Mast cells are dispensable in a genetic mouse model of chronic dermatitis
| Autor: | Eva Guiducci, Michael R. Meyer, Thorsten B. Feyerabend, Jitka Sulcova, Hans Reimer Rodewald, Sabine Werner |
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| Rok vydání: | 2014 |
| Předmět: |
Keratinocytes
Chemokine Inflammation Dermatitis Biology Pathology and Forensic Medicine Proinflammatory cytokine 03 medical and health sciences Mice 0302 clinical medicine Immune system medicine Animals Mast Cells Receptor Fibroblast Growth Factor Type 1 Receptor Fibroblast Growth Factor Type 2 Chemokine CCL2 030304 developmental biology Cell Proliferation Skin 0303 health sciences integumentary system Epidermis (botany) Mast cell Interleukin 33 stomatognathic diseases Disease Models Animal medicine.anatomical_structure Immunology biology.protein medicine.symptom Keratinocyte 030215 immunology |
| Zdroj: | The American journal of pathology. 185(6) |
| ISSN: | 1525-2191 |
| Popis: | Chronic inflammatory skin diseases, such as atopic dermatitis, affect a large percentage of the population, but the role of different immune cells in the pathogenesis of these disorders is largely unknown. Recently, we found that mice lacking fibroblast growth factor receptor 1 (Fgfr1) and Fgfr2 (K5-R1/R2 mice) in the epidermis have a severe impairment in the epidermal barrier, which leads to the development of a chronic inflammatory skin disease that shares many features with human atopic dermatitis. Using Fgfr1-/Fgfr2-deficient mice, we analyzed the consequences of the loss of mast cells. Mast cells accumulated and degranulated in the skin of young Fgfr1-/Fgfr2-deficient mice, most likely as a consequence of increased expression of the mast cell chemokine Ccl2. The increase in mast cells occurred before the development of histological abnormalities, indicating a functional role of these cells in the inflammatory skin phenotype. To test this hypothesis, we mated the Fgfr1-/Fgfr2-deficient mice with mast cell–deficient CreMaster mice. Surprisingly, loss of mast cells did not or only mildly affect keratinocyte proliferation, epidermal thickness, epidermal barrier function, accumulation and activation of different immune cells, or expression of different proinflammatory cytokines in the skin. These results reveal that mast cells are dispensable for the development of chronic inflammation in response to a defect in the epidermal barrier. |
| Databáze: | OpenAIRE |
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