Many different factors are implicated in the pathogenesis of IBD, including the gut microbiota, impaired immune response pathways, genetics and environmental triggers.1
Studies have identified 240 distinct sites in the genetic code linked to increased risk of IBD, with around 30 of these are shared between Crohn’s and ulcerative colitis. These are involved in pathways such as regulating the barrier effect of the intestine’s epithelium layer and the protective effects of the mucosa, as well as immune responses, the removal and renewal of damaged cells (autophagy), and other metabolic pathways that help maintain cell homoeostasis.5
The intestinal microbiota is considered the principal environmental factor in IBD. Gut bacterial secretions affect other gut bacteria species or strains moderating microbial numbers, balance and GI effects, with pro-inflammatory and anti-inflammatory influences on the human host’s immunology.5
Food intake is another environmental factor, with fruit and vegetable consumption associated with a lower risk of Crohn’s, while fat and sugar-rich foods may exacerbate the condition. Artificial additives may also promote intestinal inflammation by interfering with gut barrier function.
Smoking appears to adversely affect Crohn’s disease (doubling the risk), but it can be protective in ulcerative colitis. It can stimulate colonic mucosal protection and inhibit autophagy, and affects T helper cells in different ways. Other influences include gastric surgery such as appendectomy, stress and medications.2,5
Many different immune cells are found to invade the lamina propria, a connective tissue layer between the intestinal epithelium and mucosa. T cells, B cells, macrophages, dendritic cells and neutrophils can be found when the epithelium is damaged in IBD.5
High levels of pro-inflammatory cytokines such as tumour necrosis factor (TNF), interleukins, interferons, and associated pathways are also associated with IBD.