Development of Atopic Dermatitis in Mice Transgenic for Human Apolipoprotein C1

Autor: Tonny Lagerweij, C. Persoon-Deen, Jimmy F.P. Berbée, Louis M. Havekes, Arnold P. Oranje, Errol P. Prens, Lex Nagelkerken, Perry Verzaal
Přispěvatelé: TNO Kwaliteit van Leven, Dermatology, University of Groningen
Rok vydání: 2008
Předmět:
Male
Neutrophils
Administration
Topical
Immunoglobulin E
Biochemistry
immunoglobulin E
chemistry.chemical_compound
Mice
Adrenal Cortex Hormones
inflammatory cell
lipid metabolism
Mast Cells
biology
integumentary system
atopic dermatitis
article
Atopic dermatitis
medicine.anatomical_structure
priority journal
Liver
histopathology
Female
corticosteroid
PROTEIN ANTIGEN
lichenoid eruption
ECZEMA
Mice
Transgenic
Physiological Sciences
Dermatology
Article
animal tissue
Dermatitis
Atopic
Dermis
SDG 3 - Good Health and Well-being
medicine
Animals
Humans
controlled study
Biology
protein expression
Molecular Biology
mouse
Transepidermal water loss
Apolipoprotein C-I
nonhuman
Cholesterol
Pruritus
Lipid metabolism
apolipoprotein C1
Cell Biology
medicine.disease
Eosinophils
chemistry
Immunology
biology.protein
Apolipoprotein C1
Epidermis
SKIN
Spongiosis
Zdroj: Journal of Investigative Dermatology, 5, 128, 1165-1172
Journal of Investigative Dermatology, 128(5), 1165-1172. Nature Publishing Group
Journal of Investigative Dermatology, 128(5), 1165-1172. ELSEVIER SCIENCE INC
ISSN: 0022-202X
1165-1172
DOI: 10.1038/sj.jid.5701182
Popis: 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.
Databáze: OpenAIRE
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