Current concepts of the pathogenesis of inflammatory bowel disease.

Hdl Handle:
http://hdl.handle.net/10147/209243
Title:
Current concepts of the pathogenesis of inflammatory bowel disease.
Authors:
Shanahan, F
Affiliation:
Cork University Hospital, University College Cork, Ireland.
Citation:
Ir J Med Sci. 1994 Dec;163(12):544-9.
Journal:
Irish journal of medical science
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209243
PubMed ID:
7843934
Abstract:
Although the cause of inflammatory bowel disease is not known, the pathogenesis involves an immune-mediated tissue damage that is the result of an interaction among genetic predisposing factors, exogenous triggers and endogenous modifying influences. Multiple genes are involved and operate at the level of the immune response and at the target organ. Exogenous triggers include the enteric microflora which might stimulate the mucosal immune system in genetically predisposed individuals. Endogenous modifying factors such as the psychoneuroendocrine system have regulatory effects on the immune system and the inflammatory response, and may influence the course of the disease. While autoimmune phenomena do occur, particularly in ulcerative colitis, there is no evidence that they are directly responsible for the tissue damage. It appears more likely, particularly in Crohn's disease, that tissue injury may occur as an indirect or "bystander" effect of mucosal T-cell hyperactivation, perhaps in response to a normal enteric microbial antigen. Most of the immunologic and histologic features of Crohn's disease can be explained by the effects of T-cell derived and other cytokines on the epithelium, the local immune system, the microvasculature, and the recruitment of auxiliary effector cells such as neutrophils.
Language:
eng
MeSH:
Autoimmunity; Colitis, Ulcerative/diagnosis/*etiology/pathology; Crohn Disease/diagnosis/*etiology/pathology; Disease Models, Animal; Humans; Intestinal Mucosa/immunology; Neurosecretory Systems/immunology/physiopathology; T-Lymphocytes/immunology
ISSN:
0021-1265 (Print); 0021-1265 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorShanahan, Fen_GB
dc.date.accessioned2012-02-03T15:16:02Z-
dc.date.available2012-02-03T15:16:02Z-
dc.date.issued2012-02-03T15:16:02Z-
dc.identifier.citationIr J Med Sci. 1994 Dec;163(12):544-9.en_GB
dc.identifier.issn0021-1265 (Print)en_GB
dc.identifier.issn0021-1265 (Linking)en_GB
dc.identifier.pmid7843934en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209243-
dc.description.abstractAlthough the cause of inflammatory bowel disease is not known, the pathogenesis involves an immune-mediated tissue damage that is the result of an interaction among genetic predisposing factors, exogenous triggers and endogenous modifying influences. Multiple genes are involved and operate at the level of the immune response and at the target organ. Exogenous triggers include the enteric microflora which might stimulate the mucosal immune system in genetically predisposed individuals. Endogenous modifying factors such as the psychoneuroendocrine system have regulatory effects on the immune system and the inflammatory response, and may influence the course of the disease. While autoimmune phenomena do occur, particularly in ulcerative colitis, there is no evidence that they are directly responsible for the tissue damage. It appears more likely, particularly in Crohn's disease, that tissue injury may occur as an indirect or "bystander" effect of mucosal T-cell hyperactivation, perhaps in response to a normal enteric microbial antigen. Most of the immunologic and histologic features of Crohn's disease can be explained by the effects of T-cell derived and other cytokines on the epithelium, the local immune system, the microvasculature, and the recruitment of auxiliary effector cells such as neutrophils.en_GB
dc.language.isoengen_GB
dc.subject.meshAutoimmunityen_GB
dc.subject.meshColitis, Ulcerative/diagnosis/*etiology/pathologyen_GB
dc.subject.meshCrohn Disease/diagnosis/*etiology/pathologyen_GB
dc.subject.meshDisease Models, Animalen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntestinal Mucosa/immunologyen_GB
dc.subject.meshNeurosecretory Systems/immunology/physiopathologyen_GB
dc.subject.meshT-Lymphocytes/immunologyen_GB
dc.titleCurrent concepts of the pathogenesis of inflammatory bowel disease.en_GB
dc.contributor.departmentCork University Hospital, University College Cork, Ireland.en_GB
dc.identifier.journalIrish journal of medical scienceen_GB
dc.description.provinceMunster-

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