Mjj. Gijbels et al., PATHOGENESIS OF SKIN-LESIONS IN MICE WITH CHRONIC PROLIFERATIVE DERMATITIS (CPDM CPDM)/, The American journal of pathology, 148(3), 1996, pp. 941-950
Chronic proliferative dermatitis is a spontaneous mutation in C57BL/Ka
mice (cpdm/cpdm), showing alopecia, epithelial hyperproliferation, in
filtration by eosinophils and macrophages, and vascular dilatation. To
further elucidate its pathogenesis, organs of 1-, 2-, 3-, 4-, 5-, and
6-week-old cpdm/cpdm mice were examined At 4 weeks, tbe epidermal thi
ckness was increased, whereas already at 3 weeks, the bromodeoxyuridin
e incorporation was increased in the basal keratinocytes. However, alr
eady at the age of 1 week, skin, lungs, and lymph nodes were infiltrat
ed by eosinophils although no macroscopic lesions were present. Compar
ed with control animals, 6-week-old cpdm/cpdm mice had decreased serum
IgE levels and increased numbers of mast cells. From the age of 1 wee
k these mast cells became increasingly IgE positive. In contrast, the
mast cells of tbe control animals remained IgE negative. Mast cells of
control and cpdm/cpdm mice were interleukin-4 and tumor necrosis fact
or-alpha positive A likely explanation for the tissue infiltration of
eosinophils could be the release of interleukin-4 and tumor necrosis f
actor-alpha fron activated mast cells. Tumor necrosis factor-alpha may
had to the expression of E-selectin on endothelial cells, facilitatin
g interleukin-4-mediated eosinophil transendothelial migration. Althou
gh various pathogenetic aspects of the cpdm/cpdm mouse need further el
ucidation, this model can be a tool to study eosinophil infiltration,
leukocyte-endothelial cell interactions, and mast cell proliferation.
Furthermore, the cpdm/cpdm mouse can be used to study chronic inflamma
tory skin disease because of the severe epidermal proliferation.