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  1. Article ; Online: Mannitol triggers mast cell-dependent contractions of human small bronchi and prostacyclin bronchoprotection.

    Säfholm, Jesper / Manson, Martijn L / Bood, Johan / Al-Ameri, Mamdoh / Orre, Ann-Charlotte / Raud, Johan / Dahlén, Sven-Erik / Adner, Mikael

    The Journal of allergy and clinical immunology

    2019  Volume 144, Issue 4, Page(s) 984–992

    Abstract: Background: Clinical research supports that exercise-induced bronchoconstriction (EIB) is caused by hyperosmolar triggering of mast cells. The reaction can be mimicked by inhalation of mannitol, but it has paradoxically previously not been possible to ... ...

    Abstract Background: Clinical research supports that exercise-induced bronchoconstriction (EIB) is caused by hyperosmolar triggering of mast cells. The reaction can be mimicked by inhalation of mannitol, but it has paradoxically previously not been possible to replicate this mode of action of mannitol in isolated airways.
    Objective: We sought to establish an ex vivo model of EIB in human small bronchi.
    Methods: Small bronchi (inner diameter, 0.5-2 mm) from macroscopically healthy human lung tissue were obtained from 48 patients and mounted in organ baths. Contractions and mediator release were analyzed after challenge with hyperosmolar mannitol (850 mOsm).
    Results: Ten minutes of exposure to mannitol caused a small initial contraction (12% ± 1% of maximum) that was followed by a second and much larger contraction (maximum effect [E
    Conclusion: This new protocol established an in vitro model for studies of EIB in isolated human bronchi. The IP receptor might be a new target for asthma treatment.
    MeSH term(s) Asthma, Exercise-Induced/chemically induced ; Asthma, Exercise-Induced/metabolism ; Bronchi/drug effects ; Bronchial Provocation Tests/methods ; Bronchoconstriction/drug effects ; Epoprostenol/metabolism ; Humans ; Mannitol/pharmacology ; Mast Cells/drug effects ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects ; Organ Culture Techniques ; Receptors, Epoprostenol/metabolism
    Chemical Substances PTGIR protein, human ; Receptors, Epoprostenol ; Mannitol (3OWL53L36A) ; Epoprostenol (DCR9Z582X0)
    Language English
    Publishing date 2019-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2019.04.031
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  2. Article ; Online: Leukotriene E

    Lazarinis, Nikolaos / Bood, Johan / Gomez, Cristina / Kolmert, Johan / Lantz, Ann-Sofie / Gyllfors, Pär / Davis, Andy / Wheelock, Craig E / Dahlén, Sven-Erik / Dahlén, Barbro

    The Journal of allergy and clinical immunology

    2018  Volume 142, Issue 4, Page(s) 1080–1089

    Abstract: Background: Leukotriene (LT) E: Objective: We tested this hypothesis by assessing the influence of the CysLT: Methods: Fourteen patients with mild intermittent asthma and 2 patients with aspirin-exacerbated respiratory disease received 20 mg of ... ...

    Abstract Background: Leukotriene (LT) E
    Objective: We tested this hypothesis by assessing the influence of the CysLT
    Methods: Fourteen patients with mild intermittent asthma and 2 patients with aspirin-exacerbated respiratory disease received 20 mg of montelukast twice daily and placebo for 5 to 7 days in a randomized, double-blind, crossover study (NCT01841164). The PD
    Results: Montelukast completely blocked LTE
    Conclusion: LTE
    MeSH term(s) Acetates/therapeutic use ; Adult ; Aspirin/adverse effects ; Asthma/drug therapy ; Asthma/physiopathology ; Asthma/urine ; Bronchoconstriction/drug effects ; Bronchoconstrictor Agents/administration & dosage ; Bronchoconstrictor Agents/urine ; Cross-Over Studies ; Double-Blind Method ; Eicosanoids/administration & dosage ; Eicosanoids/urine ; Female ; Humans ; Leukotriene Antagonists/therapeutic use ; Male ; Mast Cells/drug effects ; Mast Cells/physiology ; Middle Aged ; Quinolines/therapeutic use ; Receptors, Leukotriene/physiology ; Young Adult
    Chemical Substances Acetates ; Bronchoconstrictor Agents ; Eicosanoids ; Leukotriene Antagonists ; Quinolines ; Receptors, Leukotriene ; leukotriene D4 receptor (LRF7RW46ID) ; montelukast (MHM278SD3E) ; Aspirin (R16CO5Y76E)
    Language English
    Publishing date 2018-03-05
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2018.02.024
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  3. Article ; Online: Urinary excretion of lipid mediators in response to repeated eucapnic voluntary hyperpnea in asthmatic subjects.

