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International audience

Additional file 1: Fig. S1. [Global ETEC survival percentages in the cumulated ileal effluents of the TIM-1]. Fig. S2. [Live/Dead flow cytometry for accurate determination of ETEC membrane physiology in the TIM-1 gastric and ileal effluents]. Fig. S3. [Spearman correlation between virulence gene expression, LT toxin production and/or ETEC survival in the TIM-1 and M-SHIME]. Fig. S4. [Phylum and species levels microbial community composition of the luminal gut regions]. Fig. S5. [Phylum and species levels microbial community composition of the mucosal gut regions]. Fig. S6. [Gut microbes concentration in the ileum and ascending colon lumen determined by total flora 16S rRNA gene quantification]. Fig. S7. [Simpson alpha diversity index over time for the six donors according to the luminal (L) and mucosal (M) gut regions]. Fig. S8. [db-RDA triplots showing the relationship of A) gut regions, B) donors and C) period pre- vs post-infection as explanatory variables to the microbial community structure at genus level]. Fig. S9. [db-RDA triplots showing the effect of ETEC pre- and post-infection on distinct microbial genera according to the gut regions]. Fig. S10. [SCFA concentrations (mM) in the ileum (ILE) and ascending colon (ASC) compartments of the M-SHIME]. Fig. S11. [Spearman correlations between the main SCFA produced in the ascending colon and ETEC survival, LT toxin production, and expression of virulence genes encoding for the enterotoxins]. Fig. S12. [High reproducibility in SCFA concentrations and microbiota composition between replicates from a same donor in a separate SHIME experiment]. Table S1. [ETEC intracellular pH (pHi) in the TIM-1 system]. Table S2. [ETEC membrane potential in the TIM-1 system]. Table S3. [Log2 fold changes in virulence genes expression in the TIM-1]. Table S4. [Log2 fold changes in virulence genes expression in the M-SHIME]. Table S5. [Parameters of the TIM-1 and M-SHIME systems]. Table S6. [General characteristic of the fecal donors involved in the M-SHIME experiments]. Table S7. [Static in vitro gastro-jejunal digestion procedure]. Table S8. [ETEC primers used in the study]. Table S9. [RDP Seqmatch and NCBI BLAST results for the most abundant species and/or species of interest in the M-SHIME].

Enterotoxigenic Escherichia coli (ETEC) and Enterohemorrhagic Escherichia coli (EHEC) are major food‐ and water‐borne pathogens that constitute a serious public health threat in low‐income and developed countries, respectively. Survival and expression of virulence genes in the human digestive tract are key features in bacterial pathogenesis, but the mechanisms behind these processes remain largely unknown due to obvious prohibition of human studies. Use of well‐controlled and multi‐parametric in vitro models can aid in addressing knowledge gaps in ETEC and EHEC pathogenesis. After a general description of the physiopathology of ETEC and EHEC infections, this chapter will give an overview of all the in vitro studies that have investigated the effect of the main physicochemical and biotic parameters of the human gut on pathogen survival and expression of virulence factors. We bring a picture of how ETEC and EHEC are able to adapt to each of the successive environments of the human gastrointestinal tract by reading many cues provided by both the host and the gut microbiota.