المؤلفون: Couderc, Elodie, Morel, Franck, Levillain, Pierre, Buffière-Morgado, Amandine, Camus, Magalie, Paquier, Camille, Bodet, Charles, Jégou, Jean-François, Pohin, Mathilde, Favot, Laure, Garcia, Martine, Huguier, Vincent, Mcheik, Jiad, Lacombe, Corinne, Yssel, Hans, Guillet, Gérard, Bernard, François-Xavier, Lecron, Jean-Claude

المصدر: PLoS ONE; 7/14/2017, Vol. 12 Issue 7, p1-13, 13p

مصطلحات موضوعية: INTERLEUKIN-17, BLOOD serum analysis, AMYLOID, KERATINOCYTES, PSORIASIS, THERAPEUTICS

مستخلص: 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. [ABSTRACT FROM AUTHOR]

: Copyright of PLoS ONE is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Weiss, Robert A., Guillet, Gerard Y.A., Freedberg, Irwin M., Farmer, Evan R., Small, Elizabeth A., Weiss, Margaret M., Sun, Tung-Tien

المصدر: Journal of Investigative Dermatology ; volume 81, issue 3, page 224-230 ; ISSN 0022-202X

مصطلحات موضوعية: Cell Biology, Dermatology, Molecular Biology, Biochemistry

الإتاحة: https://doi.org/10.1111/1523-1747.ep12518198Test
https://api.elsevier.com/content/article/PII:S0022202X15431720?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0022202X15431720?httpAccept=text/plainTest

المؤلفون: Guillet, Gérard, Braun, Lundy, Shah, Keerti, Ferenczy, Alex

المصدر: Journal of Investigative Dermatology ; volume 81, issue 6, page 513-516 ; ISSN 0022-202X

مصطلحات موضوعية: Cell Biology, Dermatology, Molecular Biology, Biochemistry

الإتاحة: https://doi.org/10.1111/1523-1747.ep12522852Test
https://api.elsevier.com/content/article/PII:S0022202X15432506?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0022202X15432506?httpAccept=text/plainTest

المؤلفون: Rabeony, Hanitriniaina, Petit-Paris, Isabelle, Garnier, Julien, Barrault, Christine, Pedretti, Nathalie, Guilloteau, Karline, Jegou, Jean-François, Guillet, Gérard, Huguier, Vincent, Lecron, Jean-Claude, Bernard, François-Xavier, Morel, Franck

المصدر: PLoS ONE; Jul2014, Vol. 9 Issue 7, p1-8, 8p

مصطلحات موضوعية: KERATINOCYTES, INTERLEUKIN-17, INTERLEUKIN-22, TUMOR necrosis factors, ONCOSTATIN M, CELL differentiation

مستخلص: Keratinocyte differentiation program leading to an organized epidermis plays a key role in maintaining the first line of defense of the skin. Epidermal integrity is regulated by a tight communication between keratinocytes and leucocytes, particularly under cytokine control. Imbalance of the cytokine network leads to inflammatory diseases such as psoriasis. Our attempt to model skin inflammation showed that the combination of IL-17A, IL-22, IL-1α, OSM and TNFα (Mix M5) synergistically increases chemokine and antimicrobial-peptide expression, recapitulating some features of psoriasis. Other characteristics of psoriasis are acanthosis and down-regulation of keratinocyte differentiation markers. Our aim was to characterize the specific roles of these cytokines on keratinocyte differentiation, and to compare with psoriatic lesion features. All cytokines decrease keratinocyte differentiation markers, but IL-22 and OSM were the most powerful, and the M5 strongly synergized the effects. In addition, IL-22 and OSM induced epidermal hyperplasia in vitro and M5 induced epidermal thickening and decreased differentiation marker expression in a mouse model, as observed in human psoriatic skin lesions. This study highlights the precise role of cytokines in the skin inflammatory response. IL-22 and OSM more specifically drive epidermal hyperplasia and differentiation loss while IL-1α, IL-17A and TNFα were more involved in the activation of innate immunity. [ABSTRACT FROM AUTHOR]

: Copyright of PLoS ONE is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)