    Bood, Johan R / Sundblad, Britt-Marie / Delin, Ingrid / Sjödin, Marcus / Larsson, Kjell / Anderson, Sandra D / Wheelock, Craig E / Dahlén, Sven-Erik / Dahlén, Barbro

    Journal of applied physiology (Bethesda, Md. : 1985)

    2015  Volume 119, Issue 3, Page(s) 272–279

    Abstract: Exercise-induced bronchoconstriction displays refractoriness manifested as a decreased response to repeated exercise challenge within hours. The refractoriness may be attenuated by inhibition of the biosynthesis of prostaglandins (PG). The aim of the ... ...

    Abstract Exercise-induced bronchoconstriction displays refractoriness manifested as a decreased response to repeated exercise challenge within hours. The refractoriness may be attenuated by inhibition of the biosynthesis of prostaglandins (PG). The aim of the study was to determine which PGs and other lipid mediators are excreted during the refractory period. First, 16 subjects with mild stable asthma performed two repeated 4-min challenges with eucapnic voluntary hyperpnea (EVH) 1 and 3 h apart. There was a similar degree of refractoriness in both protocols (∼15% protection). The 1-h interval was too short to study mediator excretion because the urinary levels did not return to baseline before the second challenge. With the 3-h protocol, there was increased urinary excretion of cysteinyl-leukotrienes and metabolites of the mast cell product PGD2 after both challenges. Next, another eight subjects performed two 6-min challenges with EVH 3 h apart, which produced a greater bronchoconstrictor response than the 4-min protocol (30.0 ± 5.4 vs. 17.7 ± 1.5%; P = 0.0029) and a greater degree of refractoriness (∼30%). Analysis by ultra-performance liquid chromatography triple quadrupole mass spectrometry confirmed excretion of the bronchoconstrictor cysteinyl-leukotrienes and PGD2 during both challenges. In addition, there was increased excretion of the bronchoprotective PGE2, and also of the main metabolite of PGI2. This is the first report of excretion of PGE2 and PGI2 during the refractory period to EVH challenge, suggesting that they may mediate the refractoriness. Maintained excretion of PGD2 and leukotriene E4 following the repeat challenge argues against mast cell mediator depletion as the mechanism of refractoriness.
    MeSH term(s) Adult ; Asthma/urine ; Biomarkers/urine ; Bronchial Provocation Tests/methods ; Bronchoconstriction ; Female ; Humans ; Lipid Metabolism ; Lipids/urine ; Male ; Middle Aged ; Prostaglandins/urine ; Respiratory Mechanics ; Urination ; Young Adult
    Chemical Substances Biomarkers ; Lipids ; Prostaglandins
    Language English
    Publishing date 2015-08-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219139-8
    ISSN 1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
    ISSN (online) 1522-1601
    ISSN 0021-8987 ; 0161-7567 ; 8750-7587
    DOI 10.1152/japplphysiol.00301.2015
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  4. Article ; Online: Prostaglandin E2 inhibits mast cell-dependent bronchoconstriction in human small airways through the E prostanoid subtype 2 receptor.

    Säfholm, Jesper / Manson, Martijn L / Bood, Johan / Delin, Ingrid / Orre, Ann-Charlotte / Bergman, Per / Al-Ameri, Mamdoh / Dahlén, Sven-Erik / Adner, Mikael

    The Journal of allergy and clinical immunology

    2015  Volume 136, Issue 5, Page(s) 1232–9.e1

    Abstract: Background: Inhaled prostaglandin (PG) E2 might inhibit asthmatic responses, but the mechanisms involved remain undefined.: Objective: We sought to characterize the direct and indirect effects of PGE2 on human small airways with particular reference ... ...

