TY - JOUR
T1 - The role of skin inflammation, barrier dysfunction, and oral tolerance in skin sensitization to gluten-derived hydrolysates in a rat model
AU - Larsen, Jeppe Madura
AU - Ballegaard, Anne Sofie Ravn
AU - Dominguez, Angela Serrano
AU - Kristoffersen, Nanna Jordahn
AU - Maryniak, Natalia Zofia
AU - Locke, Arielle Vallee
AU - Kazemi, Sahar
AU - Epstein, Michelle
AU - Madsen, Charlotte Bernhard
AU - Bøgh, Katrine Lindholm
N1 - Publisher Copyright:
© 2022 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.
PY - 2023/2
Y1 - 2023/2
N2 - Background: Adverse reactions to wheat-containing skin care products have been linked to food allergy development. Objectives: To determine the role of skin barrier dysfunction and inflammation in sensitization to gluten-derived hydrolysates via the skin in Brown Norway rats with and without oral tolerance to wheat. Methods: Skin barrier defect was induced by mechanical disruption, and skin inflammation was induced by topical application of SLS or MC903. Unmodified, enzyme hydrolyzed, or acid hydrolyzed gluten products were applied to the skin three times per week for 5 weeks. Subsequently, rats were orally gavaged with unmodified gluten. Results: Wheat-naïve rats were readily sensitized to gluten hydrolysates via the skin. Skin barrier defect and skin inflammation had little effect on the skin sensitization and hydrolysate-specific IgE levels. Oral administration of unmodified gluten promoted the production of unmodified gluten-specific IgE in rats sensitized via the skin. Sensitization through intact skin, disrupted skin barrier, or inflamed skin was unable to break tolerance to unmodified gluten in rats on a wheat-containing diet. Conclusions: Mechanical skin barrier disruption and skin inflammation play a limited role in experimental skin sensitization to gluten-derived hydrolysates.
AB - Background: Adverse reactions to wheat-containing skin care products have been linked to food allergy development. Objectives: To determine the role of skin barrier dysfunction and inflammation in sensitization to gluten-derived hydrolysates via the skin in Brown Norway rats with and without oral tolerance to wheat. Methods: Skin barrier defect was induced by mechanical disruption, and skin inflammation was induced by topical application of SLS or MC903. Unmodified, enzyme hydrolyzed, or acid hydrolyzed gluten products were applied to the skin three times per week for 5 weeks. Subsequently, rats were orally gavaged with unmodified gluten. Results: Wheat-naïve rats were readily sensitized to gluten hydrolysates via the skin. Skin barrier defect and skin inflammation had little effect on the skin sensitization and hydrolysate-specific IgE levels. Oral administration of unmodified gluten promoted the production of unmodified gluten-specific IgE in rats sensitized via the skin. Sensitization through intact skin, disrupted skin barrier, or inflamed skin was unable to break tolerance to unmodified gluten in rats on a wheat-containing diet. Conclusions: Mechanical skin barrier disruption and skin inflammation play a limited role in experimental skin sensitization to gluten-derived hydrolysates.
KW - animal model
KW - food allergy
KW - gluten
KW - oral tolerance
KW - skin barrier dysfunction
KW - skin inflammation
KW - skin sensitization
KW - wheat
UR - http://www.scopus.com/inward/record.url?scp=85140214024&partnerID=8YFLogxK
U2 - 10.1111/cod.14233
DO - 10.1111/cod.14233
M3 - Journal article
C2 - 36221232
AN - SCOPUS:85140214024
SN - 0105-1873
VL - 88
SP - 109
EP - 119
JO - Contact Dermatitis
JF - Contact Dermatitis
IS - 2
ER -