In 2011 Arumugam et al. described for the first time characteristic patterns of human gut microflora composition, which were seemingly preserved world-wide, across different nations and cultures. These patterns, named enterotypes, were defined by the significantly higher abundance of one of three bacterial genera: Bacteroides (enterotype 1), Prevotella (enterotype 2) and Ruminococcus (enterotype 3).

This simple concept of enterotypes has since divided the microbiome field. Some researchers found themselves influenced by the alluring idea of discrete microflora types, while others dismissed it out of hand as overly simplistic and as blurring what they view as a more accurate, continuous image of our gut flora. It seems, however, that at this stage it is simply a bit too early to decide once and for all who is and who isn’t right. And in this row between ‘enterotype’-ists and ‘gradualists’ it is good not to forget about probably the most important aspect of the original enterotype study: the demonstration that our gut microbiota differ not only on the individual level, but also globally, and that these differences might have a deeper biological and potentially also clinical meaning.

In an article published today in Genome Biology, Jeroen Raes follows on from the original enterotypes article, of which he was an author, and tries to answer yet another burning question: if the human gut microbiota exhibit global composition differences, does the same happen in other organisms? And if the answer is yes – what impact does it have on model animal research?

In the study, the authors take a look at five popular lab mouse strains. They identify two microbiota types eerily similar to human enterotypes 1 and 3. In addition to the standard weapon in any self-respecting microbiome researcher’s arsenal, poop sequencing, Raes and colleagues also measure the levels of an inflammatory bowel disease marker – calprotectin – in mice feces. And here comes one of their most astounding observations: they find that what they had defined as mouse enterotype 2 is significantly associated with increased calprotectin levels.

In other words, Raes and colleagues show that enterotypes in mice might be either a driver or a manifestation of inflammatory bowel disease. The implications of these results, which to the more dedicated Genome Biology readers will be reminiscent of our recent Huttenhower and colleagues article on intestinal dysbiosis in inflammatory bowel disease, are striking either way.