Host gut microbiome and mucosal immune system (Gut-Immune Axis)

The host gut microbiome and mucosal immune system constitute a dynamic and reciprocal interface essential for human health. The gut microbiota, consisting of trillions of bacteria, fungi, and viruses, provides critical signals that shape the development and function of the mucosal immune system, which in turn regulates the composition of the microbiota to prevent overgrowth of pathobionts (Belkaid & Hand, 2014). This interaction is primarily mediated through microbial-associated molecular patterns (MAMPs) and metabolites such as short-chain fatty acids (SCFAs), which promote the differentiation of regulatory T-cells (Tregs) and maintain the integrity of the intestinal epithelial barrier (Round & Mazmanian, 2009). Disruptions in this delicate balance, known as dysbiosis, are strongly linked to the pathogenesis of inflammatory bowel diseases, metabolic disorders, and systemic autoimmunity (Wu & Wu, 2012). Therapeutic strategies targeting this axis include the use of probiotics, prebiotics, and fecal microbiota transplantation (FMT) to restore microbial diversity and suppress aberrant immune responses (Thursby & Juge, 2017). Because this "target" represents a complex biological system rather than a single molecule, therapeutic outcomes often depend on the multi-component interactions between microbial communities and host immune cells (Hooper et al., 2012).

Other names

Microbiota-immune axisIntestinal microbiome-mucosal immune interfaceGut-associated lymphoid tissue (GALT)-microbiome systemHost-microbe mucosal interface

Modulation of the gut-immune axis occurs through the introduction of beneficial microbes (probiotics), substrate for microbial growth (prebiotics), or entire microbial communities (FMT) to restore diversity and produce metabolites like short-chain fatty acids (SCFAs). These metabolites bind to G protein-coupled receptors (e.g., GPR43) on immune cells to induce regulatory T-cell (Treg) differentiation and suppress pro-inflammatory cytokines, thereby restoring mucosal tolerance and barrier integrity.