Citrobacter rodentium Relies on Commensals for Colonization of the Colonic Mucosa.
Citrobacter rodentium Relies on Commensals for Colonization of the Colonic Mucosa.
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DOI：
10.1016/j.celrep.2017.11.086
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发表时间：
2017-12-19
期刊：
影响因子：
8.8
通讯作者：
Frankel G
中科院分区：
文献类型：
--
作者：
Mullineaux-Sanders C;Collins JW;Ruano-Gallego D;Levy M;Pevsner-Fischer M;Glegola-Madejska IT;Sågfors AM;Wong JLC;Elinav E;Crepin VF;Frankel G
我们研究了共生体在大肠小鼠病原体啮齿柠檬酸杆菌感染高峰期的作用。生物发光和耐卡那霉素（Kan）的啮齿鼠在持续使用Kan的小鼠盲肠腔中无毒性持续存在。单次Kan治疗足以将啮齿鼠从结肠粘膜中移除，而万古霉素（Van）或甲硝唑（Met）治疗后没有观察到这种现象。Kan， Van和Met诱导了明显的生态失调，表明啮齿鼠依赖于特定的共生体进行结肠定植。主毒力调节因子的表达在无菌小鼠中被诱导，但齿状鼠只在盲肠管中可见。此外，在常规小鼠中，单次Kan处理足以将组成性表达Ler的啮齿鼠从结肠粘膜中移除。这些结果表明，毒力基因的表达不足以定植结肠粘膜，共生菌是生理感染过程所必需的。特异性生态失调迅速将啮齿鼠柠檬酸杆菌从结肠粘膜中取代粘膜排斥与啮齿鼠毒力基因表达无关延长抗生素治疗可引起腔内无毒啮齿鼠柠檬酸杆菌的积累啮齿鼠柠檬酸杆菌依赖共生体在结肠粘膜存活，A/E病原体与肠道粘膜紧密结合。Mullineaux-Sanders等人证明，在小鼠感染鼠状柠檬酸杆菌（Citrobacter rodentium）的高峰期诱导特异性生态失调可阻止粘膜定植。这是通过一种独立于毒力基因表达调节的机制发生的，表明肠道病原体可能依赖共生菌进行有效感染。
We investigated the role of commensals at the peak of infection with the colonic mouse pathogen Citrobacter rodentium. Bioluminescent and kanamycin (Kan)-resistant C. rodentium persisted avirulently in the cecal lumen of mice continuously treated with Kan. A single Kan treatment was sufficient to displace C. rodentium from the colonic mucosa, a phenomenon not observed following treatment with vancomycin (Van) or metronidazole (Met). Kan, Van, and Met induce distinct dysbiosis, suggesting C. rodentium relies on specific commensals for colonic colonization. Expression of the master virulence regulator ler is induced in germ-free mice, yet C. rodentium is only seen in the cecal lumen. Moreover, in conventional mice, a single Kan treatment was sufficient to displace C. rodentium constitutively expressing Ler from the colonic mucosa. These results show that expression of virulence genes is not sufficient for colonization of the colonic mucosa and that commensals are essential for a physiological infection course. Specific dysbiosis rapidly displaces Citrobacter rodentium from the colonic mucosa Mucosal exclusion is independent of C. rodentium virulence gene expression Extended antibiotic treatment causes accumulation of luminal avirulent C. rodentium C. rodentium relies on commensals for survival at the colonic mucosa A/E pathogens intimately adhere to the gut mucosa. Mullineaux-Sanders et al. demonstrate that inducing specific dysbiosis at the peak of murine infection with Citrobacter rodentium prevents mucosal colonization. This occurs via a mechanism independent of virulence gene expression modulation, indicating that enteric pathogens may rely on commensals for effective infection.
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影响因子：
30.3
作者：
Kelly CJ;Zheng L;Campbell EL;Saeedi B;Scholz CC;Bayless AJ;Wilson KE;Glover LE;Kominsky DJ;Magnuson A;Weir TL;Ehrentraut SF;Pickel C;Kuhn KA;Lanis JM;Nguyen V;Taylor CT;Colgan SP
通讯作者：
Colgan SP
影响因子：
3.6
作者：
Crepin VF;Girard F;Schüller S;Phillips AD;Mousnier A;Frankel G
通讯作者：
Frankel G
影响因子：
3.2
作者：
Berdichevsky, T;Friedberg, D;Rosenshine, I
通讯作者：
Rosenshine, I
影响因子：
1.2
作者：
Collins, James William;Meganck, Jeffrey A.;Frankel, Gad
通讯作者：
Frankel, Gad
影响因子：
6.4
作者：
Spees AM;Wangdi T;Lopez CA;Kingsbury DD;Xavier MN;Winter SE;Tsolis RM;Bäumler AJ
通讯作者：
Bäumler AJ