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白色念珠菌丝裂原活化蛋白激酶磷酸酶(CPP1)突变体在小鼠乳腺炎模型中的致病性降低

Reduced pathogenicity of a Candida albicans MAP kinase phosphatase (CPP1) mutant in the murine mastitis model.

作者信息

Guhad F A, Csank C, Jensen H E, Thomas D Y, Whiteway M, Hau J

机构信息

Department of Physiology, Uppsala University, Sweden.

出版信息

APMIS. 1998 Nov;106(11):1049-55. doi: 10.1111/j.1699-0463.1998.tb00257.x.

DOI:10.1111/j.1699-0463.1998.tb00257.x
PMID:9890266
Abstract

Candida albicans strains with a deletion of the mitogen-activated protein kinase tyrosine phosphatase gene (CPP1) are derepressed in the yeast-to-hyphal transition on solid surfaces in vitro at ambient temperatures and this gene is therefore required for repression of the yeast-to-hyphal switch. The pathology caused by a CPP1 null mutant strain was compared with that of the null mutant into which the wild-type CPP1 gene was introduced by homologous recombination and with the wild-type parent strain in a murine mycotic mastitis model. The mammary glands of lactating mice (at day 5 postpartum) were infected for 2, 4 and 6 days with 1 x 10(5), 1 x 10(6) and 1 x 10(7) cell-forming units before euthanasia. Infected and non-infected control glands were evaluated histopathologically. The null mutant strains showed less severe pathology than the two control strains. The Cpplp tyrosine phosphatase may thus be considered a virulence determinant during localized infection in C. albicans.

摘要

在体外环境温度下,缺失丝裂原活化蛋白激酶酪氨酸磷酸酶基因(CPP1)的白色念珠菌菌株在固体表面从酵母形态向菌丝形态转变时不受抑制,因此该基因是抑制酵母 - 菌丝转变所必需的。在小鼠霉菌性乳腺炎模型中,将CPP1基因敲除突变株的病理学表现与通过同源重组导入野生型CPP1基因的敲除突变株以及野生型亲代菌株进行了比较。在安乐死之前,用1×10⁵、1×10⁶和1×10⁷个细胞形成单位分别感染哺乳期小鼠(产后第5天)的乳腺2天、4天和6天。对感染和未感染的对照腺体进行组织病理学评估。敲除突变株的病理学表现比两个对照菌株轻。因此,Cpplp酪氨酸磷酸酶可能被认为是白色念珠菌局部感染期间的一种毒力决定因素。

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