Ulcerative colitis pathophysiology: Difference between revisions
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==Overview== | ==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.<ref | 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.<ref name= UC pathogenesis >{{Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.}} </ref><ref name= IBD > {{Loddo, Italia, and Claudio Romano. "Inflammatory bowel disease: genetics, epigenetics, and pathogenesis." Frontiers in immunology 6 (2015): 551.}}</ref><ref name= IBD1> {{Neurath, Markus F. "Cytokines in inflammatory bowel disease." Nature Reviews Immunology 14.5 (2014): 329-342.}}</ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
*Ulcerative colitis is characterized by inflammation of the mucosa which is diffuse and primarily confined to the colon. | *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. | *The disease can extend proximally in a continuous, circular and uniform manner. | ||
*Various factors influencing the pathogenesis of ulcerative colitis include: | *Various factors influencing the pathogenesis of ulcerative colitis include:<ref name= UC pathogenesis >{{Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.}} </ref><ref name= IBD > {{Loddo, Italia, and Claudio Romano. "Inflammatory bowel disease: genetics, epigenetics, and pathogenesis." Frontiers in immunology 6 (2015): 551.}}</ref><ref name= IBD1> {{Neurath, Markus F. "Cytokines in inflammatory bowel disease." Nature Reviews Immunology 14.5 (2014): 329-342.}}</ref> | ||
**Intestinal Micro bacteria | **Intestinal Micro bacteria | ||
**Genetics | **Genetics | ||
| Line 17: | Line 18: | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
The pathogenesis of ulcerative colitis includes:<ref name="pmid28420941">{{cite journal| author=Guan Q, Zhang J| title=Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease. | journal=Mediators Inflamm | year= 2017 | volume= 2017 | issue= | pages= 4810258 | pmid=28420941 | doi=10.1155/2017/4810258 | pmc=5379128 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28420941 }} </ref> | The pathogenesis of ulcerative colitis includes:<ref name="pmid28420941">{{cite journal| author=Guan Q, Zhang J| title=Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease. | journal=Mediators Inflamm | year= 2017 | volume= 2017 | issue= | pages= 4810258 | pmid=28420941 | doi=10.1155/2017/4810258 | pmc=5379128 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28420941 }} </ref><ref name= UC pathogenesis >{{De Souza, Heitor SP, and Claudio Fiocchi. "Immunopathogenesis of IBD: current state of the art." Nature Reviews Gastroenterology & Hepatology 13.1 (2016): 13-27.}} </ref><ref name= UC pathogenesis >{{Korzenik, Joshua R., and Daniel K. Podolsky. "Evolving knowledge and therapy of inflammatory bowel disease." Nature reviews Drug discovery 5.3 (2006): 197-209.}} </ref><ref name="pmid26616476">{{cite journal| author=Berns M, Hommes DW| title=Anti-TNF-α therapies for the treatment of Crohn's disease: the past, present and future. | journal=Expert Opin Investig Drugs | year= 2016 | volume= 25 | issue= 2 | pages= 129-43 | pmid=26616476 | doi=10.1517/13543784.2016.1126247 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26616476 }} </ref> | ||
*Dysregulation of [[cytokine]] function | *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: | |||
***[[T cells]] | |||
***[[B cells]] | |||
***[[Macrophages]] | |||
***[[Dendritic cells]] | |||
***[[Neutrophils]] | |||
**Inability to control [[inflammatory]] response by regulation of immune system. | |||
*The activated lamina propria secretes many soluble mediators including | |||
**Inflammatory cytokines, such as:<ref name= UC pathogenesis >{{Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.}} </ref><ref name= IBD1> {{Neurath, Markus F. "Cytokines in inflammatory bowel disease." Nature Reviews Immunology 14.5 (2014): 329-342.}}</ref> | |||
***[[TNF]] | |||
***[[IFN-γ]] | |||
***[[IL-6]] | |||
***[[IL-12]] | |||
***[[IL-21]] | |||
***[[IL-23]] | |||
***[[IL-17]] | |||
***[[Integrin]] | |||
**Anti-inflammatory cytokines, such as:<ref name= UC pathogenesis >{{Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.}} </ref><ref name= IBD1> {{Neurath, Markus F. "Cytokines in inflammatory bowel disease." Nature Reviews Immunology 14.5 (2014): 329-342.}}</ref> | |||
***[[IL-10]] | |||
***[[TGFβ]] | |||
***[[IL-35]] | |||
*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 == | == References == | ||
Revision as of 12:36, 22 May 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.