Background: Impaired braking of inflammatory cell cysteinyl leukotriene production by prostaglandin (PG) E-2 has been implicated in the pathogenesis of aspirin exacerbated airways disease, but the mechanism is obscure. PGE(2) acts via G-protein-coupled receptors, E-prostanoid (EP)(1-4), but there is little information on the expression of PGE(2) receptors in this condition.Objective: To address the hypothesis that expression of 1 or more EP receptors on nasal mucosal inflammatory cells is deficient in patients with aspirin-sensitive compared with nonaspirin-sensitive polypoid rhinosinusitis.Methods: By using specific antibodies, immunohistochemistry, and image analysis, we measured the expression of EP1-4 in nasal biopsies from patients with aspirin-sensitive (n = 12) and nonaspirin-sensitive (n = 10) polypoid rhinosinusitis and normal controls (n = 9). Double-staining was used to phenotype inflammatory leukocytes expressing EP1-4.Results: Global mucosal expression of EP1 and EP2, but not EP3 or EP4, immunoreactivity was significantly elevated in aspirin-sensitive and nonaspirin-sensitive rhinosinusitis compared with controls (P