Prostaglandin E2 receptors in asthma and in chronic rhinosinusitis/nasal polyps with and without aspirin hypersensitivity

Respiratory Research

César Picado¹  Jordi Roca-Ferrer¹  Liliana Machado-Carvalho¹ 

[1] Centro de Investigaciones Biomédicas en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain

关键词: Prostaglandin E2 receptors;    Prostaglandin E2;    Nasal polyps;    Chronic rhinosinusitis;    Asthma;    Aspirin exacerbated respiratory disease;   

Others  :  1146263
DOI  :  10.1186/s12931-014-0100-7

 received in 2014-04-23, accepted in 2014-08-13,  发布年份 2014

【 摘 要 】

Chronic rhinosinusitis with nasal polyps (CRSwNP) and asthma frequently coexist and are always present in patients with aspirin exacerbated respiratory disease (AERD). Although the pathogenic mechanisms of this condition are still unknown, AERD may be due, at least in part, to an imbalance in eicosanoid metabolism (increased production of cysteinyl leukotrienes (CysLTs) and reduced biosynthesis of prostaglandin (PG) E₂), possibly increasing and perpetuating the process of inflammation. PGE₂ results from the metabolism of arachidonic acid (AA) by cyclooxygenase (COX) enzymes, and seems to play a central role in homeostasis maintenance and inflammatory response modulation in airways. Therefore, the abnormal regulation of PGE₂ could contribute to the exacerbated processes observed in AERD. PGE₂ exerts its actions through four G-protein-coupled receptors designated E-prostanoid (EP) receptors EP1, EP2, EP3, and EP4. Altered PGE₂ production as well as differential EP receptor expression has been reported in both upper and lower airways of patients with AERD. Since the heterogeneity of these receptors is the key for the multiple biological effects of PGE₂ this review focuses on the studies available to elucidate the importance of these receptors in inflammatory airway diseases.

【 授权许可】

   
2014 Machado-Carvalho et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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