title: Atopic dermatitis-like pruritic skin inflammation caused by feeding a special diet to HR-1 hairless mice.
abstract: Dry skin/barrier dysfunction is considered to be one of the characteristic features of atopic dermatitis (AD). When HR-1 hairless mice are fed a special diet, HR-AD, dry red skin is induced. We examined whether HR-AD-fed mouse could be used as a model for AD by showing itch-associated scratching behaviour and by analysing the immunological change. HR-1 mice were fed HR-AD from 4 weeks old. HR-AD-fed mice showed severe dry skin symptoms accompanied by a decrease in dermal water content and an increase in transepidermal water loss and prolonged scratching bout duration on day 14 or 28. These symptoms became gradually worse until day 56. Marked epidermal hyperplasia and slight increase in CD4+ cells in the skin were observed from day 28. In contrast, increases in circulating T cells and serum immunoglobulin E were seen from day 41. Other skin-infiltrating inflammatory cells, such as eosinophils and mast cells, were increased on day 56 but not on day 28. Though daily oral treatment with dexamethasone reduced the increased numbers of these cells, it did not affect the dry skin symptoms or the prolonged scratching episodes. In contrast, the development of dry skin was inhibited by feeding with 10% normal diet-containing HR-AD. The skin barrier dysfunction in HR-AD-fed mice is closely associated with the development of AD-like pruritus. Changes in the immunological parameters observed may be the consequence of skin barrier dysfunction. Our findings suggest that HR-AD-fed mouse could be used as a dry skin-based experimental model for AD.
authors.affiliation: Department of Pharmacology, Kyoto Pharmaceutical University, Kyoto, Japan.
authors.forename: Masanori
authors.initials: M
authors.lastname: Fujii
authors.forename: Junko
authors.initials: J
authors.lastname: Tomozawa
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Mizutani
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nabe
authors.forename: Kiichiro
authors.initials: K
authors.lastname: Danno
authors.forename: Shigekatsu
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000821:Animal Feed; D000818:Animals; D001834:Body Water / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000473:pathology*; D003907:Dexamethasone / Q000494:pharmacology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006965:Hyperplasia / Q000473:pathology; D007073:Immunoglobulin E / Q000097:blood / Q000737:chemistry; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology*; D008297:Male; D051379:Mice; D008812:Mice, Hairless; D011537:Pruritus / Q000473:pathology*; D012867:Skin / Q000378:metabolism / Q000473:pathology; D013997:Time Factors
chemical_list: D007073:Immunoglobulin E; D003907:Dexamethasone