Title
Development of atopic dermatitis in mice transgenic for human apolipoprotein C1
Author
Nagelkerken, L.
Verzaal, P.
Lagerweij, T.
Persoon-Deen, C.
Berbee, J.F.P.
Prens, E.P.
Havekes, L.M.
Oranje, A.P.
TNO Kwaliteit van Leven
Publication year
2008
Abstract
Mice with transgenic expression of human apolipoprotein C1 (APOC1) in liver and skin have strongly increased serum levels of cholesterol, triglycerides, and free fatty acids, indicative of a disturbed lipid metabolism. Importantly, these mice display a disturbed skin barrier function, evident from increased transepidermal water loss, and spontaneously develop symptoms of dermatitis including scaling, lichenification, excoriations, and pruritus. Histological analysis shows increased epidermal thickening and spongiosis in conjunction with elevated numbers of inflammatory cells (eosinophils, neutrophils, mast cells, macrophages, and CD4+ T cells) in the dermis. In addition, affected mice have increased serum levels of IgE and show abundant IgE+ mast cells in the dermis. Partial inhibition of disease could be achieved by restoration of the skin barrier function with topical application of a lipophilic ointment. Furthermore, the development of atopic dermatitis in these mice was suppressed by corticosteroid treatment. These findings in APOC1(+/+) mice underscore the role of skin barrier integrity in the pathogenesis of atopic dermatitis. © 2007 The Society for Investigative Dermatology.
Subject
Biology
Physiological Sciences
apolipoprotein C1
corticosteroid
immunoglobulin E
animal tissue
article
atopic dermatitis
controlled study
histopathology
inflammatory cell
lichenoid eruption
lipid metabolism
mouse
nonhuman
priority journal
protein expression
Administration, Topical
Adrenal Cortex Hormones
Animals
Apolipoprotein C-I
Dermatitis, Atopic
Eosinophils
Epidermis
Female
Humans
Immunoglobulin E
Liver
Male
Mast Cells
Mice
Mice, Transgenic
Neutrophils
Pruritus
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DOI
https://doi.org/10.1038/sj.jid.5701182
TNO identifier
240778
ISSN
0022-202X
Source
Journal of Investigative Dermatology, 128 (5), 1165-1172
Document type
article