Basophils are elevated in nasal polyps of patients with chronic rhinosinusitis without aspirin sensitivity

The level of IL-3 mRNA, a major cytokine for development and survival of basophils, is reportedly not elevated in CRS nasal and polyp tissue,13 a conclusion confirmed in a microarray analysis done by our group.14 However, as supported by the presence of basophils in IL-3-deficient mice,15 these cells can be expanded by other cytokines, such as thymic stromal lymphopoietin16 and IL-33,17 the former of which is significantly expressed in NP epithelial cells extracted from patients with CRS.18 Basophils can be activated by cross-linking of allergen-specific IgE as well as via bacterial peptidoglycans through TLR-2,2 or by formyl-methionyl-leucyl-phenylalanine19 or serine proteases through other receptors.2 Thus, bacterial infection or colonization of the sinus mucosa, commonly observed in CRS, can theoretically activate the basophils we have detected in the NP tissue. [...]we found a significantly higher number of basophils in the NP tissue than in the UT of controls and patients with CRSwNP without AERD.