Nlrp6-and ASC-Dependent Inflammasomes Do Not Shape the Commensal Gut Microbiota Composition

被引:159
作者
Mamantopoulos, Michail
Ronchi, Francesca
Van Hauwermeiren, Filip [2 ]
Vieira-Silva, Sara
Yilmaz, Bahtiyar [1 ,2 ]
Martens, Liesbet [1 ]
Saeys, Yvan
Drexler, Stefan K. [1 ]
Yazdi, Amir S. [2 ]
Raes, Jeroen [1 ]
Lamkanfi, Mohamed
McCoy, Kathy D. [1 ]
Wullaert, Andy [1 ]
机构
[1] Univ Ghent, Dept Internal Med, Ghent, Belgium
[2] VIB UGent Ctr Inflammat Res, VIB, Ghent, Belgium
基金
瑞士国家科学基金会; 欧洲研究理事会;
关键词
WIDE ASSOCIATION; INNATE IMMUNITY; RECEPTOR; COLITIS; PRIMERS; GENOME;
D O I
10.1016/j.immuni.2017.07.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The gut microbiota regulate susceptibility to multiple human diseases. The Nlrp6-ASC inflammasome is widely regarded as a hallmark host innate immune axis that shapes the gut microbiota composition. This notion stems from studies reporting dysbiosis in mice lacking these inflammasome components when compared with non-littermate wild-type animals. Here, we describe microbial analyses in inflammasome-deficient mice while minimizing non-genetic confounders using littermate-controlled Nlrp6-deficient mice and ex-germ-free littermate-controlled ASC-deficient mice that were all allowed to shape their gut microbiota naturally after birth. Careful microbial phylogenetic analyses of these cohorts failed to reveal regulation of the gut microbiota composition by the Nlrp6- and ASC-dependent inflammasomes. Our results obtained in two geographically separated animal facilities dismiss a generalizable impact of Nlrp6- and ASC-dependent inflammasomes on the composition of the commensal gut microbiota and highlight the necessity for littermate-controlled experimental design in assessing the influence of host immunity on gut microbial ecology.
引用
收藏
页码:339 / +
页数:14
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