Lactobacillus zeae protects Caenorhabditis elegans from enterotoxigenic Escherichia coli-caused death by inhibiting enterotoxin gene expression of the pathogen.
Lactobacillus zeae protects Caenorhabditis elegans from enterotoxigenic Escherichia coli-caused death by inhibiting enterotoxin gene expression of the pathogen.
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DOI：
10.1371/journal.pone.0089004
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Gong J
中科院分区：
文献类型：
--
作者：
Zhou M;Yu H;Yin X;Sabour PM;Chen W;Gong J
秀丽隐杆线虫已越来越多地用于筛选抗菌剂和益生菌，以控制病原体。它也为研究微生物与宿主的相互作用提供了一个有用的工具。本研究建立了秀丽隐杆线虫的寿命测定方法，以预先选择益生菌来控制K88+产肠毒素大肠杆菌（ETEC），这是一种引起猪腹泻的病原体，并确定了乳杆菌提供保护的潜在机制。用线虫的寿命来测定线虫对ETEC感染的反应和乳酸菌（LAB）的保护作用。在13株具有不同保护秀丽隐杆线虫免受ETEC菌株JG280诱导死亡能力的乳酸菌中，玉米乳杆菌LB1的保护水平最高（86%）。乳酸菌处理并没有减少ETEC JG280在线虫肠道中的定植。饲喂大肠杆菌菌株JFF4 （K88+，但缺乏estA、estB和elt的肠毒素基因）未引起线虫死亡。在感染ETEC JG280期间，estA、estB和elt基因的表达显著增加，而分离物LB1显著抑制了这些基因的表达。在大肠杆菌DH5α中表达estA或estB的克隆杀灭线虫的效果与ETEC JG280相同。然而，elt克隆只杀死了大约40%的蠕虫。分离物LB1也可以防止克隆的杀伤。同一分离物在体外仅部分抑制ETEC JG280和大肠杆菌DH5α肠毒素基因的表达。所建立的寿命测定法可用于控制ETEC的益生菌研究（用于有效选择和机制研究）。热稳定性肠毒素似乎是秀丽隐杆线虫死亡的主要原因。抑制ETEC肠毒素的产生，而不是干扰其肠道定植，似乎是乳杆菌提供的保护机制。
The nematode Caenorhabditis elegans has become increasingly used for screening antimicrobials and probiotics for pathogen control. It also provides a useful tool for studying microbe-host interactions. This study has established a C. elegans life-span assay to preselect probiotic bacteria for controlling K88+ enterotoxigenic Escherichia coli (ETEC), a pathogen causing pig diarrhea, and has determined a potential mechanism underlying the protection provided by Lactobacillus. Life-span of C. elegans was used to measure the response of worms to ETEC infection and protection provided by lactic acid-producing bacteria (LAB). Among 13 LAB isolates that varied in their ability to protect C. elegans from death induced by ETEC strain JG280, Lactobacillus zeae LB1 offered the highest level of protection (86%). The treatment with Lactobacillus did not reduce ETEC JG280 colonization in the nematode intestine. Feeding E. coli strain JFF4 (K88+ but lacking enterotoxin genes of estA, estB, and elt) did not cause death of worms. There was a significant increase in gene expression of estA, estB, and elt during ETEC JG280 infection, which was remarkably inhibited by isolate LB1. The clone with either estA or estB expressed in E. coli DH5α was as effective as ETEC JG280 in killing the nematode. However, the elt clone killed only approximately 40% of worms. The killing by the clones could also be prevented by isolate LB1. The same isolate only partially inhibited the gene expression of enterotoxins in both ETEC JG280 and E. coli DH5α in-vitro. The established life-span assay can be used for studies of probiotics to control ETEC (for effective selection and mechanistic studies). Heat-stable enterotoxins appeared to be the main factors responsible for the death of C. elegans. Inhibition of ETEC enterotoxin production, rather than interference of its intestinal colonization, appears to be the mechanism of protection offered by Lactobacillus.
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影响因子：
30.3
作者：
Anyanful A;Easley KA;Benian GM;Kalman D
通讯作者：
Kalman D
影响因子：
4.4
作者：
Daudelin JF;Lessard M;Beaudoin F;Nadeau E;Bissonnette N;Boutin Y;Brousseau JP;Lauzon K;Fairbrother JM
通讯作者：
Fairbrother JM
影响因子：
3.3
作者：
Frydendahl, K
通讯作者：
Frydendahl, K
影响因子：
4
作者：
Moy, Terence I.;Conery, Annie L.;Larkins-Ford, Jonah;Wu, Gang;Mazitschek, Ralph;Casadei, Gabriele;Lewis, Kim;Carpenter, Anne E.;Ausubel, Frederick M.
通讯作者：
Ausubel, Frederick M.
影响因子：
2.2
作者：
Carey, Christine M.;Kostrzynska, Magdalena;Thompson, Stacey
通讯作者：
Thompson, Stacey