Nitric Oxide Sustains IL-1β Expression in Human Dendritic Cells Enhancing Their Capacity to Induce IL-17–Producing T-Cells
The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate,...
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| Abstract | The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate, prior to exposure to lipopolysaccharide (LPS). Dose-and time-dependent experiments were performed with DCs with the aim of measuring the release and gene expression of inflammatory cytokines capable of modifying T-cell differentiation, towardsTh1, Th2 and Th17 cells. NO changed the pattern of cytokine release by LPS-matured DCs, dependent on the concentration of NO, as well as on the timing of its addition to the cells during maturation. Addition of NO before LPS-induced maturation strongly inhibited the release of IL-12, while increasing the expression and release of IL-23, IL-1β and IL-6, which are all involved in Th17 polarization. Indeed, DCs treated with NO efficiently induced the release of IL-17 by T-cells through IL-1β. Our work highlights the important role that NO may play in sustaining inflammation during an infection through the preferential differentiation of the Th17 lineage. |
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| AbstractList | The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate, prior to exposure to lipopolysaccharide (LPS). Dose-and time-dependent experiments were performed with DCs with the aim of measuring the release and gene expression of inflammatory cytokines capable of modifying T-cell differentiation, towardsTh1, Th2 and Th17 cells. NO changed the pattern of cytokine release by LPS-matured DCs, dependent on the concentration of NO, as well as on the timing of its addition to the cells during maturation. Addition of NO before LPS-induced maturation strongly inhibited the release of IL-12, while increasing the expression and release of IL-23, IL-1β and IL-6, which are all involved in Th17 polarization. Indeed, DCs treated with NO efficiently induced the release of IL-17 by T-cells through IL-1β. Our work highlights the important role that NO may play in sustaining inflammation during an infection through the preferential differentiation of the Th17 lineage. The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate, prior to exposure to lipopolysaccharide (LPS). Dose-and time-dependent experiments were performed with DCs with the aim of measuring the release and gene expression of inflammatory cytokines capable of modifying T-cell differentiation, towardsTh1, Th2 and Th17 cells. NO changed the pattern of cytokine release by LPS-matured DCs, dependent on the concentration of NO, as well as on the timing of its addition to the cells during maturation. Addition of NO before LPS-induced maturation strongly inhibited the release of IL-12, while increasing the expression and release of IL-23, IL-1β and IL-6, which are all involved in Th17 polarization. Indeed, DCs treated with NO efficiently induced the release of IL-17 by T-cells through IL-1β. Our work highlights the important role that NO may play in sustaining inflammation during an infection through the preferential differentiation of the Th17 lineage.The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate, prior to exposure to lipopolysaccharide (LPS). Dose-and time-dependent experiments were performed with DCs with the aim of measuring the release and gene expression of inflammatory cytokines capable of modifying T-cell differentiation, towardsTh1, Th2 and Th17 cells. NO changed the pattern of cytokine release by LPS-matured DCs, dependent on the concentration of NO, as well as on the timing of its addition to the cells during maturation. Addition of NO before LPS-induced maturation strongly inhibited the release of IL-12, while increasing the expression and release of IL-23, IL-1β and IL-6, which are all involved in Th17 polarization. Indeed, DCs treated with NO efficiently induced the release of IL-17 by T-cells through IL-1β. Our work highlights the important role that NO may play in sustaining inflammation during an infection through the preferential differentiation of the Th17 lineage. |
| Author | Nicod, Laurent P. Chung, Kian Fan Graf, Lukas Cesson, Valerie Obregon, Carolina |
| AuthorAffiliation | 2 Clinic and Polyclinic of Pneumology, University Hospital of Bern, Bern, Switzerland University Medical Center Freiburg, GERMANY 1 Pneumology Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland 3 Airways Disease Section, National Heart & Lung Institute, Imperial College, London, United Kingdom |
| AuthorAffiliation_xml | – name: University Medical Center Freiburg, GERMANY – name: 1 Pneumology Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland – name: 2 Clinic and Polyclinic of Pneumology, University Hospital of Bern, Bern, Switzerland – name: 3 Airways Disease Section, National Heart & Lung Institute, Imperial College, London, United Kingdom |
| Author_xml | – sequence: 1 givenname: Carolina surname: Obregon fullname: Obregon, Carolina – sequence: 2 givenname: Lukas surname: Graf fullname: Graf, Lukas – sequence: 3 givenname: Kian Fan surname: Chung fullname: Chung, Kian Fan – sequence: 4 givenname: Valerie surname: Cesson fullname: Cesson, Valerie – sequence: 5 givenname: Laurent P. surname: Nicod fullname: Nicod, Laurent P. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25853810$$D View this record in MEDLINE/PubMed |
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| Copyright | 2015 Obregon et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2015 Obregon et al 2015 Obregon et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: CO LN. Performed the experiments: LG VC CO. Analyzed the data: LG VC CO KFC. Contributed reagents/materials/analysis tools: CO LN. Wrote the paper: KFC CO LN VC LG. Competing Interests: The authors have declared that no competing interests exist. |
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| SubjectTerms | Alkenes - pharmacology Antigens Benzoates - pharmacology Cell differentiation Cytokines Dendritic cells Dendritic Cells - drug effects Dendritic Cells - immunology Dendritic Cells - metabolism Differentiation (biology) Dose-Response Relationship, Drug Gene expression Gene Expression Regulation - drug effects Helper cells Humans Imidazoles - pharmacology Inflammation Interleukin 12 Interleukin 17 Interleukin 23 Interleukin 6 Interleukin-17 - biosynthesis Interleukin-17 - metabolism Interleukin-1beta - genetics Lipopolysaccharides Lungs Lymphocytes T Maturation Nitric oxide Nitric Oxide - pharmacology Redox properties T-Lymphocytes - drug effects T-Lymphocytes - immunology T-Lymphocytes - metabolism Time Factors |
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| Title | Nitric Oxide Sustains IL-1β Expression in Human Dendritic Cells Enhancing Their Capacity to Induce IL-17–Producing T-Cells |
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