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首页> 外文期刊>Infection and immunity >Pathogenicity of Saccharomyces cerevisiae in complement factor five-deficient mice.
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Pathogenicity of Saccharomyces cerevisiae in complement factor five-deficient mice.

机译：酿酒酵母在补体因子五缺陷小鼠中的致病性。

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We have previously determined the relative virulence of isolates of Saccharomyces cerevisiae on the basis of differences in proliferation and resistance to clearance in CD-1 mice. These infections were not fatal. To further characterize S. cerevisiae pathogenesis, we studied a virulent clinical isolate, YJM128, and an avirulent nonclinical isolate, Y55, in C5-deficient mice. DBA/2N mice were infected intravenously with YJM128 or Y55, and temporal burdens of yeast cells in various organs were determined. After infection with 10(7) CFU, Y55 increased by 13-fold and YJM128 increased by 20-fold in the brain from day 0 to 3. In addition, YJM128 increased by 4-fold in the kidneys, whereas Y55 decreased by 16-fold. Both isolates declined in number in other organs. In all studies, 90% of mice infected with 10(7) CFU of YJM128 died between days 2 and 7, whereas no mice infected with equivalent numbers of Y55 died. No mice died after infection with 10(6) CFU of Y55 or YJM128. The importance of C5 was confirmed by studies using B10.D2/oSnJ (C5-) mice and their congenic C5+ counterparts. Again, the C5- mice were most susceptible to infection with S. cerevisiae, with 63% infected with YJM128 dying by day 7; no C5+ mice died. No Y55-infected mice died, and mean burdens in the brain at day 14 were sevenfold lower in C5+ mice than in C5- mice. Seven of 10 other S. cerevisiae isolates were also more virulent in DBA/2N than CD-1 mice, causing > or = 40% mortality. These data indicate that C5 is a critical factor in host resistance against S. cerevisiae infections and further confirm the pathogenic potential of some isolates of S. cerevisiae.
机译：我们先前已经根据CD-1小鼠中增殖和对清除的抵抗力的差异确定了酿酒酵母分离株的相对毒力。这些感染不是致命的。为了进一步表征酿酒酵母的发病机理，我们在C5缺陷小鼠中研究了有毒的临床分离株YJM128和无毒的非临床分离株Y55。用YJM128或Y55静脉感染DBA / 2N小鼠，并测定了各个器官中酵母细胞的时间负担。从第10天到第3天，用10（7）CFU感染后，Y55在大脑中增加了13倍，YJM128在大脑中增加了20倍。此外，肾脏中YJM128增加了4倍，而Y55减少了16-折。两种分离株在其他器官中的数量均下降。在所有研究中，感染YJM128的10（7）CFU的小鼠中有90％在第2天和第7天之间死亡，而没有感染相同数量的Y55的小鼠死亡。用Y55或YJM128的10（6）CFU感染后没有小鼠死亡。通过使用B10.D2 / oSnJ（C5-）小鼠及其同系C5 +对应物进行的研究证实了C5的重要性。同样，C5-小鼠最容易感染啤酒酵母，到第7天有63％的YJM128感染死亡。没有C5 +小鼠死亡。没有感染Y55的小鼠死亡，并且在第14天，C5 +小鼠的大脑平均负担比C5-小鼠低七倍。在DBA / 2N中，其他10株啤酒酵母中的7株也比CD-1小鼠更具毒性，导致>或= 40％的死亡率。这些数据表明C5是宿主对啤酒酵母感染的抗性的关键因素，并进一步证实了某些啤酒酵母分离株的致病潜力。

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