Additional file 1 of Dietary fibre supplementation enhances radiotherapy tumour control and alleviates intestinal radiation toxicity

Additionalfile1: Supplementary Figure S1. Differences in bacterial components in the normal chow, 0.2% cellulose and psyllium groups. Supplementary Figure S2. Differences in bacterial components in the psyllium, psyllium plus RS and psyllium plus inulin groups. Supplementary Figure S3. Local tumour and systemic immune responses in all dietary groups. Supplementary Figure S4. Discovery metabolomics analysis of caecal contents in all dietary groups. Supplementary Figure S5. Body weight changes of non-IR and IR cohorts of each dietary groups for the mice that did not receive IR or following IR. Supplementary Figure S6. Psyllium plus RS radiosensitised UPPL1591 bladder cancer cell allografts. Supplementary Figure S7. Survival analysis of tumour-bearing mice without and with IR in different dietary groups. Supplementary Figure S8. Phylogenetic composition of faecal microbiota when tumours reached 700 mm3. Supplementary Figure S9. Differences in bacterial components in responders and non-responders in the psyllium plus inulin group. Supplementary Figure S10. Principal coordinate analysis using Jaccard distance of faecal microbiota in the IR cohorts of (a) psyllium plus inulin or (b) psyllium plus RS. Supplementary Figure S11. Correlation between the gut microbiota versus the tumour growth in non-IR and IR cohorts of psyllium plus RS. Supplementary Figure S12. Beta diversity of faecal microbiota in the radiosensitisation experiment. Supplementary Figure S13. Unweighted UniFrac distance of faecal microbiota between cages in the radiosensitisation experiment. Supplementary Figure S14. Weighted UniFrac distance of faecal microbiota between cages in the radiosensitisation experiment. Supplementary Figure S15. Local tumour cytotoxic T cells in the IR cohorts of all dietary groups. Supplementary Figure S16. Local tumour immune responses in the IR cohorts of all dietary groups. Supplementary Figure S17. Local tumour and systemic immunity in psyllium plus inulin stratified by tumour response and IR. Supplementary Figure S18. Correlations between the Clostridia and Lachnospirales orders and the populations of splenic (a) leukocytes, (b) macrophages, and (c) natural killer cells in the IR cohorts of psyllium plus inulin group. Supplementary Figure S19. Metabolites and KEGG pathway that were associated with tumour growth in mice fed with psyllium plus RS. Supplementary Figure S20. Correlations between the caecal (a) threitol, (b) asparaginyl-hydroxyproline and (c) butyrate levels versus the tumour growth rate in IR cohort with or without non-IR cohort in the psyllium plus inulin group. Supplementary Figure S21. Phylogenetic composition of faecal microbiota before and after irradiation in the acute toxicity experiment. Supplementary Figure S22. Beta diversity of the gut microbiota and the metabolites profile in non-tumour-bearing mice after 3-week modified diet and 3.75 days after SARRP IR. Supplementary Figure S23. Caecal SCFAs in non-tumour-bearing mice after 3-week modified diet in acute toxicity and late toxicity experiments. Supplementary Figure S24. Overview of late normal tissue toxicity experiment. Supplementary Figure S25. Representative images of mouse large intestine sections in non-tumour-bearing mice after 22-week modified diet with or without SARRP IR. Supplementary Figure S26. Relative body weight of non-IR and IR cohorts of each dietary groups for the mice that did not receive IR or following IR. Supplementary Figure S27. Actual body weight of non-IR and IR cohorts of each dietary groups for the mice that did not receive IR or following IR. Supplementary Figure S28. Phylogenetic composition of faecal microbiota before and after irradiation in the late toxicity experiment. Supplementary Figure S29. Beta diversity of faecal microbiota in the late toxicity experiment. Supplementary Figure S30. BA+FP increased cytotoxic responses and DNA damage in T24 bladder cancer cells. Supplementary Figure S31. BA+FP increased histone acetylation levels and DNA damage in bladder cancer cells. Supplementary Figure S32. Production of SCFAs in pelvic cancer patients. Supplementary Figure S33. Comparison of bacterial and SCFA relative abundances between human samples processed serially showed similar profiles between the different processing times: 0, 24, 48 and 72 hours. Supplementary Figure S34. Correlations between Lachnospiraceae family and faecal (a) formate, (b) propionate, (c) valerate levels in cancer patients. Supplementary Figure S35. Correlations between Bacteroides genus and faecal (a) total amount of three major SCFAs, (b) acetate, (c) propionate, (d) butyrate, (e) formate, (f) valerate levels in cancer patients. Supplementary Table S1. R2 and Pr(>F) values from ADONIS test assessing unweighted and weighted UniFrac distances. Supplementary Table S2. Four most abundant phyla for human and mouse samples. Supplementary Table S3. Bacteria taxa enriched in cancer patients with low and high faecal SCFAs. Supplementary Table S4. Four most abundant phyla of three serial human faecal samples prepared at 24-hour intervals for 72-hours. Supplementary Table S5. Rodent diets without corn starch used in the study with varying levels of cellulose, psyllium, psyllium plus resistant starch, or inulin per 4000 kcal. Supplementary Table S6. Definitions of immune cell populations based on expression of cell surface markers. Supplementary Table S7. Antibody titrations and catalogue numbers. Supplementary Table S8. Effect of technical factors on sample composition (Bray-Curtis).