Ecobiotherapy Rich in Firmicutes Decreases Susceptibility to @entity1960 in a Humanized Gnotobiotic XXXX Model.

@entity1 @entity32 @entity19 @entity31 @entity2397 @entity1960 @entity636 @entity694
BACKGROUND: Alterations in the intestinal microbiota, characterized by depletion of anti-inflammatory bacteria, such as Firmicutes, in @entity1 with @entity31 ( @entity31 ) have prompted interest in microbiota-modulating strategies for this condition. The aim of this study was to evaluate the role of fecal and synthetic @entity1 microbial ecosystems, low or enriched in Firmicutes, on @entity1960 susceptibility and host immune responses. METHODS: The microbiota of selected healthy and @entity31 @entity1 donors was characterized by culture method and 16S rRNA-based sequencing. Germ-free @entity19 were colonized with fecal or a synthetic ecosystem enriched (healthy donors) or low ( @entity31 donors) in Firmicutes. Experimental @entity1960 was induced using dextran @entity2397 . Colon transcriptome and @entity694 cells were evaluated in @entity19 postcolonization by RNA-seq and flow cytometry, respectively, and T helper (TH) 17 differentiation was assessed in vitro. RESULTS: @entity19 colonized with microbiota from @entity1 with @entity31 low in Firmicutes had increased sensitivity to @entity1960 compared with @entity19 colonized with fecal or synthetic ecosystems rich in Firmicutes. Microbiota low in Firmicutes increased expression of TH17-related genes and expansion of @entity636 -expressing CD4 cells in vivo. Supplementation with bacterial isolates belonging to the Firmicutes phylum abrogated the heightened TH17 responses in vitro. CONCLUSIONS: A microbiota rich in Firmicutes derived from fecal samples of a healthy @entity1 donor, or assembled synthetically, downregulated @entity32 and TH17 pathways in @entity19 . The results support the use of ecobiotherapy strategies, enriched in Firmicutes, for the prevention or treatment of @entity31 .
