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Updated: Aug 31, 2025
Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates
Published on: February 17, 2023
Intestinal mucus-derived metabolites modulate virulence of a clade 8 enterohemorrhagic Escherichia coli O157:H7
Nicolás Garimano1, María Luján Scalise1, Fernando Gómez1
1Laboratorio de Fisiopatogenia, Instituto de Fisiología y Biofísica, IFIBIO-Houssay (UBA-CONICET), Departamento de Ciencias Fisiológicas, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Abstract:
The human colonic mucus is mainly composed of mucins, which are highly glycosylated proteins. The normal commensal colonic microbiota has mucolytic activity and is capable of releasing the monosaccharides contained in mucins, which can then be used as carbon sources by pathogens such as Enterohemorrhagic Escherichia coli (EHEC). EHEC can regulate the expression of some of its virulence factors through environmental sensing of mucus-derived sugars, but its implications regarding its main virulence factor, Shiga toxin type 2 (Stx2), among others, remain unknown. In the present work, we have studied the effects of five of the most abundant mucolytic activity-derived sugars, Fucose (L-Fucose), Galactose (D-Galactose), N-Gal (N-acetyl-galactosamine), NANA (N-Acetyl-Neuraminic Acid) and NAG (N-Acetyl-D-Glucosamine) on EHEC growth, adhesion to epithelial colonic cells (HCT-8), and Stx2 production and translocation across a polarized HCT-8 monolayer. We found that bacterial growth was maximum when using NAG and NANA compared to Galactose, Fucose or N-Gal, and that EHEC adhesion was inhibited regardless of the metabolite used. On the other hand, Stx2 production was enhanced when using NAG and inhibited with the rest of the metabolites, whilst Stx2 translocation was only enhanced when using NANA, and this increase occurred only through the transcellular route. Overall, this study provides insights on the influence of the commensal microbiota on the pathogenicity of E. coli O157:H7, helping to identify favorable intestinal environments for the development of severe disease.
Insights
Mucus sugars impact Enterohemorrhagic Escherichia coli (EHEC) pathogenicity. N-acetyl-D-glucosamine (NAG) and N-acetylneuraminic acid (NANA) enhance EHEC growth and Shiga toxin 2 (Stx2) production, while inhibiting adhesion.
Area of Science:
- Microbiology
- Gastroenterology
- Pathogen-host interactions
Background:
- Human colonic mucus, rich in mucins, provides nutrients for commensal microbiota.
- Commensal bacteria degrade mucins, releasing monosaccharides usable by pathogens like Enterohemorrhagic Escherichia coli (EHEC).
- EHEC virulence factor regulation by mucus-derived sugars, particularly Shiga toxin 2 (Stx2), is not fully understood.
Purpose of the Study:
- To investigate the impact of five abundant mucin-derived monosaccharides on EHEC growth, adhesion, and Stx2 production/translocation.
- To elucidate the role of specific sugars (Fucose, Galactose, N-acetyl-galactosamine, NANA, NAG) in EHEC pathogenicity.
- To understand how the gut microbiota's metabolic activity influences EHEC virulence.
Main Methods:
- Culturing EHEC in the presence of Fucose, Galactose, N-acetyl-galactosamine, NANA, and NAG.
- Assessing EHEC growth rates with each sugar.
- Quantifying EHEC adhesion to HCT-8 epithelial cells.
- Measuring Stx2 production and translocation across a polarized HCT-8 cell monolayer.
Main Results:
- Bacterial growth was highest with NAG and NANA.
- EHEC adhesion was reduced irrespective of the sugar tested.
- Stx2 production increased with NAG and decreased with other sugars.
- Stx2 translocation was enhanced only by NANA, specifically via the transcellular route.
Conclusions:
- Mucus-derived sugars differentially affect EHEC growth, adhesion, and Stx2 expression.
- NAG and NANA promote EHEC growth and Stx2 production, potentially increasing pathogenicity.
- These findings highlight how microbiota-derived nutrients can shape the intestinal environment for EHEC infection.
- Understanding these interactions can help identify conditions favoring severe EHEC disease.
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