Impaired braking of inflammatory cell cysteinyl leukotriene production by prostaglandin (PG) E₂ has been implicated in the pathogenesis of aspirin exacerbated airways disease, but the mechanism is obscure. PGE₂ acts via G-protein–coupled receptors, E-prostanoid (EP)_1-4, but there is little information on the expression of PGE₂ receptors in this condition.

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.

By using specific antibodies, immunohistochemistry, and image analysis, we measured the expression of EP_1-4 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 EP_1-4.

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 < .03). This was attributable principally to elevated expression on tubulin⁺ epithelial cells and Mucin 5 subtypes A and B (Muc-5AC⁺) goblet cells. In contrast, the percentages of neutrophils, mast cells, eosinophils, and T cells expressing EP₂, but not EP₁, EP₃, or EP₄, were significantly reduced (P ≤ .04) in the aspirin-sensitive compared with nonaspirin-sensitive patients.

The data suggest a possible role for PGE₂ in mediating epithelial repair in rhinitis and asthma. Because PGE₂ exerts a range of inhibitory actions on inflammatory leukocytes via the EP₂ receptor, its reduced expression in aspirin-sensitive rhinosinusitis may be partly responsible for the increased inflammatory infiltrate and production of cysteinyl leukotrienes that characterize aspirin-sensitive disease.