Tryptophan is an essential amino acid, and its metabolism in the intestine may be involved in the etiology of inflammatory bowel disease (IBD). In vivo and in vitro studies show that three major metabolic pathways of tryptophan exist, including the kynurenin pathway in immune cells and intestinal lining, the 5-hydroxytryptamine (5-HT) pathway in the enterochromaffin cells, and the indole pathway in the gut microbiota. Metabolites of all three pathways are related to aggravation or prevention of intestinal inflammation by activating the release of ligands of the aryl hydrocarbon receptor (AhR) and cytokines, affecting the function of immune cells, and changing the intestinal microbial homeostasis. Until now, most studies worked on the effect of single pathway in IBD, but the integrated changes of all tryptophan metabolic pathways still need to be clarified. In addition, the concordance between host gene expression profiles and metabolites found in the intestine is less understood. In order to gain mechanistic understanding of tryptophan metabolism in IBD patients, we perform a meta-analysis of publicly available transcriptomic datasets, and summarize metabolomic data from the Human Metabolome Project and previous publications. For the meta-analysis, 14 transcriptomic datasets comparing gene expression between IBD patients and non-IBD controls were included after screening, analyzed for quality control, and datasets were individually-processed. Differential expression analysis will be carried out for each study, focusing on genes involved in tryptophan metabolic pathways, AhR signaling, Th17 cell differentiation. Preliminary data indeed show that tryptophan metabolism in the intestinal biopsies is altered in IBD patients. Subsequently, results will be meta-analytically aggregated. Additionally, functional enrichment analyses will be performed to study how these pathways change in IBD patients. Furthermore, the concentration of tryptophan and its metabolites in serum and fecal samples will be compared between IBD patients and non-IBD controls. On basis of these results, a network of tryptophan metabolism in IBD patients will be established, which will increase our understanding of the potential of tryptophan and its metabolites as diagnostic marker and/or therapeutic target.