Although the etio-pathogenesis of inflammatory bowel diseases (IBD) is not entirely clear, the interaction between genetic and adverse environmental factors may reduce the variety of the intestinal microbiota (dysbiosis), resulting in a chronic inflammation having effects on the large-scale brain network through the gut-brain axis. In this paper, we hypothesized the presence of inflammation-related changes in brain topology of IBD patients, regardless of the specific clinical form (ulcerative colitis (UC) or Crohn’s disease (CD)). To test this hypothesis, we analyzed source-reconstructed magnetoencephalography (MEG) signals in 25 IBD patients and 28 healthy controls (HC) in resting-state condition, and evaluated the brain network topology. Finally, to assess whether these changes were linked to IBD clinical evolution, we correlated brain topology to disease duration. We found that the betweenness centrality (BC) of the left hippocampus was higher in patients as compared to controls, in the gamma frequency band. BC is a nodal topological parameter indicating how much a brain region is involved in the flow of information through the brain network. Furthermore, the comparison among UC, CD and HC showed statistically significant differences between UC and HC and between CD and HC, but not between the two clinical forms. Our results demonstrated that the topological changes observed in IBD patients were not dependent on the specific clinical form, but due to the gastro-intestinal inflammatory process itself. However, although these findings are promising, we need to enlarge the sample size to monitor the brain involvement in IBD and to clarify the clinical impact.