Zentralinstitut für Ernährungs und Lebensmittelforschung, Abteilung Mikrobiologie, Technische Universität München, 85354 Freising, Germany.
Appl Environ Microbiol. 2010 Sep;76(18):6277-85. doi: 10.1128/AEM.01274-10. Epub 2010 Jul 16.
Caenorhabditis elegans is a validated model to study bacterial pathogenicity. We report that Yersinia enterocolitica strains W22703 (biovar 2, serovar O:9) and WA314 (biovar 1B, serovar O:8) kill C. elegans when feeding on the pathogens for at least 15 min before transfer to the feeding strain Escherichia coli OP50. The killing by Yersinia enterocolitica requires viable bacteria and, in contrast to that by Yersinia pestis and Yersinia pseudotuberculosis strains, is biofilm independent. The deletion of tcaA encoding an insecticidal toxin resulted in an OP50-like life span of C. elegans, indicating an essential role of TcaA in the nematocidal activity of Y. enterocolitica. TcaA alone is not sufficient for nematocidal activity because E. coli DH5alpha overexpressing TcaA did not result in a reduced C. elegans life span. Spatial-temporal analysis of C. elegans infected with green fluorescent protein-labeled Y. enterocolitica strains showed that Y. enterocolitica colonizes the nematode intestine, leading to an extreme expansion of the intestinal lumen. By low-dose infection with W22703 or DH5alpha followed by transfer to E. coli OP50, proliferation of Y. enterocolitica, but not E. coli, in the intestinal lumen of the nematode was observed. The titer of W22703 cells within the worm increased to over 10(6) per worm 4 days after infection while a significantly lower number of a tcaA knockout mutant was recovered. A strong expression of tcaA was observed during the first 5 days of infection. Y. enterocolitica WA314 (biovar 1B, serovar O:8) mutant strains lacking the yadA, inv, yopE, and irp1 genes known to be important for virulence in mammals were not attenuated or only slightly attenuated in their toxicity toward the nematode, suggesting that these factors do not play a significant role in the colonization and persistence of this pathogen in nematodes. In summary, this study supports the hypothesis that C. elegans is a natural host and nutrient source of Y. enterocolitica.
秀丽隐杆线虫是研究细菌致病性的有效模型。我们报告,在转移到喂食菌株大肠杆菌 OP50 之前,至少喂食 15 分钟,肠耶尔森菌 W22703(生物型 2,血清型 O:9)和 WA314(生物型 1B,血清型 O:8)菌株可以杀死秀丽隐杆线虫。肠耶尔森菌的杀伤需要活菌,并且与鼠疫耶尔森菌和假结核耶尔森菌菌株的杀伤不同,肠耶尔森菌的杀伤不依赖生物膜。编码一种杀虫毒素的 tcaA 的缺失导致秀丽隐杆线虫的 OP50 样寿命,表明 TcaA 在肠耶尔森菌的线虫杀伤活性中起关键作用。TcaA 本身不足以引起线虫杀伤活性,因为过度表达 TcaA 的大肠杆菌 DH5alpha 并没有导致秀丽隐杆线虫寿命缩短。用绿色荧光蛋白标记的肠耶尔森菌菌株感染秀丽隐杆线虫的时空分析表明,肠耶尔森菌定植于线虫肠道,导致肠道腔极度扩张。通过低剂量感染 W22703 或 DH5alpha 后转移到大肠杆菌 OP50,观察到线虫肠道中肠耶尔森菌的增殖,而不是大肠杆菌的增殖。感染后 4 天,蠕虫内 W22703 细胞的滴度增加到超过 10(6)个/蠕虫,而回收的 tcaA 敲除突变体的数量明显减少。在感染的前 5 天观察到 tcaA 的强烈表达。已知对哺乳动物具有重要毒力的 yadA、inv、yopE 和 irp1 基因缺失的肠耶尔森菌 WA314(生物型 1B,血清型 O:8)突变菌株在对线虫的毒性方面没有减弱或仅略有减弱,这表明这些因素在该病原体在线虫中的定植和持续存在中不起重要作用。总之,这项研究支持秀丽隐杆线虫是肠耶尔森菌的天然宿主和营养来源的假说。