Prostanoid Receptors as Possible Targets for Anti-Allergic Drugs: Recent Advances in Prostanoids on Allergy and Immunology

Tetsuya      Honda; Yoshiki      Tokura; Yoshiki      Miyachi; Kenji      Kabashima

doi:10.2174/1389450111009011605

Abstract

Prostanoids, consisting of prostaglandins and thromboxane, are cyclooxygenase metabolites of arachidonic acid released in various pathophysiological conditions which exert a range of actions mediated through their respective receptors expressed on target cells. Although it has been difficult to analyze the physiological role of prostanoids, recent developments in both the disruption of the respective gene and receptor selective compounds have enabled us to investigate the physiological roles for each receptor. It has been demonstrated that each prostanoid receptor has multiple functions, and that their expression is regulated in a context-dependent manner that sometimes results in opposite, excitatory and inhibitory, outcomes. The balance of prostanoid production and receptor expression has been revealed to be important for homeostasis of the human body. Here, we review new findings on the roles of prostanoids in allergic and immune diseases, focusing on contact dermatitis, atopic dermatitis, asthma, rheumatoid arthritis, and encephalomyelitis, and also discuss the clinical potentials of receptor-selective drugs.

Keywords: Prostanoid, atopic dermatitis, contact dermatitis, NSAID, prostaglandin, asthma, rheumatoid arthritis, encephalomyelitis, allergy, prostaglandins, thromboxane, cyclooxygenase, arachidonic acid, encephalomyelitis, allergy, rhinitis, hyperglycemia, osteoporosis, arachidonic acid (AA), leukotrienes (LTs), hydroxy-eicosatetraenoic acids (HETEs), 15-lipoxygenase (LO), phorbol ester TPA, thromboxane (TX), rhodopsin, prostanoids, allergic, keratinocytes (KCs), dendritic cells (DCs), Langerhans cells (LCs), dermal DCs (dDCs), lipopolysaccharide (LPS), anti-inflammatory drugs (NSAIDs), ibuprofen piconol, Propionibacterium acnes, contact hypersensitivity (CHS) model, Schistosoma mansoni, lymph nodes, T helper type 2, ovalbumin-induced, polymorphism analysis of the human DP gene (PTGDR), aspirin-induced asthmatic attacks (AIA), Rheumatoid arthritis (RA), synovial hyperplasia, collageninduced arthritis (CIA), synovial fibroblasts, experimental encephalomyelitis (EAE), psoriasis, rheumatoid arthritis