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Neuroinflammation in inflammatory bowel disease.

Lakhan SE, Kirchgessner A - J Neuroinflammation (2010)

Bottom Line: Gut inflammation causes significant changes in neurally controlled gut functions including cramping, abdominal pain, fecal urgency, and explosive diarrhea.Inflammatory mediators include 5-hydroxytryptamine and cytokines, as well as reactive oxygen species and the production of oxidative stress.This review will discuss the effects of inflammation on enteric neural activity and potential therapeutic strategies that target neuroinflammation in the enteric nervous system.

View Article: PubMed Central - HTML - PubMed

Affiliation: Global Neuroscience Initiative Foundation, Los Angeles, CA, USA. slakhan@gnif.org

ABSTRACT
Inflammatory bowel disease is a chronic intestinal inflammatory condition, the pathology of which is incompletely understood. Gut inflammation causes significant changes in neurally controlled gut functions including cramping, abdominal pain, fecal urgency, and explosive diarrhea. These symptoms are caused, at least in part, by prolonged hyperexcitability of enteric neurons that can occur following the resolution of colitis. Mast, enterochromaffin and other immune cells are increased in the colonic mucosa in inflammatory bowel disease and signal the presence of inflammation to the enteric nervous system. Inflammatory mediators include 5-hydroxytryptamine and cytokines, as well as reactive oxygen species and the production of oxidative stress. This review will discuss the effects of inflammation on enteric neural activity and potential therapeutic strategies that target neuroinflammation in the enteric nervous system.

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Related in: MedlinePlus

Immunoreactivity to hemeoxygenase-1 (HO-1) and substance P (SP) in a cryostat section of human colon. An HO-1-positive macrophage (orange) is seen in close proximity to a SP-containing nerve fiber (green) in the colonic mucosa.
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Figure 1: Immunoreactivity to hemeoxygenase-1 (HO-1) and substance P (SP) in a cryostat section of human colon. An HO-1-positive macrophage (orange) is seen in close proximity to a SP-containing nerve fiber (green) in the colonic mucosa.

Mentions: In addition to colonic epithelial cells, HO-1 is expressed in macrophages. In both mouse and human colon, HO-1 immunoreactivity is displayed by macrophages in close proximity to SP-containing nerve fibers (Figure 1). Macrophages have pro- and anti-inflammatory activities, depending on their phenotype. For example, CD206+/HO-1+ gastric macrophages protect against oxidative stress-induced damage and are required for prevention of diabetic gastroparesis in mice [84]. Thus, expression of HO-1 in macrophages could constitute an important component of the anti-inflammatory effect by increasing antioxidant protection and decreasing the inflammatory component of IBD lesions. Moreover, the expression of HO-1 in macrophages close to enteric nerves could act as a natural defense mechanism to alleviate enteric nerve injury in the GI tract. Therefore, induction of HO-1 expression in macrophages might be a therapeutic option to protect neurons in patients with IBD; however, this idea remains to be tested.


Neuroinflammation in inflammatory bowel disease.

Lakhan SE, Kirchgessner A - J Neuroinflammation (2010)

Immunoreactivity to hemeoxygenase-1 (HO-1) and substance P (SP) in a cryostat section of human colon. An HO-1-positive macrophage (orange) is seen in close proximity to a SP-containing nerve fiber (green) in the colonic mucosa.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2909178&req=5

Figure 1: Immunoreactivity to hemeoxygenase-1 (HO-1) and substance P (SP) in a cryostat section of human colon. An HO-1-positive macrophage (orange) is seen in close proximity to a SP-containing nerve fiber (green) in the colonic mucosa.
Mentions: In addition to colonic epithelial cells, HO-1 is expressed in macrophages. In both mouse and human colon, HO-1 immunoreactivity is displayed by macrophages in close proximity to SP-containing nerve fibers (Figure 1). Macrophages have pro- and anti-inflammatory activities, depending on their phenotype. For example, CD206+/HO-1+ gastric macrophages protect against oxidative stress-induced damage and are required for prevention of diabetic gastroparesis in mice [84]. Thus, expression of HO-1 in macrophages could constitute an important component of the anti-inflammatory effect by increasing antioxidant protection and decreasing the inflammatory component of IBD lesions. Moreover, the expression of HO-1 in macrophages close to enteric nerves could act as a natural defense mechanism to alleviate enteric nerve injury in the GI tract. Therefore, induction of HO-1 expression in macrophages might be a therapeutic option to protect neurons in patients with IBD; however, this idea remains to be tested.

Bottom Line: Gut inflammation causes significant changes in neurally controlled gut functions including cramping, abdominal pain, fecal urgency, and explosive diarrhea.Inflammatory mediators include 5-hydroxytryptamine and cytokines, as well as reactive oxygen species and the production of oxidative stress.This review will discuss the effects of inflammation on enteric neural activity and potential therapeutic strategies that target neuroinflammation in the enteric nervous system.

View Article: PubMed Central - HTML - PubMed

Affiliation: Global Neuroscience Initiative Foundation, Los Angeles, CA, USA. slakhan@gnif.org

ABSTRACT
Inflammatory bowel disease is a chronic intestinal inflammatory condition, the pathology of which is incompletely understood. Gut inflammation causes significant changes in neurally controlled gut functions including cramping, abdominal pain, fecal urgency, and explosive diarrhea. These symptoms are caused, at least in part, by prolonged hyperexcitability of enteric neurons that can occur following the resolution of colitis. Mast, enterochromaffin and other immune cells are increased in the colonic mucosa in inflammatory bowel disease and signal the presence of inflammation to the enteric nervous system. Inflammatory mediators include 5-hydroxytryptamine and cytokines, as well as reactive oxygen species and the production of oxidative stress. This review will discuss the effects of inflammation on enteric neural activity and potential therapeutic strategies that target neuroinflammation in the enteric nervous system.

Show MeSH
Related in: MedlinePlus