    Abstract Background: Inhaled prostaglandin (PG) E2 might inhibit asthmatic responses, but the mechanisms involved remain undefined.
    Objective: We sought to characterize the direct and indirect effects of PGE2 on human small airways with particular reference to the receptors mediating the responses.
    Methods: Contraction and relaxation were studied in isolated human bronchi with an inner diameter of 1 mm or less.
    Results: Low concentrations of PGE2 (0.01-1 μmol/L) relaxed the bronchi precontracted by histamine. The bronchodilator response was inhibited by the E prostanoid (EP) subtype 4 receptor antagonist ONO-AE3-208 but unaffected by the EP2 receptor antagonist PF-04418948. Higher concentrations of PGE2 (10-100 μmol/L) contracted the small airways. However, the TP receptor agonists U-46,619, PGF2α, and PGD2 were more potent than PGE2. Moreover, the bronchoconstrictor responses to PGE2 and all other tested prostanoids, including the EP1/EP3 receptor agonist 17-phenyl trinor PGE2 and the partial FP receptor agonist AL-8810, were uniformly abolished by the TP receptor antagonist SQ-29,548. In the presence of TP and EP4 antagonists, PGE2 inhibited the mast cell-mediated bronchoconstriction resulting from anti-IgE challenge. Measurement of the release of histamine and cysteinyl leukotrienes documented that this bronchoprotective action of PGE2 was mediated by the EP2 receptor, unrelated to bronchodilation, and increased with time of exposure.
    Conclusion: The pharmacology of PGE2 in isolated human small airways was different from its profile in animal models. This first demonstration of powerful EP2 receptor-mediated inhibition of IgE-dependent contractions in human airways introduces a new selective target for the treatment of asthma. This EP2 control of mast cell-mediated bronchoconstriction is presumably exaggerated in patients with aspirin-exacerbated respiratory disease.
    MeSH term(s) 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology ; Asthma/drug therapy ; Asthma/metabolism ; Azetidines/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic ; Bronchi/drug effects ; Bronchi/immunology ; Bronchi/pathology ; Bronchoconstriction/drug effects ; Cells, Cultured ; Dinoprost/analogs & derivatives ; Dinoprost/pharmacology ; Dinoprostone/analogs & derivatives ; Dinoprostone/pharmacology ; Fatty Acids, Unsaturated ; Histamine/metabolism ; Humans ; Hydrazines/pharmacology ; Immunoglobulin E/immunology ; In Vitro Techniques ; Mast Cells/immunology ; Molecular Targeted Therapy ; Naphthalenes/pharmacology ; Phenylbutyrates/pharmacology ; Prostaglandin D2/pharmacology ; Receptors, Prostaglandin/agonists ; Receptors, Prostaglandin E, EP1 Subtype/agonists ; Receptors, Prostaglandin E, EP2 Subtype/antagonists & inhibitors ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & inhibitors ; Receptors, Thromboxane/agonists ; Receptors, Thromboxane/antagonists & inhibitors
    Chemical Substances 17-phenyltrinorprostaglandin E2 ; 4-(4-cyano-2-(2-(4-fluoronaphthalen-1-yl)propionylamino)phenyl)butyric acid ; Azetidines ; Bridged Bicyclo Compounds, Heterocyclic ; Fatty Acids, Unsaturated ; Hydrazines ; Naphthalenes ; PTGER4 protein, human ; Phenylbutyrates ; Receptors, Prostaglandin ; Receptors, Prostaglandin E, EP1 Subtype ; Receptors, Prostaglandin E, EP2 Subtype ; Receptors, Prostaglandin E, EP4 Subtype ; Receptors, Thromboxane ; prostaglandin F2alpha receptor ; AL 8810 (12QE8J6004) ; Immunoglobulin E (37341-29-0) ; 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid (76898-47-0) ; Histamine (820484N8I3) ; SQ 29548 (88SD2J5ZNX) ; Dinoprost (B7IN85G1HY) ; 1-(4-fluorobenzoyl)-3-(((6-methoxy-2-naphthyl)oxy)methyl)azetidine-3-carboxylic acid (I7Z38E70VF) ; Dinoprostone (K7Q1JQR04M) ; Prostaglandin D2 (RXY07S6CZ2)
    Language English
    Publishing date 2015-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2015.04.002
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  5. Article ; Online: The effect of omega-3 fatty acids on bronchial hyperresponsiveness, sputum eosinophilia, and mast cell mediators in asthma.

    Brannan, John D / Bood, Johan / Alkhabaz, Ahmad / Balgoma, David / Otis, Joceline / Delin, Ingrid / Dahlén, Barbro / Wheelock, Craig E / Nair, Parameswaran / Dahlén, Sven-Erik / O'Byrne, Paul M

    Chest

    2014  Volume 147, Issue 2, Page(s) 397–405

    Abstract: Background: Omega-3 fatty acid supplements have been reported to inhibit exercise-induced bronchoconstriction (EIB). It has not been determined whether omega-3 supplements inhibit airway sensitivity to inhaled mannitol, a test for bronchial ... ...

