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__NOTOC__
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{{Ulcerative colitis}}
{{CMG}}; {{AE}}{{USAMA}}
==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 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==
*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:<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
**Genetics
**Immunological abnormalities
**Environmental factors
===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><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
*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.


{{Ulcerative colitis}}
*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]]


Please help WikiDoc by adding content here.  It's easy!  Click  [[Help:How to Edit a Page|here]]  to learn about editing.
*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 ==
{{reflist|2}}
{{Reflist|2}}
 
{{WH}}
{{WH}}
{{WS}}
{{WS}}


[[Category:Autoimmune diseases]]
[[Category:Gastroenterology]]
[[Category:Inflammations]]
[[Category:Conditions diagnosed by stool test]]
[[Category:Abdominal pain]]
[[Category:Needs content]]
[[Category:Needs content]]

Latest revision as of 00:33, 30 July 2020

https://https://www.youtube.com/watch?v=dYQrqeTxC9g%7C350}}

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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.Invalid parameter in <ref> tag[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:Invalid parameter in <ref> tag[1][2]
    • Intestinal Micro bacteria
    • Genetics
    • Immunological abnormalities
    • Environmental factors

Pathogenesis

The pathogenesis of ulcerative colitis includes:[3]Invalid parameter in <ref> tagInvalid parameter in <ref> tag[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.
  • 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. ↑ 1.0 1.1 Template:Loddo, Italia, and Claudio Romano. "Inflammatory bowel disease: genetics, epigenetics, and pathogenesis." Frontiers in immunology 6 (2015): 551.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.

Template:WH Template:WS

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