A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice

Harm HogenEsch, Marion J J Gijbels, Erik Offerman, Joop Van Hooft, Dirk W. Van Bekkum, Chris Zurcher

Research output: Contribution to journalArticle

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Abstract

Chronic proliferative dermatitis is a new spontaneous mutation in C57BL/Ka mice. Breeding results suggest an autosomal recessive mode of inheritance. Mutant mice develop skin lesions at the age of 5 to 6 weeks. The lesions occur in the ventral and dorsal skin of the body, whereas ears, footpads, and tail are not involved. The lesions are characterized by epidermal hyperplasia, hyper- and parakeratosis, and single cell necrosis of keratinocytes. The dermis and epidermis are infiltrated by granulocytes and macrophages, and occasionally subcorneal and intracorneal microabscesses are formed. The number of mast cells in the dermis progressively increases with age. There is dilatation and proliferation of dermal capillaries. Similar lesions develop in the mouth, esophagus, and forestomach, which, in the mouse, are all lined by orthokeratinizing stratified squamous cell epithelium. Studies with bromodeoxyuridine confirm the increased rate of epithelial cell proliferation. Most inflammatory cells in the affected skin express Mac-1, and few express the T lymphocyte marker CD3. There is increased expression of intercellular adhesion molecule-1 on keratinocytes and endothelial cells. Infiltration of neutrophils and macrophages are also seen in the liver, lung, and several joints. The disease could not be transferred by bone marrow or spleen transplants into irradiated normal syngeneic hosts. Treatment of the mice with triamcinolone, a long-acting corticosteroid, resulted in nearly complete regression of the lesions over a period of 4 weeks, whereas systemic cyclosporin A treatment was ineffective.

Original languageEnglish (US)
Pages (from-to)972-982
Number of pages11
JournalAmerican Journal of Pathology
Volume143
Issue number3
StatePublished - Sep 1993
Externally publishedYes

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Dermatitis
Inbred C57BL Mouse
Skin
Mutation
Dermis
Keratinocytes
Epithelial Cells
Macrophages
Parakeratosis
Triamcinolone
Neutrophil Infiltration
Intercellular Adhesion Molecule-1
Bromodeoxyuridine
Granulocytes
Epidermis
Mast Cells
Cyclosporine
Esophagus
Hyperplasia
Breeding

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

HogenEsch, H., Gijbels, M. J. J., Offerman, E., Van Hooft, J., Van Bekkum, D. W., & Zurcher, C. (1993). A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice. American Journal of Pathology, 143(3), 972-982.

A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice. / HogenEsch, Harm; Gijbels, Marion J J; Offerman, Erik; Van Hooft, Joop; Van Bekkum, Dirk W.; Zurcher, Chris.

In: American Journal of Pathology, Vol. 143, No. 3, 09.1993, p. 972-982.

Research output: Contribution to journalArticle

HogenEsch, H, Gijbels, MJJ, Offerman, E, Van Hooft, J, Van Bekkum, DW & Zurcher, C 1993, 'A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice', American Journal of Pathology, vol. 143, no. 3, pp. 972-982.
HogenEsch H, Gijbels MJJ, Offerman E, Van Hooft J, Van Bekkum DW, Zurcher C. A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice. American Journal of Pathology. 1993 Sep;143(3):972-982.
HogenEsch, Harm ; Gijbels, Marion J J ; Offerman, Erik ; Van Hooft, Joop ; Van Bekkum, Dirk W. ; Zurcher, Chris. / A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice. In: American Journal of Pathology. 1993 ; Vol. 143, No. 3. pp. 972-982.
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