Immunological cell situation in the skin of atopic model mice.
BACKGROUND
We observed nishikinezumi, cinnamon-coloured (NC)/Fujita (F) mice aged between 5 and 28 weeks. These NC mice have skin eruptions that resemble human atopic dermatitis (AD) under conventional circumstances.


OBJECTIVE
We investigated the skin of eruptive and non-eruptive lesions in NC/F mice by using haematoxylin-eosin (H&E) staining, toluidine blue staining and immunohistopathological study with immunoglobulin (Ig)EepsilonRI, CD23, interleukin (IL)-4, IL-5, interferon (INF)-gamma and Ia antigen.


RESULTS
Histological examination of the eruptive lesions revealed the perivascular infiltration of many lymphocytes and mast cells into the upper dermis. Intracellular oedema of the epidermis, lymphocyte infiltration into the epidermis and liquefaction degeneration of the basal layer were also observed. The numbers of IL-4 and IL-5 positive cells in the eruptive lesions were larger than those of the non-eruptive lesions. IL-4 and IL-5 positive cells in the eruptive lesions increased weekly. Some IFN-gamma positive cells were observed in the eruptive lesions after 21 weeks. IFN-gamma positive cells were scarce in the skin of both the non-eruptive and eruptive lesions before 21 weeks. Serum IgE increased from 7 weeks to 21 weeks.


CONCLUSIONS
We confirmed that these findings indicated that T helper (Th)2-dominant immunological activation transformed to a Th1-dominant situation. Many IgEepsilonRI positive cells were recognized in the dermis of the eruptive lesions by the time IgE had decreased. We assumed that the dermatitis before 21 weeks was an IgE-mediated allergy. We have previously reported that older NC/F mice had positive patch-test reactions to mites. Because serum IgE decreased after 21 weeks, dermatitis after 21 weeks might be associated more with cell-mediated delayed hypersensitivity than with IgE-mediated immediate allergy.
Department of Environmental Dermatology, Nagoya University, School of Medicine, 1-1-20, Daikominami, Higashi-ku, Nagoya, Aichi 461-0047, Japan. ksugiura@med.nagoya-u.ac.jp
K
K
Sugiura
K
K
Hiramoto
M
M
Shamoto
M
M
Sugiura
R
R
Hayakawa
Y
Y
Kato
M
M
Shinzato
A
A
Osada
N
N
Sakamoto
H
H
Takahashi
D000818:Animals; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D007073:Immunoglobulin E / Q000097:blood; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D051379:Mice; D008815:Mice, Inbred Strains; D017455:Receptors, IgE / Q000032:analysis; D012867:Skin / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology
D015848:Interleukin-5; D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma