Role of prostaglandin D 2 and E 2 terminal synthases in chronic rhinosinusitis

• Published in: Clinical and experimental allergy Vol. 36; no. 8; pp. 1028 - 1038
• Main Authors: Okano, M., Fujiwara, T., Yamamoto, M., Sugata, Y., Matsumoto, R., Fukushima, K., Yoshino, T., Shimizu, K., Eguchi, N., Kiniwa, M., Urade, Y., Nishizaki, K.
• Format: Journal Article
• Language: English
• Published: 01.08.2006
• ISSN: 0954-7894; 1365-2222
• DOI: 10.1111/j.1365-2222.2006.02528.x

Summary Background Prostaglandin (PG)D 2 and E 2 , two major cyclooxygenase (COX) products, are generated by PGD 2 synthase (PGDS) and PGE 2 synthase (PGES), respectively, and appear to mediate airway inflammation. Objective We sought to determine the role of PGDS and PGES in the pathophysiology of chronic rhinosinusitis (CRS). Methods The study examined the expression of PGDS and PGES in nasal polyps of 22 CRS patients. As controls, uncinate process mucosae were obtained from 12 CRS patients not having nasal polyps and five subjects without sinusitis. Immunohistochemistry and quantitative real‐time PCR were used to evaluate the expression. Results Both PGDS and PGES were detected in nasal polyps by immunohistochemistry. Significantly greater levels of PGDS mRNA and lesser levels of PGES mRNA were observed in the nasal polyps as compared with uncinate process mucosae, and an inverse correlation between PGDS and PGES expression was observed. Levels of PGDS mRNA in nasal polyps were positively correlated with degree of infiltration by EG2+ eosinophils, whereas the levels of PGES were inversely correlated. Significantly increased levels of PGDS and conversely decreased levels of PGES were observed in asthmatics as compared with non‐asthmatics. In addition, PGDS and PGES levels were positively and inversely correlated with the radiological severity of sinusitis, respectively. Conclusions These results suggest that PGDS and PGES display an opposite and important role in the pathophysiology of CRS such as polyp formation, and more specifically, a biased expression of these synthases might contribute to the development of CRS by affecting eosinophilic inflammation.