The monoamine serotonin, 5-hydroxytryptamine (5-HT), is a remarkable molecule with conserved production in prokaryotes and eukaryotes and a wide range of functions. In the gastrointestinal tract, enterochromaffin cells are the most important source for 5-HT production. Some intestinal bacterial species are also able to produce 5-HT. Besides its role as a neurotransmitter, 5-HT acts on immune cells to regulate their activation. Several lines of evidence indicate that intestinal 5-HT signaling is altered in patients with inflammatory bowel disease. In this review, we discuss the current knowledge on the production, secretion, and signaling of 5-HT in the intestine. We present an inventory of intestinal immune and epithelial cells that respond to 5-HT and describe the effects of these signaling processes on intestinal homeostasis. Further, we detail the mechanisms by which 5-HT could affect inflammatory bowel disease course and describe the effects of interventions that target intestinal 5-HT signaling.

Recent studies have suggested a major role for endospore forming bacteria within the gut microbiota, not only as pathogens but also as commensal and beneficial members contributing to gut homeostasis. In this review the sporulation processes, spore properties, and germination processes will be explained within the scope of the human gut. Within the gut, spore-forming bacteria are known to interact with the host’s immune system, both in vegetative cell and spore form. Together with the resistant nature of the spore, these characteristics offer potential for spores’ use as delivery vehicles for therapeutics. In the last part of the review, the therapeutic potential of spores as probiotics, vaccine vehicles, and drug delivery systems will be discussed.

Background This study aimed to obtain a holistic view of remission in pediatric Crohn’s Disease (CD) by integrating six omics datasets from three anatomical compartments. Methods Patients with fecal calprotectin below 250 mg/kg were considered in remission (n = 27), above 250 mg/kg as having active disease (n = 31). Proteome and microbiomes (fungi and bacteria) were analyzed in feces. Metabolomes in feces, urine, and plasma. Datasets were integrated into a multi-omics model. Results The use of individual datasets shows multiple differences between remission and active disease. Integration yielded a good model (AUC of 0.8) predicting remission. The most important features in this model are fecal bacteria (40%), fecal metabolites (22%), fecal proteins (16%), plasma metabolites (12%), fecal fungi (6%), and urine metabolites (4%). The interactome reveals Ruminococcaceae and Faecalibacterium as key players, with a correlation between antifungal urine hydroxyphenyllactic acid and fecal fungi. Pathway analysis shows an association of purine metabolism with remission, independent of thiopurine use. Changes in purine metabolism are confirmed in a pediatric CD public dataset. Conclusion The pathways and correlations identified as playing a role in remission may remain undetectable if individual omics datasets or single anatomical compartments are used, highlighting the need for a holistic approach that integrates multiple datasets from multiple anatomical compartments.