Interleukin-17A-induced production of acute serum amyloid A by keratinocytes contributes to psoriasis pathogenesis
Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines. We investigate...
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| Published in | PloS one Vol. 12; no. 7; p. e0181486 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
14.07.2017
Public Library of Science (PLoS) |
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| Abstract | Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines.
We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients.
NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay.
IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed.
Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. |
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| AbstractList | Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines.
We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients.
NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay.
IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed.
Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines.We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients.NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay.IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed.Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-[kappa]B, C/EBP[beta], STAT3 activated by proinflammatory cytokines. We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients. NHEK were stimulated by A-SAA or the cytokines IL-1[alpha], IL-17A, IL-22, OSM, TNF-[alpha] alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay. IL-1[alpha], TNF-[alpha] and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed. Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. Background Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-[kappa]B, C/EBP[beta], STAT3 activated by proinflammatory cytokines. Objectives We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients. Methods NHEK were stimulated by A-SAA or the cytokines IL-1[alpha], IL-17A, IL-22, OSM, TNF-[alpha] alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay. Results IL-1[alpha], TNF-[alpha] and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed. Conclusion Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. Background Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines. Objectives We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients. Methods NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay. Results IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed. Conclusion Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. Background Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines. Objectives We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients. Methods NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay. Results IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed. Conclusion Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. BACKGROUNDAcute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPβ, STAT3 activated by proinflammatory cytokines.OBJECTIVESWe investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients.METHODSNHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay.RESULTSIL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed.CONCLUSIONKeratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment. |
| Audience | Academic |
| Author | Couderc, Elodie Lacombe, Corinne Camus, Magalie Guillet, Gérard Lecron, Jean-Claude Favot, Laure Mcheik, Jiad Morel, Franck Garcia, Martine Bernard, François-Xavier Levillain, Pierre Buffière-Morgado, Amandine Huguier, Vincent Jégou, Jean-François Pohin, Mathilde Bodet, Charles Paquier, Camille Yssel, Hans |
| AuthorAffiliation | 6 Service d’Immunologie et Inflammation, CHU de Poitiers, Poitiers, France Centre National de la Recherche Scientifique, FRANCE 3 Service d’Anatomopathologie, CHU de Poitiers, Poitiers, France 4 Service de Chirurgie plastique, CHU de Poitiers, Poitiers, France 5 Service de Chirurgie pédiatrique, CHU de Poitiers, Poitiers, France 7 Centre d'Immunologie et des Maladies Infectieuses, Inserm U1135, Hôpital Pitié-Salpêtrière, Paris, France 8 Laboratoire BIOalternatives, Gencay, France 1 Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France 2 Service de Dermatologie, CHU de Poitiers, Poitiers, France |
| AuthorAffiliation_xml | – name: 4 Service de Chirurgie plastique, CHU de Poitiers, Poitiers, France – name: 2 Service de Dermatologie, CHU de Poitiers, Poitiers, France – name: 6 Service d’Immunologie et Inflammation, CHU de Poitiers, Poitiers, France – name: 7 Centre d'Immunologie et des Maladies Infectieuses, Inserm U1135, Hôpital Pitié-Salpêtrière, Paris, France – name: 1 Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – name: 3 Service d’Anatomopathologie, CHU de Poitiers, Poitiers, France – name: 8 Laboratoire BIOalternatives, Gencay, France – name: 5 Service de Chirurgie pédiatrique, CHU de Poitiers, Poitiers, France – name: Centre National de la Recherche Scientifique, FRANCE |
| Author_xml | – sequence: 1 givenname: Elodie surname: Couderc fullname: Couderc, Elodie organization: Service de Dermatologie, CHU de Poitiers, Poitiers, France – sequence: 2 givenname: Franck surname: Morel fullname: Morel, Franck organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 3 givenname: Pierre surname: Levillain fullname: Levillain, Pierre organization: Service d'Anatomopathologie, CHU de Poitiers, Poitiers, France – sequence: 4 givenname: Amandine surname: Buffière-Morgado fullname: Buffière-Morgado, Amandine organization: Service de Dermatologie, CHU de Poitiers, Poitiers, France – sequence: 5 givenname: Magalie surname: Camus fullname: Camus, Magalie organization: Service de Dermatologie, CHU de Poitiers, Poitiers, France – sequence: 6 givenname: Camille surname: Paquier fullname: Paquier, Camille organization: Service de Dermatologie, CHU de Poitiers, Poitiers, France – sequence: 7 givenname: Charles surname: