In a recent paper, researchers from Canada have coined the term ‘ecobiotherapy’ to refer to “the use of microbial ecosystems for a therapeutic purpose.” The ecosystem need not be fully characterized; it may be an ecosystem as used in classic cases of fecal microbiota transplantation, or it may be assembled from select, isolated bacteria that are chosen for their demonstrated beneficial effects in the host. Authors told GMFH editors, however, that this working definition may change over time and/or become more specific as this area of research evolves.

Scientists have previously observed a depletion of anti-inflammatory bacteria, particularly Firmicutes, in the intestines of patients with ulcerative colitis (UC). This study evaluated how microbial ecosystems low or enriched in Firmicutes could affect colitis susceptibility and host immune responses in mice. Researchers tested both fecal samples and synthetic mixtures of microbes.

In this study, researchers characterized the microbiota of healthy human donors and those with UC. The fecal microbiota of healthy donors was indeed enriched in Firmicutes, and the microbiota of UC donors was low in Firmicutes. Germ-free mice were colonized with either a fecal sample from these donors or a synthetic ecosystem enriched or low in Firmicutes.

Colitis was induced in the mice with dextran sodium sulfate. Mice with microbiota low in Firmicutes (as in the UC donors) showed an increased sensitivity to colitis, compared to mice colonized with ecosystems rich in Firmicutes. In the mice, low Firmicutes increased the expression of Th17-related genes and expansion of interleukin-17A-expressing CD4+ cells.

A Firmicutes-rich microbiota — whether it was taken from healthy human donors or put together synthetically — decreased colonic inflammation and downregulated Th17 pathways in mice. These experiments support the use of ecobiotherapy strategies for prevention or treatment of UC.

Natividad JM, et al. (2015) Ecobiotherapy rich in Firmicutes decreases susceptibility to colitis in a humanized gnotobiotic mouse model. Inflammatory Bowel Diseases doi: 10.1097/MIB.0000000000000422