Additional file 1 of Pathobionts from chemically disrupted gut microbiota induce insulin-dependent diabetes in mice

Additional file 1: Fig. S1. Fasting C-Peptide in the mice with and without 0.2% DSS. Fig. S2. Serum amylase (AMS) and serum lipase levels in each group. Fig. S3. 0.2% DSS increased food and water intake but did not change energy intake of mice. Fig. S4. 0.2% DSS did not change the lipid accumulation in mice. Fig. S5. 0.2% DSS did not impair gut barrier integrity and induce inflammation. Fig. S6. qPCR of 16S rRNA gene in fecal samples. Fig. S7. The gut microbiota had been depleted by more than 99% in the mice with a cocktail of antibiotics for 5 weeks. Fig. S8. The recipient mice developed a gut microbiota more similar to their donor mice. Fig. S9. Optimal classification performance of the sPLS-DA model of the gut microbial structure in NC and DSS mice. Fig. S10. Fluorescence in situ hybridization (FISH) of 16S rRNA in the pancreas of antibiotic treated mice. Fig. S11. Fluorescence in situ hybridization (FISH) of 16S rRNA in the pancreas in fecal microbiota transplanted mice. Fig. S12. The bacterial load in the liver as measured by real-time qPCR of 16S rRNA gene. Fig. S13. Flow cytometry evaluation of subtypes of leukocytes in the pancreas of FMNC and FMDSS mice. Fig. S14. 0.2% DSS did not enrich bacteria in pacreas and disrupt the immune tolerance in antibiotic treated mice. Fig. S15. Identification of Muribaculaceae strain MF 13079. Fig. S16. Functional annotation of flagella-related genes and motility test of MF13079. Fig. S17. Bacteria load in mesenteric lymph nodes (MLN) in Akk and Muri mice. Fig. S18. Bray-Curtis Distance based on 16S rRNA sequencing data of gut microbiota between recipient mice and human donors. Fig. S19. Fluorescence in situ hybridization (FISH) of 16S rRNA in the pancreas. Tables S1. Culture medium used for isolation of Muribaculeae. Table S2. COG in the genome of MF 13079.