Bodet fullname: Bodet, Charles organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 8 givenname: Jean-François surname: Jégou fullname: Jégou, Jean-François organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 9 givenname: Mathilde surname: Pohin fullname: Pohin, Mathilde organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 10 givenname: Laure surname: Favot fullname: Favot, Laure organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 11 givenname: Martine surname: Garcia fullname: Garcia, Martine organization: Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France – sequence: 12 givenname: Vincent surname: Huguier fullname: Huguier, Vincent organization: Service de Chirurgie plastique, CHU de Poitiers, Poitiers, France – sequence: 13 givenname: Jiad surname: Mcheik fullname: Mcheik, Jiad organization: Service de Chirurgie pédiatrique, CHU de Poitiers, Poitiers, France – sequence: 14 givenname: Corinne surname: Lacombe fullname: Lacombe, Corinne organization: Service d'Immunologie et Inflammation, CHU de Poitiers, Poitiers, France – sequence: 15 givenname: Hans surname: Yssel fullname: Yssel, Hans organization: Centre d'Immunologie et des Maladies Infectieuses, Inserm U1135, Hôpital Pitié-Salpêtrière, Paris, France – sequence: 16 givenname: Gérard surname: Guillet fullname: Guillet, Gérard organization: Service de Dermatologie, CHU de Poitiers, Poitiers, France – sequence: 17 givenname: François-Xavier surname: Bernard fullname: Bernard, François-Xavier organization: Laboratoire BIOalternatives, Gencay, France – sequence: 18 givenname: Jean-Claude orcidid: 0000-0003-3990-5213 surname: Lecron fullname: Lecron, Jean-Claude organization: Service d'Immunologie et Inflammation, CHU de Poitiers, Poitiers, France |
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| Copyright | COPYRIGHT 2017 Public Library of Science 2017 Couderc 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. Distributed under a Creative Commons Attribution 4.0 International License 2017 Couderc et al 2017 Couderc et al |
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| DOI | 10.1371/journal.pone.0181486 |
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| DocumentTitleAlternate | A-SAA in psoriasis pathogenesis |
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| Editor | Ryffel, Bernhard |
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| Keywords | expression differentiation secretion oncostatin-m Protein-coupled receptor binding cd36 skin inflammation kappa-b rheumatoid-arthritis |
| Language | English |
| License | Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Creative Commons Attribution License |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 PMCID: PMC5510841 Competing Interests: Regarding the role of the commercial company “BIOalternatives”, we confirmed that they participate in the study design and analysis of the data, and preparation of the manuscript, and that we have no competing interest. It can be fully considered as an academic collaboration. This commercial affiliation does not alter our adherence to all PLOS ONE policies on sharing data and materials. |
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| Snippet | Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been... Background Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin... BACKGROUNDAcute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin... Background; Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the... Background Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin... |
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| SubjectTerms | Acute phase proteins Acute phase substances Adaptive immunology Adult Aged Aminoquinolines - pharmacology Animals Assaying Atopic dermatitis Biochemistry, Molecular Biology Biology and Life Sciences CCAAT/enhancer-binding protein CCL20 protein CCR6 protein Cells, Cultured Chemokine CCL20 - metabolism Chemokine CCL20 - pharmacology Cream Cytokines Cytokines - genetics Cytokines - metabolism Dermatitis Dermatitis, Atopic - metabolism Dermatitis, Atopic - pathology Dermatology Disease Models, Animal Enzyme-linked immunosorbent assay Female Gene expression Genetic aspects Genomics Glycoproteins Helper cells Human health and pathology Humans Imiquimod Immunity Immunology Inflammation Inflammatory diseases Inflammatory response Innate immunity Interleukin Interleukin 1 Interleukin 22 Interleukin-17 Interleukin-17 - genetics Interleukin-17 - metabolism Interleukin-17 - pharmacology Keratinocytes Keratinocytes - cytology Keratinocytes - drug effects Keratinocytes - metabolism Life Sciences Ligands Liver Liver - drug effects Liver - metabolism Lymphocytes Lymphocytes T Male Medicine and Health Sciences Metabolism Mice Mice, Inbred C57BL Middle Aged Mimicry NF-κB protein Pathogenesis Patients Proteins Psoriasis Psoriasis - metabolism Psoriasis - pathology Receptors, CCR6 - metabolism Recombinant Proteins - biosynthesis Recombinant Proteins - isolation & purification Recombinant Proteins - pharmacology Recruitment Research and Analysis Methods Rodents Serum Amyloid A Protein - analysis Serum Amyloid A Protein - genetics Serum Amyloid A Protein - metabolism Skin Skin - drug effects Skin - metabolism Skin diseases Stimulation Synthesis Th17 Cells - cytology Th17 Cells - metabolism Transcription factors Tumor necrosis factor-TNF Up-Regulation - drug effects β-Amyloid |
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| Title | Interleukin-17A-induced production of acute serum amyloid A by keratinocytes contributes to psoriasis pathogenesis |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/28708859 https://www.proquest.com/docview/1919497409 https://search.proquest.com/docview/1920200032 https://hal.science/hal-01703911 https://pubmed.ncbi.nlm.nih.gov/PMC5510841 https://doaj.org/article/3f290c89fca648e39fea7fd29d34aa73 http://dx.doi.org/10.1371/journal.pone.0181486 |
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