Rationale: Allergic airway inflammation is generally considered to be a Th2-type immune response. However, Th17-type immune responses also play important roles in this process, especially in the pathogenesis of neutrophilic airway inflammation, a hallmark of severe asthma. Anti-IgE Ab is an effective treatment for patients with severe allergic asthma. It reduces not only the rate of asthma exacerbations or emergency visits but also the intensity of allergic airway inflammation, especially eosinophilic inflammation. However, whether anti-IgE treatment can suppress neutrophilic airway inflammation is still unknown.

Methods: In this study, we examined whether anti-IgE Ab treatment suppresses neutrophilic airway inflammation in ovalbumin (OVA)-T cell receptor-transgenic DO11.10 mice and then elucidated the mechanism of its action. DO11.10 mice were nebulized with OVA or PBS from days 0 to 2. Some mice received an anti-IgE Ab i.p. on day -1. On day 3, the mice were analyzed. 

Results: The anti-IgE Ab treatment significantly suppressed OVA-induced neutrophilic airway inflammation in DO11.10 mice. It also inhibited the production of IL-17 and the infiltration of Th17 cells in the lungs.

Conclusions: These results indicate that the anti-IgE Ab could suppress Th17-mediated neutrophilic airway inflammation, raising the possibility that anti-IgE Ab serves as an important strategy for treating neutrophil-dominant severe asthma.