Epithelial cells, stromal cells, immune cells and microbiota are fundamental components of the intestinal mucosa, and together they are necessary to preserve homeostasis in the gut. Crohn’s disease (CD) and ulcerative colitis (UC) are the most common entities that comprise the inflammatory bowel diseases (IBD). Both conditions are characterized by chronic gut inflammation, and a relapsing remitting disease progression that can be considered as a mosaic of acute inflammation, chronic inflammation and healing.
The incidence of IBD worldwide has increased noticeably in the past years, however the reasons for this remain poorly understood. However, there is growing evidence that several risk factors can contribute to the development and progression of IBD including: (i) genetic predisposition, (ii) dysbiosis of the gut microbiota, (iii) alterations in the gut environment, and (iv) immune dysregulation in the gut.
Alterations in (i) mucosal barrier function, (ii) innate and adaptive immune responses towards the gut microbiota, (iii) endoplasmic reticulum stress, (iv) autophagy, (v) alterations in metabolic pathways, and other processes are also suggested to contribute to IBD pathogenesis. Therefore, it is our aim for these components to be profiled in this Research Topic. We welcome the submission of Review, Mini-Review and Original Research articles that include, but are not limited to, the following topics:
1. The role of ILCs in mucosal immunology.
2. The role of innate immune cells, including dendritic cells, in intestinal homeostasis and inflammation.
3. Alterations in adaptive immune responses in the presence of intestinal mucosa inflammation.
4. Mouse models for studying inflammatory bowel disease.
5. Genetic predisposition to inflammatory bowel disease.
6. Autoimmunity in the gut.
7. Dietary components involved in intestinal homeostasis.
8. Colitis pathogenesis and associated cancers.
Epithelial cells, stromal cells, immune cells and microbiota are fundamental components of the intestinal mucosa, and together they are necessary to preserve homeostasis in the gut. Crohn’s disease (CD) and ulcerative colitis (UC) are the most common entities that comprise the inflammatory bowel diseases (IBD). Both conditions are characterized by chronic gut inflammation, and a relapsing remitting disease progression that can be considered as a mosaic of acute inflammation, chronic inflammation and healing.
The incidence of IBD worldwide has increased noticeably in the past years, however the reasons for this remain poorly understood. However, there is growing evidence that several risk factors can contribute to the development and progression of IBD including: (i) genetic predisposition, (ii) dysbiosis of the gut microbiota, (iii) alterations in the gut environment, and (iv) immune dysregulation in the gut.
Alterations in (i) mucosal barrier function, (ii) innate and adaptive immune responses towards the gut microbiota, (iii) endoplasmic reticulum stress, (iv) autophagy, (v) alterations in metabolic pathways, and other processes are also suggested to contribute to IBD pathogenesis. Therefore, it is our aim for these components to be profiled in this Research Topic. We welcome the submission of Review, Mini-Review and Original Research articles that include, but are not limited to, the following topics:
1. The role of ILCs in mucosal immunology.
2. The role of innate immune cells, including dendritic cells, in intestinal homeostasis and inflammation.
3. Alterations in adaptive immune responses in the presence of intestinal mucosa inflammation.
4. Mouse models for studying inflammatory bowel disease.
5. Genetic predisposition to inflammatory bowel disease.
6. Autoimmunity in the gut.
7. Dietary components involved in intestinal homeostasis.
8. Colitis pathogenesis and associated cancers.
