice, this was also the case for the AHR changes in both of BALB/c and C57BL/6 mice. The number of neutrophils in BAL fluid and the IgE levels in the serum were significantly increased in Nrf2-/- compared with Nrf2+/+ in BALB/c mice; in contrast, there was no significantly different between Nrf2-/- and Nrf2+/+ in C57BL/6 mice.
In conclusion, the role of Nrf2 in the generation of allergic airway inflammation differs markedly between mouse strains. Our results suggest that Nrf2 may play a key role in the development of allergic airway inflammation related to neutrophils in BALB/c mice.