Figure 2. The intestinal mucosa in the normal bowel and IBD.
Upon exposure to environmental factors, patients with IBD develop microbial dysbiosis with
decrease of short-chain fatty acids (SCFA) producing bacteria and increase in
Proteobacteria. Mechanisms that maintain the intestinal barrier are also disrupted in the IBD
mucosa, including: down regulation of E-cadherin in tight junctions; thickness of the mucus
layer; abnormal goblet cell function, including Muc2 and RELMβ proteins; and
dysfunctional Paneth cells associated mechanisms, including secretion of antimicrobial
products, NOD2 and ATG16L1 gene associated functions. From the innate immune system
perspective, the IBD mucosa has been shown to exhibit: a decrease in colonic macrophages
expressing CD14, defective CX3CR1 antigen presentation by dendritic cells; and impaired
Autophagy. Lastly, while leukocyte migration via integrin cellular adhesion molecules
(CAMs) interactions also occurs in the normal mucosa, the balance between Effector and
regulatory T cells (T-reg) appears to be disturbed in the IBD mucosa, resulting in
uncontrolled activation of different T-cell lineages that migrate to the inflamed intestine.
