Prostaglandin E2 is required for ultraviolet B-induced skin inflammation via EP2 and EP4 receptors
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چکیده
منابع مشابه
Prostaglandin E2 is generally required for human dendritic cell migration and exerts its effect via EP2 and EP4 receptors.
The control of dendritic cell (DC) migration is pivotal for the initiation of cellular immune responses. In this study, we demonstrate that the migration of human monocyte-derived (Mo)DCs as well as of ex vivo peripheral blood DCs toward CCL21, CXCL12, and C5a is stringently dependent on the presence of the proinflammatory mediator PGE2, although DCs expressed CXCR4 and C5aR on their surface an...
متن کاملPotential therapeutic interventions via EP2/EP4 prostaglandin receptors.
Prevention and treatment of pathological inflammatory processes requires application of various classes of immune suppressors, such as calcineurin inhibitors, steroids and non-steroid inhibitors of prostaglandin synthesis. However, each type of these immune suppressors causes less or more serious adverse side-effects. Exploration of the role played by prostanoids in the immune response and iden...
متن کاملProstaglandin E2 Prevents Hyperosmolar-Induced Human Mast Cell Activation through Prostanoid Receptors EP2 and EP4
BACKGROUND Mast cells play a critical role in allergic and inflammatory diseases, including exercise-induced bronchoconstriction (EIB) in asthma. The mechanism underlying EIB is probably related to increased airway fluid osmolarity that activates mast cells to the release inflammatory mediators. These mediators then act on bronchial smooth muscle to cause bronchoconstriction. In parallel, prote...
متن کاملCyclooxygenase-2 inhibits UVB-induced apoptosis in mouse skin by activating the prostaglandin E2 receptors, EP2 and EP4.
Cyclooxygenase-2 (COX-2) is induced by UVB light and reduces UVB-induced epidermal apoptosis; however, the mechanism is unclear. Therefore, wild-type (WT) and COX-2-/- mice were acutely treated with UVB (5 kJ/m(2)), and apoptotic signaling pathways were compared. Following exposure, apoptosis was 2.5-fold higher in COX-2-/- compared with WT mice. Because prostaglandin E(2) (PGE(2)) is the major...
متن کاملProstaglandin E2 modulates dendritic cell function via EP2 and EP4 receptor subtypes.
We have reported previously that PGE(2) inhibits dendritic cells (DC) functions. Because E prostanoid receptor (EPR) subtypes involved in this action are unknown, expression and functions of these receptors were examined in DC. Western blot and flow cytometry analyses showed that all EPRs were coexpressed in DC. In a dose-dependent manner, lipopolysaccharide (LPS) enhanced EP(2)R/EP(4)R but not...
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ژورنال
عنوان ژورنال: Laboratory Investigation
سال: 2006
ISSN: 0023-6837,1530-0307
DOI: 10.1038/labinvest.3700491