Chen C G, Yang Y L, Cheng H H, Su C L, Huang S F, Chen C T, Liu Y T, Su I J, Lo H J
Division of Clinical Research, National Health Research Institutes, Miaoli, Taiwan.
Int J Immunopathol Pharmacol. 2006 Jul-Sep;19(3):561-5. doi: 10.1177/039463200601900312.
The cph1/cph1 efg1/efg1 Candida albicans mutant cells were non-lethal in a mouse model of systemic infection. We investigated in vivo proliferation and invasion of C. albicans cells in infected mice to elucidate the interaction between the host and the pathogen. Homogenates of kidneys from the mice infected with the wild-type and the mutant C. albicans cells yielded a mean of 2.1 x 10 7 CFU/g and 2.2 x 10 6 CFU/g, respectively. The kidneys from the mice infected with the wild-type cells showed extensive renal cortical necrosis associated with neutrophilic infiltration. There were also wild-type hyphal cells present in abundance. Hence, tubular necrosis leading to renal failure in the mice may be the cause of death. Although the cph1/cph1 efg1/efg1 mutant cells were not lethal, they were capable of establishing restricted zones of infection and colonization near the renal pelvis instead of simply being cleared by the immune system in mice.
cph1/cph1 efg1/efg1白色念珠菌突变细胞在系统性感染的小鼠模型中无致死性。我们研究了白色念珠菌细胞在感染小鼠体内的增殖和侵袭情况,以阐明宿主与病原体之间的相互作用。感染野生型和突变型白色念珠菌细胞的小鼠肾脏匀浆分别产生平均2.1×10⁷CFU/g和2.2×10⁶CFU/g的菌落形成单位。感染野生型细胞的小鼠肾脏显示出广泛的肾皮质坏死,并伴有嗜中性粒细胞浸润。同时也有大量野生型菌丝细胞存在。因此,导致小鼠肾衰竭的肾小管坏死可能是死亡原因。虽然cph1/cph1 efg1/efg1突变细胞无致死性,但它们能够在肾盂附近建立有限的感染和定植区域,而不是简单地被小鼠免疫系统清除。