Development of an animal model for rosacea‑like skin lesions caused by Demodex
To develop an animal model of rosacea-like skin lesions caused by Demodex mites, a suspension of Demodex mites was injected into the skin of Japanese rabbits. The pathology of the skin lesion was assessed using H&E staining after 4 weeks of modeling. The skin lesions observed after 4 weeks were...
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Published in | Experimental and therapeutic medicine Vol. 24; no. 4 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Athens
Spandidos Publications
01.10.2022
Spandidos Publications UK Ltd D.A. Spandidos |
Subjects | |
Online Access | Get full text |
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Summary: | To develop an animal model of rosacea-like skin lesions caused by Demodex mites, a suspension of Demodex mites was injected into the skin of Japanese rabbits. The pathology of the skin lesion was assessed using H&E staining after 4 weeks of modeling. The skin lesions observed after 4 weeks were further treated with the recombinant bovine basic fibroblast growth factor (rbFGF) gel. Untreated lesions in the same rabbit were considered as the blank control. Erythema papules were observed in the model rabbit skin and could be observed most clearly in the 2nd week. Lumpy foreign bodies, telangiectasia and granuloma-like structure were observed in the model rabbit in the 1st, 2nd, and 3rd weeks, respectively. An organized granuloma-like structure was observed in the 4th week. The color of the skin lesions became lighter than that of the self-control after 4 weeks of rbFGF treatment. In conclusion, the model of Demodex-induced rosacea-like skin lesions can be developed through intradermal injection of suspension of Demodex mites into Japanese rabbits. The model can mimic the phenotype of skin lesions and histopathological manifestations in the Demodex mite-positive patient with rosacea. |
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Bibliography: | Abbreviations: rbFGF, recombinant bovine basic fibroblast growth factor; H&E, hematoxylin-eosin; PBS, phosphate buffer saline Contributed equally |
ISSN: | 1792-0981 1792-1015 |
DOI: | 10.3892/etm.2022.11555 |