FIGURE 1.

Transferrable dysbiosis in RAI16^–/– mice is responsible for exacerbated colitis. (A–D) Separately housed RAI16^–/– mice, WT mice and co‐housed WT (WT(RAI16^–/–) mice or RAI16^–/– (WT) mice were administrated of 2.5% DSS for 6 days. Body weight loss (A) and disease activity index (B) of separately housed RAI16^–/–, WT, co‐housed WT (WT(RAI16^–/–) and RAI16^–/– (WT) mice were monitored daily, colon length (C) and histopathology (D) were determined at day 7 post DSS treatment. (E, H) Pretreated for 3 weeks with an antibiotics cocktail (ABx: ampicillin, kanamycin, vancomycin and metronidazole), then recolonised with either WT or RAI16^–/– faecal material by oral gavage, mice were administrated of 2.5% DSS as usual. Body weight loss (E), disease activity index (F), colon length (G) and histopathology (H) were determined as before. (I) Bacterial 16S rRNA‐based analysis of the faecal microbiota from WT and RAI16^–/– mice. (J) The indicated key microbial species were tested by quantitative PCR (WT and RAI16^–/– mice, n = 8–12). The increased abundance of Prevotella and Bacterroidase and the decreased abundance of Clostridia were shown. (K) Relative abundance of Prevotella DNA at 0, 2 and 4 weeks of co‐housing was measured by quantitative PCR. (L, N) Pretreated for 3 weeks with ABx as before, then recolonised with Prevotella spp. by oral gavage or not, mice were administrated of 2.5% DSS as usual. Body weight loss (L), disease activity index (M) and histopathology (N) were determined as before.