Mucins, gut microbiota, and postbiotics role in colorectal cancer

Abstract

An imbalance in the crosstalk between the host and gut microbiota affects the intestinal barrier function, which results in inflammatory diseases and colorectal cancer. The colon epithelium protects itself from a harsh environment and various pathogenic organisms by forming a double mucus layer, primarily comprising mucins. Recent studies are focusing on how dietary patterns alter the gut microbiota composition, which in turn regulates mucin expression and maintains the intestinal layers. In addition, modulation of gut microbiota by microbiotic therapy (involving fecal microbiota transplantation) has emerged as a significant factor in the pathologies associated with dysbiosis. Therefore, proper communication between host and gut microbiota via different dietary patterns (prebiotics and probiotics) is needed to maintain mucus composition, mucin synthesis, and regulation. Here, we review how the interactions between diet and gut microbiota and bacterial metabolites (postbiotics) regulate mucus layer functionalities and mucin expression in human health and disease.

Keywords: Mucins; colorectal cancer; gut microbiota; postbiotics; prebiotics; probiotics.

Figure 1.

Amelioration of gut microbiota and mucins. (1). Consumption of a Western-style diet (rich in high-fat calories and low in fiber) and other factors mediates microbiota alterations (dysbiosis) in the colon. (2). This altered microbiota, along with their metabolites, are responsible for increasing the intestinal permeability and reducing the mucus layer thickness by decreasing MUC2 expression; the result is the invasion of pathogens into the epithelium. (3). Administration of pre- (GOS and FOS) and probiotics (majorly bifidobacteria and lactobacilli) and prudent diet improves the intestinal layer functionalities and maintains proper gut health (eubiosis)

Figure 2.

Mechanism(s) of action of prebiotics and probiotics. The health benefits of prebiotics on the host are involved with various mechanisms, viz., 1) Selectively stimulate the growth of beneficial probiotic organisms. 2) Modulate various cytokines to inhibit the secretion of pro-inflammatory markers. 3) & 4) Release SCFAs and increase the absorption of minerals. In case of probiotics: A) Mediate the secretion of metabolites from the prebiotics (e.g., fiber) or directly involved in the inhibition of CRC tumor growth by increasing apoptosis. B) Suppress the growth of harmful bacteria by reducing intestinal luminal pH. C) Secrete the anti-microbial peptides (bacteriocins and β-defensins) to inhibit the growth of pathobionts. D) Decrease colonic inflammation by reducing Th17 and increasing Treg cells

Figure 3.

Mucin regulation and intestinal barrier function by gut microbiota metabolites