Modulating Composition and Metabolic Activity of the Gut Microbiota in IBD Patients

Abstract

The healthy intestine represents a remarkable interface where sterile host tissues come in contact with gut microbiota, in a balanced state of homeostasis. The imbalance of gut homeostasis is associated with the onset of many severe pathological conditions, such as inflammatory bowel disease (IBD), a chronic gastrointestinal disorder increasing in incidence and severely influencing affected individuals. Despite the recent development of next generation sequencing and bioinformatics, the current scientific knowledge of specific triggers and diagnostic markers to improve interventional approaches in IBD is still scarce. In this review we present and discuss currently available and emerging therapeutic options in modulating composition and metabolic activity of gut microbiota in patients affected by IBD. Therapeutic approaches at the microbiota level, such as dietary interventions alone or with probiotics, prebiotics and synbiotics, administration of antibiotics, performing fecal microbiota transplantation (FMT) and the use of nematodes, all represent a promising opportunities towards establishing and maintaining of well-being as well as improving underlying IBD symptoms.

Keywords: dietary interventions; fecal microbiota transplantation (FMT); gut microbiota; inflammatory bowel disease (IBD); nematodes; probiotics.

Figure 1

A schematic representation of intestinal mucosa in (A) healthy; and (B) inflammatory bowel disease (IBD)-affected individual. A thick mucus layer overlies the entire epithelium of the healthy intestine. Bacteria are distributed throughout the outer mucus layer, while the inner layer is thick and resistant to bacterial penetration due to the antimicrobial peptides secreted by the epithelial cells, and immunoglobulin A (IgA) produced by B cells and transcytosed across the epithelial layer. Commensal microbiota suppresses the proliferation of pathobionts (opportunistic bacteria that coexist with commensals in low extent) and enteric pathogens, tuning the host responses towards immunological tolerance and maintaining intestinal homeostasis. Genetic and environmental factors influence intestinal microbiota composition and can lead to mucosal dysbiosis—disruption of commensal microbial community, resulting in outgrowth of pathobionts and colonization of the intestine by pathogen species. These bacterial species produce and secrete toxins, thinning the protective mucus layer, damaging the epithelial layer and, thus, reducing the integrity of the epithelial barrier. The bacteria can gain access to epithelium and mucosal tissue resulting in a strong inflammatory response by the host immune system.