Metabolic re-programming of keratinocytes in response to contact allergens
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Metabolic re-programming of keratinocytes in response to contact allergens. / Menzel, Mandy; Mraz, Veronika; Vaher, Helen; Geisler, Carsten; Menné Bonefeld, Charlotte.
In: Contact Dermatitis, Vol. 90, No. 3, 2024, p. 235-244.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Metabolic re-programming of keratinocytes in response to contact allergens
AU - Menzel, Mandy
AU - Mraz, Veronika
AU - Vaher, Helen
AU - Geisler, Carsten
AU - Menné Bonefeld, Charlotte
N1 - Publisher Copyright: © 2023 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.
PY - 2024
Y1 - 2024
N2 - Background: Allergic contact dermatitis (ACD) is a common skin disease caused by the recognition of haptens by the immune system. Keratinocytes play an important role in the initiation and facilitation of inflammatory responses in ACD. Immune responses are associated with major changes in metabolism. However, metabolic re-programming is not well studied in ACD; specifically, knowledge of metabolic alterations in structural cells is lacking. Methods: Metabolic re-programming in ACD was studied using publicly available transcriptome datasets. Primary pooled keratinocytes and a keratinocyte cell line (HaCaT) were stimulated with contact allergens, and inflammatory responses and expression of metabolic markers were measured by qPCR and flow cytometry, respectively. Results: ACD is characterized by metabolic re-programming with a metabolic profile similar to atopic dermatitis. Exposure to contact allergens causes a wide array of metabolic alterations. Stimulation of keratinocytes with contact allergens induced inflammatory responses typical for ACD and was associated with an up-regulation of proteins representative for glucose uptake, fatty acid metabolism, oxidative phosphorylation and to some extent arginine biosynthesis. Changes in these metabolic pathways were also observed when comparing lesional with non-lesional contact dermatitis skin. Conclusions: ACD is, similarly to other inflammatory skin diseases, characterized by metabolic re-programming. Contact allergen exposure induces expression of a wide array of metabolic pathways, which is at least in part mediated through metabolic re-programming of keratinocytes.
AB - Background: Allergic contact dermatitis (ACD) is a common skin disease caused by the recognition of haptens by the immune system. Keratinocytes play an important role in the initiation and facilitation of inflammatory responses in ACD. Immune responses are associated with major changes in metabolism. However, metabolic re-programming is not well studied in ACD; specifically, knowledge of metabolic alterations in structural cells is lacking. Methods: Metabolic re-programming in ACD was studied using publicly available transcriptome datasets. Primary pooled keratinocytes and a keratinocyte cell line (HaCaT) were stimulated with contact allergens, and inflammatory responses and expression of metabolic markers were measured by qPCR and flow cytometry, respectively. Results: ACD is characterized by metabolic re-programming with a metabolic profile similar to atopic dermatitis. Exposure to contact allergens causes a wide array of metabolic alterations. Stimulation of keratinocytes with contact allergens induced inflammatory responses typical for ACD and was associated with an up-regulation of proteins representative for glucose uptake, fatty acid metabolism, oxidative phosphorylation and to some extent arginine biosynthesis. Changes in these metabolic pathways were also observed when comparing lesional with non-lesional contact dermatitis skin. Conclusions: ACD is, similarly to other inflammatory skin diseases, characterized by metabolic re-programming. Contact allergen exposure induces expression of a wide array of metabolic pathways, which is at least in part mediated through metabolic re-programming of keratinocytes.
KW - allergic contact dermatitis
KW - keratinocytes
KW - metabolic re-programming
U2 - 10.1111/cod.14462
DO - 10.1111/cod.14462
M3 - Journal article
C2 - 37985405
AN - SCOPUS:85177163140
VL - 90
SP - 235
EP - 244
JO - Contact Dermatitis. Supplement
JF - Contact Dermatitis. Supplement
SN - 1396-6669
IS - 3
ER -
ID: 374653740