Inflammatory Bowel Disease (IBD), which comprises Crohn’s disease and ulcerative colitis, is a chronic inflammatory condition with a relapsing course. As IBD is associated with psychiatric disorders such as depression and anxiety as well as cognitive impairment, it was suggested that these psychological factors might predispose an individual to develop the disease. Now it is clear that there is bi-directional communication between the gut and the central nervous system (Kennedy et al, 2012) and our recent finding identifies a new mechanism by which IBD might cause behavioral manifestations (Zonis et al, 2015).

The generation of new neurons continues throughout adulthood in the subgranular zone of the dentate gyrus of the hippocampus. It is well accepted that adult hippocampal neurogenesis is involved in memory and learning (Aimone et al, 2014) and various aspects of emotion and the stress response (Cameron and Glover, 2015). Thus, disruption of hippocampal neurogenesis could have profound effects on a wide range of behaviors. Among many other factors, inflammation and pro-inflammatory cytokines negatively affect neurogenesis. Peripheral inflammation can signal the brain by activating the vagus nerve and Toll-like receptors in the circumventricular organs, and pro-inflammatory cytokines can enter the brain through saturable transport systems. Engagement of this immune-to-brain communication ultimately leads to the activation of resident microglia, which is a major source of pro-inflammatory cytokines in the brain.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account
Continue with Google
Continue with ORCiD