BACKGROUND: Prostaglandin D2 (PGD2) is the major prostanoid produced in the acute phase of allergic reactions. However, its pathophysiological role in addition to the pathway of production in allergic rhinitis remains unclear. We sought to determine the expression of synthases and receptors for PGD2 in human nasal mucosa. These expressions were compared between allergic and nonallergic patients. METHODS: The expression and localization of hematopoietic-type (h)-PGD2 synthase (PGDS) and lipocalin-type (l)-PGDS were detected by immunohistochemistry. The expression of D prostanoid (DP) receptor and chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) was determined by quantitative real-time PCR. RESULTS: The h-PGDS but not l-PGDS was clearly expressed in nasal mucosa. The expression of h-PGDS in allergic patients was significantly higher than in control patients without mucosal hypertrophy. A variety of infiltrating cells including mast cells, eosinophils, macrophages, and lymphocytes as well as constitutive cells such as epithelial cells and fibroblasts expressed h-PGDS. The expression of both DP and CRTH2 was confirmed also. Although either the amount of DP or the amount of CRTH2 was not correlated with serum levels of IgE, the amount of CRTH2 but not DP was highly and significantly correlated with the number of eosinophils infiltrating into nasal musosa. CONCLUSION: These results suggest that PGD2 is released via the action of h-PGDS from various cells, and the expression of h-PGDS may be associated with the hypertrophic inflammation in the nose. In addition, ligation of PGD2 to CRTH2 appears to be selectively involved in eosinophil recruitment into the nose regardless of atopic status.
BACKGROUND:Prostaglandin D2 (PGD2) is the major prostanoid produced in the acute phase of allergic reactions. However, its pathophysiological role in addition to the pathway of production in allergic rhinitis remains unclear. We sought to determine the expression of synthases and receptors for PGD2 in human nasal mucosa. These expressions were compared between allergic and nonallergic patients. METHODS: The expression and localization of hematopoietic-type (h)-PGD2 synthase (PGDS) and lipocalin-type (l)-PGDS were detected by immunohistochemistry. The expression of D prostanoid (DP) receptor and chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) was determined by quantitative real-time PCR. RESULTS: The h-PGDS but not l-PGDS was clearly expressed in nasal mucosa. The expression of h-PGDS in allergicpatients was significantly higher than in control patients without mucosal hypertrophy. A variety of infiltrating cells including mast cells, eosinophils, macrophages, and lymphocytes as well as constitutive cells such as epithelial cells and fibroblasts expressed h-PGDS. The expression of both DP and CRTH2 was confirmed also. Although either the amount of DP or the amount of CRTH2 was not correlated with serum levels of IgE, the amount of CRTH2 but not DP was highly and significantly correlated with the number of eosinophils infiltrating into nasal musosa. CONCLUSION: These results suggest that PGD2 is released via the action of h-PGDS from various cells, and the expression of h-PGDS may be associated with the hypertrophic inflammation in the nose. In addition, ligation of PGD2 to CRTH2 appears to be selectively involved in eosinophil recruitment into the nose regardless of atopic status.
Authors: Tatiana Luna-Gomes; Kelly G Magalhães; Fabio P Mesquita-Santos; Ilka Bakker-Abreu; Rafaela F Samico; Raphael Molinaro; Andrea S Calheiros; Bruno L Diaz; Patrícia T Bozza; Peter F Weller; Christianne Bandeira-Melo Journal: J Immunol Date: 2011-11-18 Impact factor: 5.422
Authors: Amr E El-Shazly; Dominique Y Begon; Gaelle Kustermans; Mohammad Arafa; Estelle Dortu; Monique Henket; Philippe P Lefebvre; Renaud Louis; Philippe Delvenne Journal: J Biol Chem Date: 2012-11-20 Impact factor: 5.157
Authors: Merritt L Fajt; Stacy L Gelhaus; Bruce Freeman; Crystal E Uvalle; John B Trudeau; Fernando Holguin; Sally E Wenzel Journal: J Allergy Clin Immunol Date: 2013-03-16 Impact factor: 10.793