Figure 1.

Cross-communication in the gut, showing bacteria–bacteria, bacteria–host, and host–bacteria communication. In the bacteria–bacteria communication, elevated AI-2 induces the growth of native gut bacterial residents such as Firmicutes and Bifidobacteria but suppresses the expansion of pathogens such as V. cholera. 3-Oxo-C12:2 is positively associated with Firmicutes. Indole enhances the proliferation of beneficial bacteria. In the bacteria–host communication, 3-oxo-C12:2 protect tight junction integrity. Indoles enhances epithelial barrier function via the aryl hydrocarbon receptor (AhR). While AI-3 induces pro-inflammatory reactions by stimulating the expression of cytokines IL-8, 3-oxo-C12:2-HSL reduces inflammation by repressing the expression of IL-1, IL-8, and TNF. 3-Oxo-C12 exacts a negative impact on the epithelial barrier by disrupting the tight junctions. Gram-positive signal peptides, such as competence and sporulation factor (CSF) bind to the cation transporter (OCTN2), and subsequently activate heat shock protein (HSP), p38 MAP, and protein kinase B (Akt), to protect intestinal barriers from oxidative stress damage, and impairment. The QS peptide, EntF*, promotes colorectal cancer (CRC) metastasis through interference with the epithelial cells’ integrity. The host–bacteria communication means, from the host end, the microenvironment in the lumen (pH, Temperature, Osmotic pressure, and Bile acids) which inactivates QS signals such as AI-2 is modulated. Also, paraoxonases (PONs) exert lactonase-like activity against AHLs signals. AI-2 mimics, and catecholamines (epinephrine (EPI)/norepinephrine (NE)) are recognized by the bacterial QS receptors to modulate gut microbial balance (created using BioRender.com, accessed on 12 December 2022).