Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion
TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine I...
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| Published in | Journal of allergy and clinical immunology Vol. 132; no. 2; pp. 297 - 304.e3 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.08.2013
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10.
We sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2D3).
PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture.
Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2D3-mediated inhibition of the IL-17A response.
Patients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)2D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. |
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| AbstractList | TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10.
We sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2D3).
PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture.
Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2D3-mediated inhibition of the IL-17A response.
Patients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)2D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. Background TH 17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10. Objective We sought to investigate the production of the TH 17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2 D3). Methods PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2 D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH 17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture. Results Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2 D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2 D3-mediated inhibition of the IL-17A response. Conclusion Patients with severe asthma exhibit increased levels of TH 17 cytokines, which are not inhibited by steroids. 1,25(OH)2 D3 inhibits TH 17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. BACKGROUND: TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10. OBJECTIVE: We sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]₂D3). METHODS: PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)₂D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture. RESULTS: Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)₂D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)₂D3-mediated inhibition of the IL-17A response. CONCLUSION: Patients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)₂D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. Background: T sub(H)17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10. Objective: We sought to investigate the production of the T sub(H)17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1 alpha ,25-dihydroxyvitamin D3 (1,25[OH] sub(2)D3). Methods: PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH) sub(2)D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the T sub(H)17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture. Results: Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH) sub(2)D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH) sub(2)D3-mediated inhibition of the IL-17A response. Conclusion: Patients with severe asthma exhibit increased levels of T sub(H)17 cytokines, which are not inhibited by steroids. 1,25(OH) sub(2)D3 inhibits T sub(H)17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10.BACKGROUNDTH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10.We sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2D3).OBJECTIVEWe sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2D3).PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture.METHODSPBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture.Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2D3-mediated inhibition of the IL-17A response.RESULTSAsthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2D3-mediated inhibition of the IL-17A response.Patients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)2D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients.CONCLUSIONPatients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)2D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients. |
| Author | Timms, Peter M. Griffiths, Christopher J. Black, Cheryl Nanzer, Alexandra M. Richards, David F. Ryanna, Kimuli Corrigan, Christopher J. Hawrylowicz, Catherine M. Chambers, Emma S. Martineau, Adrian R. |
| Author_xml | – sequence: 1 givenname: Alexandra M. surname: Nanzer fullname: Nanzer, Alexandra M. organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 2 givenname: Emma S. surname: Chambers fullname: Chambers, Emma S. organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 3 givenname: Kimuli surname: Ryanna fullname: Ryanna, Kimuli organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 4 givenname: David F. surname: Richards fullname: Richards, David F. organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 5 givenname: Cheryl surname: Black fullname: Black, Cheryl organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 6 givenname: Peter M. surname: Timms fullname: Timms, Peter M. organization: Homerton University NHS Foundation Trust, London, United Kingdom – sequence: 7 givenname: Adrian R. surname: Martineau fullname: Martineau, Adrian R. organization: Centre for Primary Care and Public Health, Blizard Institute, Queen Mary, University of London, London, United Kingdom – sequence: 8 givenname: Christopher J. surname: Griffiths fullname: Griffiths, Christopher J. organization: Centre for Primary Care and Public Health, Blizard Institute, Queen Mary, University of London, London, United Kingdom – sequence: 9 givenname: Christopher J. surname: Corrigan fullname: Corrigan, Christopher J. organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom – sequence: 10 givenname: Catherine M. surname: Hawrylowicz fullname: Hawrylowicz, Catherine M. email: catherine.hawrylowicz@kcl.ac.uk organization: MRC and the Asthma UK Centre for Allergic Mechanisms in Asthma, King's College London, London, United Kingdom |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27609652$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/23683514$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2013 American Academy of Allergy, Asthma & Immunology American Academy of Allergy, Asthma & Immunology 2014 INIST-CNRS Copyright © 2013 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved. |
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| Keywords | SS IL-17A vitamin D Treg 1,25(OH)2D3 GR Asthma steroid resistant steroid sensitive glucocorticoids Foxp3 TH17 SR T H17 1α,25-Dihydroxyvitamin D3 Forkhead box protein 3 Glucocorticoid receptor Regulatory T 1,25(OH) 2D3 Human Steroid Immunopathology 17 Calcitriol Cytokine Biosynthesis Glucocorticoid Resistance Immunology Vitamin D T Inhibitor Severe asthma Th17 lymphocyte 1,25(OH)D3 T(H)17 Steroid resistant Steroid sensitive |
| Language | English |
| License | https://www.elsevier.com/tdm/userlicense/1.0 CC BY 4.0 Copyright © 2013 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved. |
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| Snippet | TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing... Background TH 17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a... Background: T sub(H)17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a... BACKGROUND: TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a... |
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| SubjectTerms | Adult Allergy and Immunology antagonists anti-inflammatory activity Asthma Asthma - drug therapy Asthma - immunology Asthma - physiopathology Biological and medical sciences Cells, Cultured dexamethasone Drug Resistance enzyme-linked immunosorbent assay Female flow cytometry Fundamental and applied biological sciences. Psychology Fundamental immunology glucocorticoids Glucocorticoids - pharmacology Glucocorticoids - therapeutic use Humans IL-17A interleukin-10 Interleukin-10 - biosynthesis Interleukin-10 - genetics interleukin-17 Interleukin-17 - biosynthesis Interleukin-17 - genetics Interleukin-22 Interleukins - biosynthesis Interleukins - genetics Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Lymphocyte Activation Male Medical sciences mononuclear leukocytes patients quantitative polymerase chain reaction Real-Time Polymerase Chain Reaction Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Severity of Illness Index steroid resistant steroid sensitive steroids TH17 Th17 Cells - immunology Th17 Cells - metabolism Up-Regulation vitamin D Vitamin D - analogs & derivatives Vitamin D - pharmacology Vitamin D - therapeutic use |
| Title | Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion |
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