التفاصيل البيبلوغرافية
| العنوان: |
Interleukin-17A-induced production of acute serum amyloid A by keratinocytes contributes to psoriasis pathogenesis. |
| المؤلفون: |
Couderc, Elodie1,2, Morel, Franck1, Levillain, Pierre3, Buffière-Morgado, Amandine1,2, Camus, Magalie1,2, Paquier, Camille1,2, Bodet, Charles1, Jégou, Jean-François1, Pohin, Mathilde1, Favot, Laure1, Garcia, Martine1, Huguier, Vincent1,2,3,4, Mcheik, Jiad1,2,3,4,5, Lacombe, Corinne3,6, Yssel, Hans7, Guillet, Gérard1,2, Bernard, François-Xavier8, Lecron, Jean-Claude1,6 Jean-Claude.Lecron@univ-poitiers.fr |
| 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] |
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