Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic inflammatory disorders of the intestinal tract. They are summarized as inflammatory bowel disease (IBD). In UC, the inflammation occurs in the mucosa and mucosal ulceration can develop. UC is mainly localized in the rectum and spreads to proximal parts of the intestine to a different extent. In CD, any part of the gastrointestinal tract can be affected, however the main site of inflammation is the terminal ileum and inflammation can occur segmental and discontinuously. In contrast to UC, not only the mucosa is affected but also all layers of the intestinal wall and granuloma are formed in CD. The pathogenesis of both diseases is not yet fully elucidated. Different factors such as genetics, immune dysregulation, and the microbial flora in the intestine and barrier dysfunction of intestinal epithelial cells may lead to the pathology of IBD. The pathogenesis of IBD is poorly understood because of the variability in clinical manifestations and complexity of the mechanisms of chronic inflammation.
There is increasing evidence that IBD tissue injury involves many cell types present in the bowel wall. The epithelial cell has been traditionally considered an important component of IBD pathogenesis, especially in UC. Due to the variability, complexity, and chronicity of gut inflammation in IBD, intestinal epithelial cells (IEC) constantly adapt to the multiple events occurring in the mucosal microenvironment, a phenomenon that has been long recognized. This adaptation might cause IEC to undergo changes in growth and differentiation, metabolism, secretary pattern, immune function, and antigen expression.
Taking into account the practical importance of searching for new effective approaches for Inflammatory Bowel Diseases treatment and prevention, we dedicate a special issue of the journal to this problem.

Aims and Scope:

1. Ulcerative colitis
2. Crohn’s disease
3. Gut Immunology
4. Gut genetic factors
5. Gut Microbiota
6. Gut micro RNA