Rationale Aspirin sensitive asthma involves impaired “braking” of leukotriene-induced bronchospasm by PGE 2. PGE 2 acts via 4 G-protein-coupled receptors, EP 1–4. Methods Using specific antibodies, immunohistochemistry and image analysis, we measured, semi-quantitatively, the expression and distribution of EP 1–4 in sections of nasal biopsies from aspirin-sensitive (AS, n=12) and non-aspirin-sensitive (NAS, n=10) patients with rhinosinusitis, compared with normal controls (NC, n=9). The slides were analyzed in a blind manner on an Olympus microscope connected with a Zeiss Vision KS300 image system. Because the majority of EP receptors were located on structural tissues, positive staining was quantified as the percentage of the total stainable area of the sections defined by hematoxylin. Results The amount of staining for each receptor, expressed as percentage of the total stainable area of the sections is AS: 17.7 ± 4.4 ∗, 24.8 ± 5.2 ∗, 6.8 ± 1.4, and 4.4 ± 0.9; NAS: 13.3 ± 2.9, 21.2 ± 3.0 ∗∗, 7.9 ± 2.7, and 5.6 ± 1.5; NC: 6.0 ± 2.7, 8.7 ± 2.1, 4.3 ± 1.8, and 1.9 ± 0.7, for EP1–4, respectively, ( ∗ p<0.05 and ∗∗ p<0.01 vs NC). EP 2 was found on epithelium, glands and ducts, blood vessels and inflammatory cells, while EP 1, EP3, and EP4 were located mainly on epithelium, including epithelial glands and ducts, and to a lesser extent on submucosal inflammatory cells. Conclusions EP1 and EP2 expressed significantly higher in nasal biopsy of rhinosinusitis than those in normal although global staining for EP1–4 did not significantly differ between AS and NAS. Further work will assess their differential distribution on inflammatory leukocytes.