Abstract
Alterations of the gut microbiota may cause dysregulated mucosal immune responses leading to the onset of inflammatory bowel diseases (IBD) in genetically susceptible hosts. Restoring immune homeostasis through the normalization of the gut microbiota is now considered a valuable therapeutic approach to treat IBD patients. The customization of microbe-targeted therapies, including antibiotics, prebiotics, live biotherapeutics and faecal microbiota transplantation, is therefore considered to support current therapies in IBD management. In this review, we will discuss recent advancements in the understanding of host−microbe interactions in IBD and the basis to promote homeostatic immune responses through microbe-targeted therapies. By considering gut microbiota dysbiosis as a key feature for the establishment of chronic inflammatory events, in the near future it will be suitable to design new cost-effective, physiologic, and patient-oriented therapeutic strategies for the treatment of IBD that can be applied in a personalized manner.
Highlights
The pathogenesis of inflammatory bowel diseases (IBD) is still incompletely understood
ATCC15707 [142,143,144] can influence the immunoregulatory capacity of human antigen presenting cells (APCs). Both peptides are capable to increase the pro-inflammatory profile of IBD-derived APC, as demonstrated by the enhanced expression of human leukocyte antigen-DR (HLA-DR) on cDC prompted by peptide B7, which expanded IL-1β production of B-cells and on pDC by B12
We showed that therapeutic faecal microbiota transplantation (FMT) administration in the context of a chronic experimental colitis setting, a condition more similar to that of IBD patients, stably decreased colonic inflammation by modulating the expression of pro-inflammatory genes, such as Ifng, Tnf, Il1b, Il-17, and Il-6 [107]
Summary
The pathogenesis of inflammatory bowel diseases (IBD) is still incompletely understood. Impairment of intestinal barrier functions, which results in the translocation of gut microbes, promotes the hyper-activation of the mucosal immune system and the production of pro-inflammatory cytokines that altogether contribute to fuelling the inflammation observed in IBD patients [1,2,3]. The gut microbiota has to modulate and regulate several aspects of host’s immune system towards tolerance rather than responsiveness Any disruption of this delicate equilibrium has potentially pathological consequences on the health status of the host. Dysbiosis (i.e., altered microbial composition) of the gut microbiota can lead to chronic inflammation as observed in IBDs. IBDs appear to be caused by a dysregulated immune response to commensal microorganisms harbouring virulence traits in their genome (the so-called pathobionts) in genetically susceptible hosts. We will recapitulate the mechanisms by which the gut microbiota and the immune system reciprocally influence their functions in homeostasis and during IBD as well as the basis for therapeutic restoration of homeostatic immune function by manipulating the gut microbiota through existing microbe-targeted therapies, including antibiotics, prebiotics, probiotics, and faecal microbiota transplantation
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