Expression profiles of prostaglandin E2 receptor subtypes in aspirin tolerant adult Chinese with chronic rhinosinusitis

Abstract

Background: Several studies have indicated that prostaglandin E2 and E-prostanoid (EP) receptors play a role in the pathogenesis of chronic rhinosinusitis (CRS) in white populations. However, until now there was no report about EP receptor expression and its role in the pathophysiology of CRS in Chinese patients. Objective: To investigate the expression profiles of EP receptors, including EP1, EP2, EP3, and EP4 receptors in different Chinese patients with CRS with aspirin tolerance. Methods: Nasal biopsy specimens were obtained from 12 controls, 12 patients with CRS without nasal polyps (CRSsNP), 12 with eosinophilic CRS with nasal polyps (CRSwNP), and 16 with noneosinophilic CRSwNP. Histopathologic characteristics were observed under a light microscope. Immunostaining was used to examine tissue localization of EP receptors. Messenger RNA and protein expression of EP receptors were examined by means of quantitative RT-polymerase chain reaction and Western blot, respectively. Results: Different types of CRS presented different histopathologic hallmarks. EP receptors were expressed mainly on epithelium, glands, and infiltrating inflammatory cells in nasal tissue. In controls, patients with CRSsNP, and those with noneosinophilic CRSwNP, EP4 mRNA levels were higher than EP1, EP2, and EP3 receptors. EP2 was downexpressed, and EP1 was upexpressed in patients with eosinophilic CRSwNP. When comparing EP receptor expression among different groups, Messenger RNA and protein of EP1 receptor were significantly enhanced in eosinophilic CRSwNP, but EP2, EP3, and EP4 receptors did not show significant differences. Conclusion: EP receptor expressions present different features in healthy subjects and patients with CRS. The upregulated EP1 receptor in eosinophilic CRSwNP might be associated with excessive infiltrations of eosinophils and other inflammatory cells. The accurate role of the four EP receptors in the pathogenesis of different CRS remains to be further explored.