Salmonella typhimurium proliferates and establishes a persistent infection in the intestine of Caenorhabditis elegans
Salmonella typhimurium proliferates and establishes a persistent infection in the intestine of Caenorhabditis elegans
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DOI：
10.1016/s0960-9822(00)00830-7
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发表时间：
2000-11-30
期刊：
影响因子：
9.2
通讯作者：
Ausubel, FM
中科院分区：
文献类型：
--
作者：
Aballay, A;Yorgey, P;Ausubel, FM
由于缺乏这种相互作用的遗传易处理模型，宿主-病原体相互作用的遗传分析受到阻碍。我们之前表明，人类机会性病原体铜绿假单胞菌可以杀死秀丽隐杆线虫，可以鉴定出影响这种杀灭作用的铜绿假单胞菌和秀丽隐杆线虫基因，并且大多数铜绿假单胞菌基因对于哺乳动物的发病机制也很重要。在这里，我们证明鼠伤寒沙门氏菌以及其他肠炎沙门氏菌血清型（包括肠炎沙门氏菌和都柏林沙门氏菌）也可以杀死秀丽隐杆线虫。当线虫被放置在鼠伤寒沙门氏菌的菌苔上时，细菌会在蠕虫肠腔中积聚，线虫会在几天内死亡。这种杀灭需要与活细菌细胞接触。当将蠕虫放置在鼠伤寒沙门氏菌菌苔上相对较短的时间（3-5小时）然后转移到大肠杆菌菌苔上时，蠕虫会以类似的动力学死亡。转移到大肠杆菌后，高滴度的鼠伤寒沙门氏菌会在线虫的余生中持续存在于秀丽隐杆线虫的肠腔中。此外，用 1:1000 的鼠伤寒沙门氏菌和大肠杆菌的混合物喂养 5 小时，然后转移到 100% 大肠杆菌，也会导致几天后死亡。这种杀灭与秀丽隐杆线虫管腔中鼠伤寒沙门氏菌滴度的增加相关，每条蠕虫达到 10,000 个细菌。这些数据表明，与铜绿假单胞菌相反，鼠伤寒沙门氏菌的少量接种物可以在秀丽隐杆线虫肠道中增殖并建立持续感染。 PhoP/PhoQ 信号转导系统中的鼠伤寒沙门氏菌突变导致对秀丽隐杆线虫的杀伤显着减少。
Genetic analysis of host-pathogen interactions has been hampered by the lack of genetically tractable models of such interactions. We showed previously that the human opportunistic pathogen Pseudomonas aeruginosa kills Caenorhabditis elegans, that P. aeruginosa and C. elegans genes can be identified that affect this killing, and that most of these P. aeruginosa genes are also important for mammalian pathogenesis. Here, we show that Salmonella typhimurium as well as other Salmonella enterica serovars including S. enteritidis and S. dublin can also kill C. elegans. When C. elegans is placed on a lawn of S. typhimurium, the bacteria accumulate in the lumen of the worm intestine and the nematodes die over the course of several days. This killing requires contact with live bacterial cells. The worms die with similar kinetics when placed on a lawn of S. typhimurium for a relatively short time (3-5 hours) before transfer to a lawn of E. coli. After the transfer to E. coli, a high titer of S. typhimurium persists in the C. elegans intestinal lumen for the rest of the worms' life. Furthermore, feeding for 5 hours on a 1:1000 mixture of S. typhimurium and E. coli followed by transfer to 100% E. coli, also led to death after several days. This killing correlated with an increase in the titer of S. typhimurium in the C. elegans lumen, which reached 10,000 bacteria per worm. These data indicate that, in contrast to P. aeruginosa, a small inoculum of S. typhimurium can proliferate in the C. elegans intestine and establish a persistent infection. S. typhimurium mutated in the PhoP/PhoQ signal transduction system caused significantly less killing of C. elegans.