Effect of IFN-γ on the kynurenine/tryptophan ratio in monolayer-cultured keratinocytes and a 3D reconstructed human epidermis model.


Journal

Journal of dermatological science
ISSN: 1873-569X
Titre abrégé: J Dermatol Sci
Pays: Netherlands
ID NLM: 9011485

Informations de publication

Date de publication:
Sep 2020
Historique:
received: 16 03 2020
revised: 10 07 2020
accepted: 15 07 2020
pubmed: 13 8 2020
medline: 16 6 2021
entrez: 13 8 2020
Statut: ppublish

Résumé

Interferon-gamma (IFN-γ) represents a potent inducer for keratinocyte inflammatory and immune activation in vitro. Since tryptophan (trp) conversion to kynurenine (kyn) is involved in inflammation, the topical kyn/trp ratio may serve as a biomarker of skin inflammation. However, the trp metabolism in keratinocytes exposed to IFN-γ is not yet fully understood. The aim of this study was to establish a human epidermis model in order to quantify cytokine and kyn/trp secretion from IFN-γ stimulated cells and tissues. Moreover, to compare the cell response of 2D-cultured keratinocytes and the 3D epidermis model. Polycarbonate filters were used on which primary keratinocytes could attach and stratify in order to form the typical layers of reconstructed human epidermis (RHE). After IFN-γ treatment, secretion of kyn/trp was measured by high performance liquid chromatography. Gene and protein expression of indoleamine 2,3-dioxygenase 1 (IDO) was analyzed with real-time PCR and immunohistochemistry. The secretion of cytokines was quantified with ELISA. Trp catabolism to kyn was significantly increased (P < 0.01) in the 2D culture in response to IFN-γ treatment. Before kyn secretion, IDO was strongly upregulated (P < 0.001). IFN-γ treatment also increased the secretion of IL-6 and IL-8 from the keratinocytes. In the RHE, IDO was upregulated by IFN-γ, and kyn secretion could be detected. Interestingly, IDO expression was only present in the basal cells of the RHE. Our results suggest that IFN-γ acts as an inducer of trp degradation preferentially in undifferentiated keratinocytes, indicated by the IDO expression in the basal layer of the RHE.

Sections du résumé

BACKGROUND BACKGROUND
Interferon-gamma (IFN-γ) represents a potent inducer for keratinocyte inflammatory and immune activation in vitro. Since tryptophan (trp) conversion to kynurenine (kyn) is involved in inflammation, the topical kyn/trp ratio may serve as a biomarker of skin inflammation. However, the trp metabolism in keratinocytes exposed to IFN-γ is not yet fully understood.
OBJECTIVE OBJECTIVE
The aim of this study was to establish a human epidermis model in order to quantify cytokine and kyn/trp secretion from IFN-γ stimulated cells and tissues. Moreover, to compare the cell response of 2D-cultured keratinocytes and the 3D epidermis model.
METHODS METHODS
Polycarbonate filters were used on which primary keratinocytes could attach and stratify in order to form the typical layers of reconstructed human epidermis (RHE). After IFN-γ treatment, secretion of kyn/trp was measured by high performance liquid chromatography. Gene and protein expression of indoleamine 2,3-dioxygenase 1 (IDO) was analyzed with real-time PCR and immunohistochemistry. The secretion of cytokines was quantified with ELISA.
RESULTS RESULTS
Trp catabolism to kyn was significantly increased (P < 0.01) in the 2D culture in response to IFN-γ treatment. Before kyn secretion, IDO was strongly upregulated (P < 0.001). IFN-γ treatment also increased the secretion of IL-6 and IL-8 from the keratinocytes. In the RHE, IDO was upregulated by IFN-γ, and kyn secretion could be detected. Interestingly, IDO expression was only present in the basal cells of the RHE.
CONCLUSION CONCLUSIONS
Our results suggest that IFN-γ acts as an inducer of trp degradation preferentially in undifferentiated keratinocytes, indicated by the IDO expression in the basal layer of the RHE.

Identifiants

pubmed: 32782183
pii: S0923-1811(20)30234-6
doi: 10.1016/j.jdermsci.2020.07.005
pii:
doi:

Substances chimiques

CXCL8 protein, human 0
Culture Media 0
IDO1 protein, human 0
IFNG protein, human 0
IL6 protein, human 0
Indoleamine-Pyrrole 2,3,-Dioxygenase 0
Interleukin-6 0
Interleukin-8 0
Recombinant Proteins 0
Kynurenine 343-65-7
Interferon-gamma 82115-62-6
Tryptophan 8DUH1N11BX

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

177-184

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no conflict of interest to declare.

Auteurs

Anna Gustafsson (A)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden. Electronic address: anna.gustafsson@mau.se.

Zdenka Prgomet (Z)

Department of Oral Biology, Faculty of Odontology, Malmö University, Malmö, Sweden.

Skaidre Jankovskaja (S)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden.

Tautgirdas Ruzgas (T)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden.

Johan Engblom (J)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden.

Lars Ohlsson (L)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden.

Anette Gjörloff Wingren (A)

Biofilms - Research Center for Biointerfaces, Malmö University, Malmö, Sweden; Department of Biomedical Science, Faculty of Health and Society, Malmö University, Malmö, Sweden.

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Classifications MeSH