Literature DB >> 22572831

Comparative evaluation of establishing a human gut microbial community within rodent models.

Melissa Wos-Oxley1, André Bleich, Andrew P A Oxley, Silke Kahl, Lydia M Janus, Anna Smoczek, Hannes Nahrstedt, Marina C Pils, Stefan Taudien, Matthias Platzer, Hans-Jürgen Hedrich, Eva Medina, Dietmar H Pieper.   

Abstract

The structure of the human gut microbial community is determined by host genetics and environmental factors, where alterations in its structure have been associated with the onset of different diseases. Establishing a defined human gut microbial community within inbred rodent models provides a means to study microbial-related pathologies, however, an in-depth comparison of the established human gut microbiota in the different models is lacking. We compared the efficiency of establishing the bacterial component of a defined human microbial community within germ-free (GF) rats, GF mice, and antibiotic-treated specific pathogen-free mice. Remarkable differences were observed between the different rodent models. While the majority of abundant human-donor bacterial phylotypes were established in the GF rats, only a subset was present in the GF mice. Despite the fact that members of the phylum Bacteriodetes were well established in all rodent models, mice enriched for phylotypes related to species of Bacteroides. In contrary to the efficiency of Clostridiales to populate the GF rat in relative proportions to that of the human-donor, members of Clostridia cluster IV only poorly colonize the mouse gut. Thus, the genetic background of the different recipient rodent systems (that is, rats and mice) strongly influences the nature of the populating human gut microbiota, determining each model's biological suitability.

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Year:  2012        PMID: 22572831      PMCID: PMC3427216          DOI: 10.4161/gmic.19934

Source DB:  PubMed          Journal:  Gut Microbes        ISSN: 1949-0976


  67 in total

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6.  Human gut microbiota transferred to germ-free NOD mice modulate the progression towards type 1 diabetes regardless of the pace of beta cell function loss in the donor.

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