Table 1 Bacterial mucosal receptors

E. coli binding to Neu5Gc-containing glycans

Influence the gut microbiota population and metabolism.

Cause stomach disorders (Sreevalsan and Safe, 2013) and loss of short chain fatty acids (SCFAs).

Diet rich in fibre promotes the growth of bacteria that generate SCFAs.

Changes in mucosal glycosylation (due to inflammation)

Affects a low number among bacteriophages and less eradicating effects on bacteria specific for mucus-penetrating (Kamada et al., 2013).

The resulting dysbiosis is associated with intestinal permeability (Kamada et al., 2013).

Akkermansia muciniphila is a promising probiotics, improving metabolic functions and immune response (Zhang et al., 2019)

Increased free fucose in the colon

Confers locus of Enterocyte Effacement (LEE) virulence genes produced by Enterohaemorrhagic E.coli (Wells et al., 2011).

LEE effacing lesion, leading to a brush border or lumen and microvili destruction, loss of ion and induce severe diarrhea.

Eat diet rich in fibre to supply SCFAs and fermented food to heal the gut.

Thinner mucus in the distal colon (diet with Microbiota-accessible carbohydrates (MACs depletion)

Increases the proximity of microbes to the epithelium.

The expression of an

inflammation marker REGIIIβ is increased (Gebhart et al., 2015).

Faecalibacterium prausnitzii has anti-inflammatory effects partially via the elevation of IL-10 production (Yan et al., 2008).

TGF-β also suppresses an inflammatory response and mediates immune tolerance (Hornung et al., 2009).

Shiga, bacterial toxins of type AB5 and pertussis toxins

Get adhered to the surface of intestinal glycan (Sreevalsan and Safe, 2013).

Influence the gut microbiota population and metabolism. Eventually cause stomach disorders (Sreevalsan and Safe, 2013).

Akkermansia muciniphila is a promising probiotic, improving metabolic functions and immune response (Zhang et al., 2019)

Monosaccharide (from intestinal glycans)

Utilized by bacteria devoid of glycosidases.

Mediate a strong proliferating response leading to dysbiosis (Rahman et al., 2016).

Same intervention as above.

Obstructed mucin glycosylation

Obstruction of carbohydrates for bacterial utilizing mucinglycans as source of carbon (Rahman et al., 2016)

Dysbiosis in the gut

microbiota is the resulting

consequences.

Same intervention as above.

The junctional adhesion molecule A (JAM-A) knockout

Increase of Desulfovibrionaceae and decrease of Akkermansia (Kashiwagi et al., 2015)

Wound-induced inflammation and angiogenesis.

Probiotics, dietary fiber, antioxidants, mucosal nutrients stimulating digestive enzymes.