Ulcerative colitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]
Overview
Ulcerative colitis is characterized by inflammation of the mucosa which is diffuse and primarily confined to the colon. The disease can extend proximally in a continuous, circular and uniform manner. Various factors influencing the pathogenesis of ulcerative colitis including intestinal micro bacteria, genetics, immunological abnormalities, and environmental factors.[1][2]
Pathophysiology
- Ulcerative colitis is characterized by inflammation of the mucosa which is diffuse and primarily confined to the colon.
- The disease can extend proximally in a continuous, circular and uniform manner.
- Various factors influencing the pathogenesis of ulcerative colitis include:[1][2]
- Intestinal Micro bacteria
- Genetics
- Immunological abnormalities
- Environmental factors
Pathogenesis
The pathogenesis of ulcerative colitis includes:[3][4]
- Dysregulation of cytokine function
- Immunological abnormalities lead to:
- Damage of the epithelium, characterized by:
- Abnormal production of mucus
- Abnormalities in the repair of epithelium
- The inflammation extends by the help of the flora of the intestine.
- Many cells also infiltrate the lamina propria. These may include:
- Inability to control inflammatory response by regulation of immune system.
- Damage of the epithelium, characterized by:
- The activated lamina propria secretes many soluble mediators including:
- Ulcerative colitis is considered to be caused by:
- Th2 and Th9
- It is associated with excessive production of
- IL-13
- IL-5 and
- IL-9
References
- ↑ 1.0 1.1 Template:Loddo, Italia, and Claudio Romano. "Inflammatory bowel disease: genetics, epigenetics, and pathogenesis." Frontiers in immunology 6 (2015): 551.
- ↑ 2.0 2.1 2.2 2.3 Template:Neurath, Markus F. "Cytokines in inflammatory bowel disease." Nature Reviews Immunology 14.5 (2014): 329-342.
- ↑ Guan Q, Zhang J (2017). "Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease". Mediators Inflamm. 2017: 4810258. doi:10.1155/2017/4810258. PMC 5379128. PMID 28420941.
- ↑ Berns M, Hommes DW (2016). "Anti-TNF-α therapies for the treatment of Crohn's disease: the past, present and future". Expert Opin Investig Drugs. 25 (2): 129–43. doi:10.1517/13543784.2016.1126247. PMID 26616476.