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首页> 外文期刊>Comparative Medicine >Ulcerative Dermatitis in C57BL/6 Mice Lacking Stearoyl CoA Desaturase 1
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Ulcerative Dermatitis in C57BL/6 Mice Lacking Stearoyl CoA Desaturase 1

机译：缺乏硬脂酰辅酶A去饱和酶1的C57BL / 6小鼠的溃疡性皮肤炎

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摘要

Ulcerative dermatitis (UD) is a common cause of morbidity and euthanasia in mice with a C57BL/6 (B6) background. The purposes of the current study were to determine whether UD lesions could be reliably produced in B6 mice lacking stearoyl-CoA desaturase 1 (SCD1(-/-) mice), to ascertain whether the UD lesions in SCD1(-/-) mice were similar to those found in other B6 mice, and to characterize the cell invasion phenotype of Staphlococcus xylosus cultured from the lesions. S. xylosus isolates from the environment and human skin were used as controls. SCD1(-/-) (n = 8 per group) and nontransgenic B6 control mice (n = 22 mice pooled from 3 groups that received different concentrations of conjugated linoleic acid) were fed standard rodent chow or a semipurified diet (NIH AIN76A) for 4 wk. Samples from other B6 mice with UD (field cases; n = 7) also were submitted for histology and culture. All of the SCD1(-/-) mice developed UD lesions by 4 wk on NIH AIN76A. None of SCD1(-/-) fed standard rodent chow and none of the wildtype B6 mice fed NIH AIN76A developed UD. Supplementation with conjugated linoleic acid did not affect ulcerogenesis. UD lesions in SCD1(-/-) mice and field cases were grossly and histologically similar. S. xylosits was isolated from SCD1(-/-) mice with UD (71%) and field cases of UD (43%). These isolates were the most cell-invasive, followed by the environmental isolate, and finally the human skin isolate. Our results provide a basis for further pathologic and clinical study of UD.
机译：溃疡性皮炎（UD）是具有C57BL / 6（B6）背景的小鼠发病和安乐死的常见原因。本研究的目的是确定是否可以在缺乏硬脂酰辅酶A去饱和酶1的B6小鼠（SCD1（-/-）小鼠）中可靠地产生UD损伤，以确定SCD1（-/-）小鼠中的UD损伤是否类似于在其他B6小鼠中发现的那些，并表征了从病灶培养的木糖葡萄球菌的细胞入侵表型。来自环境和人类皮肤的木糖链球菌分离物用作对照。为SCD1（-/-）（每组n = 8）和非转基因B6对照小鼠（n = 22只小鼠，从接受不同浓度的共轭亚油酸的3组小鼠中混合）喂食标准啮齿动物或半纯化饮食（NIH AIN76A），用于4周。来自其他B6小鼠的UD样品（现场病例; n = 7）也被提交进行组织学和培养。所有SCD1（-/-）小鼠在NIH AIN76A上第4周都出现了UD病变。用SCD1（-/-）饲喂标准啮齿动物食物，饲喂NIH AIN76A的野生型B6小鼠均未发育出UD。补充共轭亚油酸不会影响溃疡的发生。 SCD1（-/-）小鼠和野外病例的UD病变在组织学和组织学上均相似。从具有UD（71％）和现场UD病例（43％）的SCD1（-/-）小鼠中分离出S. xylosits。这些分离株是最具细胞入侵性的，其次是环境分离株，最后是人类皮肤分离株。我们的结果为进一步的UD病理和临床研究提供了基础。

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