Additional file 2 of Host tp53 mutation induces gut dysbiosis eliciting inflammation through disturbed sialic acid metabolism

Additional file 1: Supplementary methods and Supplementary Figures. Figure S1. tp53 mutant GITs are aberrantly infiltrated by increased numbers of neutrophils and exhibit hyperimmune responses similar to those induced by DSS treatment. Figure S2. Overview of the experimental procedure and comparisons of gross anatomy between the wild type and tp 53 mutants. Figure S3. The increased number of Alcian blue-positive goblet cells in tp53 mutants are due to Gram (-) bacteria. Figure S4. Gamma-proteobacteria class is enriched in the GITs of tp53 mutants. Figure S5. Aeromonas spp., Citrobacter spp., and Pseudomonas spp. are enriched in the tp53 mutant GITs. Figure S6. E. coli does not induce the increase of Alcian blue-positive goblet cells. Figure S7. Photobacterium damselae DreWT1 isolated from GITs of WT does not induce the increase of NFκB-EGFP activity. Figure S8. Endogenous Aeromonas spp. as well as Pseudomonas spp. and Citrobacter spp. were isolated from tp53 mutants in AMB agar plate culture. Figure S9. tp53 mutation alters metabolic pathways in GITs. Figure S10. SCFA levels show no differences between WT and tp53 mutants. Figure S11. Oseltamivir treatment does not alter free sialic acid levels of the host. Figure S12. Neu5Gc, but not Neu5Ac is utilized as a carbon source by Aeromonas jandaei TP531 for its growth. Figure S13. Elevated inflammation elicited by exogenous addition of mCherry-tagged A. jandaei TP531 in tp53 mutants is abolished by limiting available sialic acids with oseltamivir. Figure S14. Neu5Gc supplementation elevates intestinal inflammation but does barely promote Aeromonas blooming. Figure S15. Neu5Ac supplementation elevates intestinal inflammation in a microbiota-dependent manner, but does not promote blooming of Aeromonas spp.. Figure S16. Citrobacter spp. may outcompete Aeronomas spp. when Neu5Gc and Neu5Ac are supplemented as carbon sources. Figure S17. Monoassociation with A. jandaei TP531 does not induce the lethality and the increase of Alcian blue-positive goblet cells. Figure S18. A proposed working model illustrates dysbiosis and intestinal inflammation by tp53 mutation via imbalanced sialometabolism and a potential therapeutic intervention.