title: Characterization of dermatitis arising spontaneously in DS-Nh mice maintained under conventional conditions: another possible model for atopic dermatitis.
abstract: DS-Nh (DS Nh/+) mice spontaneously develop dermatitis when they are housed in a conventional environment. In this study, we analyzed the clinical and histopathological features of dermatitis in DS-Nh mice, which is characterized by erythema, edema, and erosion on the face, neck, chest and flexor surfaces of their forelegs with marked scratching behavior. Histopathological examination, including immunohistochemistry, revealed that inflammatory cells consisting of mast cells, eosinophils, CD4-positive T cell-dominant lymphocytes and CD11b-positive macrophages infiltrated the skin lesions. The cytokine production pattern of inflammatory cells in a lesional skin tissue was shifted to the Th2-type (IL-4) rather than the Th1 type (IFN-gamma). Serum IgE levels were elevated and correlated with the severity of the clinical skin conditions. These skin symptoms were observed in association with a colonization of Staphylococcus aureus. Similar clinical and histopathological symptoms were inducible with repeated percutaneous immunization of heat-killed S. aureus on the back of SPF DS-Nh mice. These results suggest that the spontaneous dermatitis that occurs in conventionally raised DS-Nh mice is comparable to a certain type of human atopic dermatitis (AD), which is associated with S. aureus, a recognized environmental factor. Thus, we consider that DS-Nh mice offer a useful model for investigating the pathogenesis of AD and for developing new therapeutic approaches or drugs for treating AD.
authors.affiliation: Department of Dermatology, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, 650-0017 Kobe, Japan.
authors.forename: Ichiro
authors.initials: I
authors.lastname: Hikita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yoshioka
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Mizoguchi
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Tsukahara
authors.forename: Kenta
authors.initials: K
authors.lastname: Tsuru
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagai
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Hirasawa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Tsuruta
authors.forename: Ryuji
authors.initials: R
authors.lastname: Suzuki
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Ichihashi
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Horikawa
mesh_terms: D000818:Animals; D003872:Dermatitis / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D003876:Dermatitis, Atopic; D004195:Disease Models, Animal; D005145:Face; D005856:Germ-Free Life; D006651:Histocytochemistry; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics; D012867:Skin / Q000378:metabolism / Q000382:microbiology; D013203:Staphylococcal Infections; D013210:Staphylococcus / Q000302:isolation & purification; D013211:Staphylococcus aureus
chemical_list: D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma