TABLE 1.
Major bacterial components and metabolites and their effect on gastrointestinal (GI) motility.
| Major bacterial components and metabolites | Effects on gastrointestinal (GI) motility |
| Lipopeptides and peptidoglycan | Signaling through toll-like receptor 2 (TLR2), maintaining adult enteric nervous system and nitrergic neurons |
| Lipopolysaccharides (LPS) | Signaling via TLR4, playing dual function of improving and delaying motility in different manners |
| Deoxycholic acid (DCA) and lithocholic acid (LCA) | By activating Taketa G-protein-coupled receptor 5 (TGR5), modulating the release of 5-hydroxytryptamine (5-HT) and promoting GI motility |
| 7-ketodeoxycholic acid and muricholic acid | Associated with faster GI transit |
| Short-chain fatty acids (SCFAs) | Stimulation of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) production, modulating the release of 5-HT, playing dual function of increasing and decreasing GI motility |
| Tryptamine | By activating epithelial 5-HT4, accelerating GI transit |
| Indole-3-carboxaldehyde (IAld) | Activating cholinergic enteric neurons to promote GI motility |
| 5-hydroxytryptophan (5-HTP) | Converted to 5-hydroxyindole (5-HI) by bacterial tryptophanase, improving GI motility directly through activation of L-type voltage-dependent calcium channels (L-VDCCs) |
| Quercetin | Promoting GI motility and mucin secretion |
| Putrescine and cadaverine | Regulating intestinal peristalsis |
| γ-aminobutyric acid (GABA) | Modulating both motor and secretory GI activity |