Disease relevance of cpdm

• Mutant cpdm/cpdm mice develop a chronic skin disease characterized by epidermal hyperplasia and inflammation [1].
• In contrast, T cell function appeared normal as assessed by evaluation of the contact hypersensitivity response in cpdm/cpdm mice [2].
• The ability of the cpdm/cpdm mice to mount a delayed-type hypersensitivity response was greatly reduced [3].
• Chronic proliferative dermatitis (cpdm/cpdm) mutant mice develop a persistent eosinophilic dermatitis associated with increased T(H)2 cytokines in the skin [4].
• C57BL/Ka mice with chronic proliferative dermatitis (cpdm/cpdm) develop chronic persistent skin lesions characterized by epidermal hyperplasia, infiltration by granulocytes and macrophages, and vascular dilatation [5].

High impact information on cpdm

• The cpdm mutation causes a complex phenotype that is characterized by multiorgan inflammation and the defective development of lymphoid tissues [2].
• The cpdm/cpdm mouse may be a useful model to study the factors that control the development of lymphoid tissues, in particular the Peyer's patches, and the mechanisms that control the humoral immune response [2].
• Furthermore, the cpdm/cpdm mouse can be used to study chronic inflammatory skin disease because of the severe epidermal proliferation [6].
• Compared with control animals, 6-week-old cpdm/cpdm mice had decreased serum IgE levels and increased numbers of mast cells [6].
• Although various pathogenetic aspects of the cpdm/cpdm mouse need further elucidation, this model can be a tool to study eosinophil infiltration, leukocyte-endothelial cell interactions, and mast cell proliferation [6].

Chemical compound and disease context of cpdm

• Quantification of spontaneous scratching by chronic proliferative dermatitis mice or histamine and Compound 48/80-treated C57BL/Ka mice was performed visually (using a video recording showing both the mice and the computer-generated signal) and using the pruritus detection system (PDS = SDU plus computer program) [7].

Anatomical context of cpdm

• These results indicate that the differentiation of keratinocytes in cpdm/cpdm mice was normal [1].
• Chronic proliferative dermatitis is a spontaneous mutation in C57BL/Ka mice (cpdm/cpdm) and is characterized by epithelial hyperproliferation, infiltration by eosinophils and macrophages, and vascular dilatation [8].
• This study demonstrates that the pathologic features found in the cpdm/cpdm mice are the result of a disorder in the epidermis or dermis and not due to a systemic defect [8].
• Expression patterns of chemokines in the skin of cpdm/cpdm mice were evaluated to define the mechanisms driving cutaneous infiltration by leukocytes [4].
• In correlation with the relative absence of lymphocytes in the cpdm/cpdm skin no lymphocyte binding could be observed, but avid adhesion of neutrophils was seen [9].

Associations of cpdm with chemical compounds

• An increased number of proliferating keratinocytes was present in the cpdm/cpdm skin-graft transplanted to nudes or to C57BL/Ka mice based on short-term bromodeoxyuridine labeling [8].
• Treatment of the cpdm/cpdm mice with calcipotriene (5 microg/day for 3 weeks) inhibited epidermal proliferation and the number of eosinophils [10].
• The correlation between visual and automatic quantification of spontaneous cpdm mouse scratching was 81.7+/-2.5% (mean +/- S.E.M.). For histamine, the correlation was 85.6+/-3.6% (mean +/- S.E.M.) and for Compound 48/80, 85.8+/-3.1% (mean +/- S.E.M.). The PDS routinely detected less than 5% false-positive signals [7].

Other interactions of cpdm

• Treatment of cpdm/cpdm mice with CCL11-neutralizing polyclonal antibodies did not affect the number of eosinophils in the skin or the severity of the dermatitis [4].
• Asebia (ab), flaky skin (fsn), and chronic proliferative dermatitis (cpd) are spontaneous mouse mutations with psoriasiform skin alterations of unclear pathogenesis [11].
• These data are consistent with impaired type 1 and excessive type 2 cytokine production in cpdm/cpdm mice [3].

Analytical, diagnostic and therapeutic context of cpdm

• Intercellular adhesion molecule-1 continued to be expressed by basal keratinocytes of the cpdm/cpdm grafts after transplantation [8].
• Maintenance of donor phenotype after full-thickness skin transplantation from mice with chronic proliferative dermatitis (cpdm/cpdm) to C57BL/Ka and nude mice and vice versa [8].
• Western blot analysis with an antibody against Chi3L3 and Chi3L4 confirmed the increased amount of these proteins in the skin of cpdm/cpdm mice [12].
• The concentration of CCL11 protein was increased two- to threefold in the skin of cpdm/cpdm mice by enzyme-linked immunosorbent assay [4].

References