    Abstract Background: Omega-3 fatty acid supplements have been reported to inhibit exercise-induced bronchoconstriction (EIB). It has not been determined whether omega-3 supplements inhibit airway sensitivity to inhaled mannitol, a test for bronchial hyperresponsiveness (BHR) and model for EIB in people with mild to moderate asthma.
    Methods: In a double-blind, crossover trial, subjects with asthma who had BHR to inhaled mannitol (n = 23; 14 men; mean age, 28 years; one-half taking regular inhaled corticosteroids) were randomized to omega-3 supplements (4.0 g/d eicosapentaenoic acid and 2.0 g/d docosahexaenoic acid) or matching placebo for 3 weeks separated by a 3-week washout. The primary outcome was the provoking dose of mannitol (mg) to cause a 15% fall in FEV1 (PD15). Secondary outcomes were sputum eosinophil count, spirometry, Asthma Control Questionnaire (ACQ) score, serum triacylglyceride level, and lipid mediator profile in urine and serum.
    Results: PD15 (geometric mean, 95% CI) to mannitol following supplementation with omega-3s (78 mg, 51-119 mg) was not different from placebo (88 mg, 56-139 mg, P = .5). There were no changes in sputum eosinophils (mean ± SD) in a subgroup of 11 subjects (omega-3, 8.4% ± 8.2%; placebo, 7.8% ± 11.8%; P = .9). At the end of each treatment period, there were no differences in FEV1 % predicted (omega-3, 85% ± 13%; placebo, 84% ± 11%; P = .9) or ACQ score (omega-3, 1.1% ± 0.5%; placebo, 1.1% ± 0.5%; P = .9) (n = 23). Omega-3s caused significant lowering of blood triglyceride levels and expected shifts in serum fatty acids and eicosanoid metabolites, confirming adherence to the supplements; however, no changes were observed in urinary mast cell mediators.
    Conclusions: Three weeks of omega-3 supplements does not improve BHR to mannitol, decrease sputum eosinophil counts, or inhibit urinary excretion of mast cell mediators in people with mild to moderate asthma, indicating that dietary omega-3 supplementation is not useful in the short-term treatment of asthma.
    Trial registry: ClinicalTrials.gov; No.: NCT00526357; URL: www.clinicaltrials.gov.
    MeSH term(s) Adult ; Asthma/physiopathology ; Bronchial Hyperreactivity/drug therapy ; Cross-Over Studies ; Dietary Supplements ; Dose-Response Relationship, Drug ; Double-Blind Method ; Eosinophilia/drug therapy ; Eosinophils ; Fatty Acids, Omega-3/metabolism ; Fatty Acids, Omega-3/pharmacology ; Fatty Acids, Omega-3/therapeutic use ; Female ; Forced Expiratory Volume ; Humans ; Leukocyte Count ; Male ; Mannitol/administration & dosage ; Mast Cells/physiology ; Sputum/cytology ; Triglycerides/blood ; Young Adult
    Chemical Substances Fatty Acids, Omega-3 ; Triglycerides ; Mannitol (3OWL53L36A)
    Language English
    Publishing date 2014-10-16
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.14-1214
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  6. Article ; Online: Urinary Leukotriene E

    Kolmert, Johan / Gómez, Cristina / Balgoma, David / Sjödin, Marcus / Bood, Johan / Konradsen, Jon R / Ericsson, Magnus / Thörngren, John-Olof / James, Anna / Mikus, Maria / Sousa, Ana R / Riley, John H / Bates, Stewart / Bakke, Per S / Pandis, Ioannis / Caruso, Massimo / Chanez, Pascal / Fowler, Stephen J / Geiser, Thomas /
    Howarth, Peter / Horváth, Ildikó / Krug, Norbert / Montuschi, Paolo / Sanak, Marek / Behndig, Annelie / Shaw, Dominick E / Knowles, Richard G / Holweg, Cécile T J / Wheelock, Åsa M / Dahlén, Barbro / Nordlund, Björn / Alving, Kjell / Hedlin, Gunilla / Chung, Kian Fan / Adcock, Ian M / Sterk, Peter J / Djukanovic, Ratko / Dahlén, Sven-Erik / Wheelock, Craig E

    American journal of respiratory and critical care medicine

    2020  Volume 203, Issue 1, Page(s) 37–53

    Abstract: Rationale: ...

    Abstract Rationale:
    MeSH term(s) Adult ; Asthma/metabolism ; Asthma/physiopathology ; Biomarkers/urine ; Female ; Humans ; Inflammation/metabolism ; Inflammation/physiopathology ; Leukotriene E4/metabolism ; Leukotriene E4/urine ; Male ; Middle Aged ; Prostaglandins/metabolism ; Prostaglandins/urine
    Chemical Substances Biomarkers ; Prostaglandins ; Leukotriene E4 (75715-89-8)
    Language English
    Publishing date 2020-07-14
    Publishing country United States
    Document type Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201909-1869OC
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