Activation of the Prostaglandin E2 receptor EP2 prevents house dust mite‐induced airway hyperresponsiveness and inflammation by restraining mast cells’ activity

Prostaglandin E2 (PGE2) has been proposed to exert antiasthmatic effects in patients, to prevent antigen‐induced airway pathology in murine models, and to inhibit mast cells (MC) activity in vitro.

[1]  D. Aronoff,et al.  Prostaglandin E₂ suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells. , 2014, The Journal of allergy and clinical immunology.

[2]  N. Pullen,et al.  Characterization of the EP receptor subtype that mediates the inhibitory effects of prostaglandin E2 on IgE‐dependent secretion from human lung mast cells , 2013, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[3]  J. Mullol,et al.  Low prostaglandin E2 and cyclooxygenase expression in nasal mucosa fibroblasts of aspirin‐intolerant asthmatics , 2013, Respirology.

[4]  C. Bortner,et al.  Cyclooxygenase-2 inhibits T helper cell type 9 differentiation during allergic lung inflammation via down-regulation of IL-17RB. , 2013, American journal of respiratory and critical care medicine.

[5]  C. Picado,et al.  Locally administered prostaglandin E2 prevents aeroallergen-induced airway sensitization in mice through immunomodulatory mechanisms. , 2013, Pharmacological research.

[6]  A. Olivera,et al.  E‐prostanoid 2 receptors dampen mast cell degranulation via cAMP/PKA‐mediated suppression of IgE‐dependent signaling , 2012, Journal of leukocyte biology.

[7]  S. Wenzel.  Asthma phenotypes: the evolution from clinical to molecular approaches , 2012, Nature Medicine.

[8]  B. Koller,et al.  Prostaglandin E2 Produced by the Lung Augments the Effector Phase of Allergic Inflammation , 2012, The Journal of Immunology.

[9]  P. Kalinski.  Regulation of Immune Responses by Prostaglandin E2 , 2012, The Journal of Immunology.

[10]  J. Mullol,et al.  Reduced expression of COXs and production of prostaglandin E(2) in patients with nasal polyps with or without aspirin-intolerant asthma. , 2011, The Journal of allergy and clinical immunology.

[11]  D. Broide,et al.  Chronic allergen challenge induces bronchial mast cell accumulation in BALB/c but not C57BL/6 mice and is independent of IL-9 , 2010, Immunogenetics.

[12]  L. Pujols,et al.  Activity of the cyclooxygenase 2-prostaglandin-E prostanoid receptor pathway in mice exposed to house dust mite aeroallergens, and impact of exogenous prostaglandin E2 , 2009, Journal of Inflammation.

[13]  K. Austen,et al.  Innate cells and T helper 2 cell immunity in airway inflammation. , 2009, Immunity.

[14]  J. Foidart,et al.  Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production , 2009, Inflammation Research.

[15]  C. Picado,et al.  Un inhibidor selectivo de la ciclooxigenasa-2 empeora la función respiratoria y fomenta la actividad de los mastocitos en ratones sensibilizados a la ovalbúmina , 2009 .

[16]  C. Picado,et al.  [A cyclooxygenase-2 selective inhibitor worsens respiratory function and enhances mast cell activity in ovalbumin-sensitized mice]. , 2009, Archivos de bronconeumologia.

[17]  J. Roca‐Ferrer,et al.  Subcutaneous Prostaglandin E2 Restrains Airway Mast Cell Activity in vivo and Reduces Lung Eosinophilia and Th2 Cytokine Overproduction in House Dust Mite-Sensitive Mice , 2009, International Archives of Allergy and Immunology.

[18]  G. Sturm,et al.  Prostaglandin E2 Inhibits Eosinophil Trafficking through E-Prostanoid 2 Receptors1 , 2008, The Journal of Immunology.

[19]  C. Brightling,et al.  Engagement of the EP2 prostanoid receptor closes the K+ channel KCa3.1 in human lung mast cells and attenuates their migration , 2008, European journal of immunology.

[20]  S. Galli,et al.  Mast cell-derived TNF contributes to airway hyperreactivity, inflammation, and TH2 cytokine production in an asthma model in mice. , 2007, The Journal of allergy and clinical immunology.

[21]  Chunli Feng,et al.  Human mast cells express multiple EP receptors for prostaglandin E2 that differentially modulate activation responses. , 2006, Blood.

[22]  L. Kay,et al.  Prostaglandin E2 activates EP2 receptors to inhibit human lung mast cell degranulation , 2006, British journal of pharmacology.

[23]  J. Morrow,et al.  Allergen-induced airway hyperresponsiveness mediated by cyclooxygenase inhibition is not dependent on 5-lipoxygenase or IL-5, but is IL-13 dependent. , 2006, Journal of immunology.

