RESUMEN
Seasonal allergic rhinitis caused by Japanese cedar pollen (SAR-JCP) is a serious social problem in Japan, affecting 38.8% of the population (1). Omalizumab, a recombinant humanised monoclonal anti-immunoglobulin (Ig)E antibody, reduces serum-free IgE levels by 84-99% (2). The reduction of serum-free IgE levels induced by omalizumab ultimately downregulates FcεRI expression in basophils and mast cells (3). Omalizumab significantly reduces nasal symptoms and improves the quality of life in patients with allergic rhinitis (4,5); however, other than a decrease in free IgE, its biomarker activity is unclear. Allergic rhinitis reactions are more pronounced in nasal secretions and mucosa than in serum; however, no studies have examined the changes in proteins in nasal secretions after omalizumab administration. In this study, we aimed to elucidate the pathophysiology of the effect of omalizumab. This may serve as a basis for the identification of new biomarkers through the examination of proinflammatory proteins in nasal secretions, which may reflect the pathophysiology more accurately than peripheral blood.