[24]  J. Morrow,et al.  Allergen-Induced Airway Hyperresponsiveness Mediated by Cyclooxygenase Inhibition Is Not Dependent on 5-Lipoxygenase or IL-5, but Is IL-13 Dependent1 , 2005, The Journal of Immunology.

[25]  S. Narumiya,et al.  Suppression of allergic inflammation by the prostaglandin E receptor subtype EP3 , 2005, Nature Immunology.

[26]  K. Chung,et al.  Evaluation of Selective Prostaglandin E2 (PGE2) Receptor Agonists as Therapeutic Agents for the Treatment of Asthma , 2005, Science's STKE.

[27]  P. Henry,et al.  Stimulation of protease‐activated receptor‐2 inhibits airway eosinophilia, hyperresponsiveness and bronchoconstriction in a murine model of allergic inflammation , 2005, British journal of pharmacology.

[28]  K. Yamagata,et al.  Augmentation of allergic inflammation in the airways of cyclooxygenase‐2‐deficient mice , 2005, Respirology.

[29]  J. Morrow,et al.  Cyclooxygenase Inhibition Augments Allergic Inflammation through CD4-Dependent, STAT6-Independent Mechanisms1 , 2005, The Journal of Immunology.

[30]  M. Yacoub,et al.  Identification in human airways smooth muscle cells of the prostanoid receptor and signalling pathway through which PGE2 inhibits the release of GM‐CSF , 2004, British journal of pharmacology.

[31]  M. Sanak,et al.  Deficient prostaglandin E2 production by bronchial fibroblasts of asthmatic patients, with special reference to aspirin-induced asthma. , 2003, The Journal of allergy and clinical immunology.

[32]  M. Jordana,et al.  Intranasal exposure of mice to house dust mite elicits allergic airway inflammation via a GM-CSF-mediated mechanism , 2003 .

[33]  J. Morrow,et al.  Selective cyclooxygenase-1 and -2 inhibitors each increase allergic inflammation and airway hyperresponsiveness in mice. , 2002, American journal of respiratory and critical care medicine.

[34]  J. Moreau,et al.  FunctionsIL-10, Which Down-Regulates Dendritic Cell Enhances the Production of Endogenous 2 Cyclooxygenase-2-Issued Prostaglandin E , 2002 .

[35]  R. Tanaka,et al.  Noninvasive system for evaluating the allergen-specific airway response in a murine model of asthma. , 1999, Laboratory investigation; a journal of technical methods and pathology.

[36]  D. Zeldin,et al.  Allergic lung responses are increased in prostaglandin H synthase-deficient mice. , 1999, The Journal of clinical investigation.

[37]  J. Mullol,et al.  Cyclooxygenase-2 mRNA is downexpressed in nasal polyps from aspirin-sensitive asthmatics. , 1999, American journal of respiratory and critical care medicine.

[38]  E. Gelfand,et al.  Noninvasive measurement of airway responsiveness in allergic mice using barometric plethysmography. , 1997, American journal of respiratory and critical care medicine.

[39]  R. M. Refini,et al.  Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma. , 1996, American journal of respiratory and critical care medicine.

[40]  J. Shelhamer,et al.  Airway Inflammation , 1995, Annals of Internal Medicine.

[41]  P. O'Byrne,et al.  Effect of inhaled PGE2 on exercise-induced bronchoconstriction in asthmatic subjects. , 1994, American journal of respiratory and critical care medicine.

[42]  S. Galli,et al.  125I-fibrin deposition in IgE-dependent immediate hypersensitivity reactions in mouse skin. Demonstration of the role of mast cells using genetically mast cell-deficient mice locally reconstituted with cultured mast cells. , 1987, Journal of immunology.

[43]  P. Howarth,et al.  The mast cell as a primary effector cell in the pathogenesis of asthma. , 1986, The Journal of allergy and clinical immunology.

[44]  D. Katz,et al.  Monoclonal dinitrophenyl-specific murine IgE antibody: preparation, isolation, and characterization. , 1980, Journal of immunology.

[45]  C. Picado,et al.  The PGE2-EP2-mast cell axis: an antiasthma mechanism. , 2015, Molecular immunology.

[46]  M. Peters-Golden,et al.  Prostaglandin E 2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells , 2014 .

[47]  P. Barnes.  Severe asthma: advances in current management and future therapy. , 2012, The Journal of allergy and clinical immunology.

[48]  C. Vancheri,et al.  The lung as a privileged site for the beneficial actions of PGE2. , 2004, Trends in immunology.

[49]  P. O'Byrne,et al.  Protective effects of inhaled PGE2 on allergen-induced airway responses and airway inflammation. , 1999, American journal of respiratory and critical care medicine.

[50]  T. Standiford,et al.  Regulation of human alveolar macrophage- and blood monocyte-derived interleukin-8 by prostaglandin E2 and dexamethasone. , 1992, American journal of respiratory cell and molecular biology.