Fibrogenesis in Crohn's Disease

Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains lim...

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Published inThe American journal of gastroenterology Vol. 102; no. 2; pp. 439 - 448
Main Authors BURKE, John P, MULSOW, Jurgen J, O'KEANE, Conor, DOCHERTY, Neil G, WATSON, R. William G, RONAN O'CONNELL, P
Format Journal Article
LanguageEnglish
Published Oxford Blackwell Publishing 01.02.2007
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
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Abstract Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains limited. The aim of this review is to discuss the current understanding of fibrogenesis in CD and to outline potential directions in research and therapeutics. The electronic literature (January 1966 to May 2006) on CD-associated fibrosis was reviewed. Further references were obtained by cross-referencing from key articles. CD-associated fibrosis results from chronic transmural inflammation and a complex interplay among intestinal mesenchymal cells, cytokines, and local inflammatory cells. The fibroblast is the key cell type mediating stricture formation. The cytoarchitecure of the bowel wall is altered with disruption of the muscularis mucosa, thickening of the muscularis propria, and deposition of collagen throughout. The cytokine TGF-beta appears critical in this process, acting to increase growth factor and extracellular matrix (ECM) production and dysregulate ECM turnover. Potential therapeutic interventions are likely to concentrate on modulating down-stream targets of TGF-beta. Greater understanding of the biology of fibrostenosis is likely to yield significant advances in our ability to care for patients with stricturing CD. Potential dividends of this approach include identification of novel therapeutic targets and biomarkers useful for prognostication and therapeutic monitoring.
AbstractList Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains limited. The aim of this review is to discuss the current understanding of fibrogenesis in CD and to outline potential directions in research and therapeutics. The electronic literature (January 1966 to May 2006) on CD-associated fibrosis was reviewed. Further references were obtained by cross-referencing from key articles. CD-associated fibrosis results from chronic transmural inflammation and a complex interplay among intestinal mesenchymal cells, cytokines, and local inflammatory cells. The fibroblast is the key cell type mediating stricture formation. The cytoarchitecure of the bowel wall is altered with disruption of the muscularis mucosa, thickening of the muscularis propria, and deposition of collagen throughout. The cytokine TGF-beta appears critical in this process, acting to increase growth factor and extracellular matrix (ECM) production and dysregulate ECM turnover. Potential therapeutic interventions are likely to concentrate on modulating down-stream targets of TGF-beta. Greater understanding of the biology of fibrostenosis is likely to yield significant advances in our ability to care for patients with stricturing CD. Potential dividends of this approach include identification of novel therapeutic targets and biomarkers useful for prognostication and therapeutic monitoring.
INTRODUCTION:Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains limited. The aim of this review is to discuss the current understanding of fibrogenesis in CD and to outline potential directions in research and therapeutics.METHODS:The electronic literature (January 1966 to May 2006) on CD-associated fibrosis was reviewed. Further references were obtained by cross-referencing from key articles.RESULTS:CD-associated fibrosis results from chronic transmural inflammation and a complex interplay among intestinal mesenchymal cells, cytokines, and local inflammatory cells. The fibroblast is the key cell type mediating stricture formation. The cytoarchitecure of the bowel wall is altered with disruption of the muscularis mucosa, thickening of the muscularis propria, and deposition of collagen throughout. The cytokine TGF-β appears critical in this process, acting to increase growth factor and extracellular matrix (ECM) production and dysregulate ECM turnover. Potential therapeutic interventions are likely to concentrate on modulating down-stream targets of TGF-β.CONCLUSIONS:Greater understanding of the biology of fibrostenosis is likely to yield significant advances in our ability to care for patients with stricturing CD. Potential dividends of this approach include identification of novel therapeutic targets and biomarkers useful for prognostication and therapeutic monitoring.
INTRODUCTIONOver one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains limited. The aim of this review is to discuss the current understanding of fibrogenesis in CD and to outline potential directions in research and therapeutics.METHODSThe electronic literature (January 1966 to May 2006) on CD-associated fibrosis was reviewed. Further references were obtained by cross-referencing from key articles.RESULTSCD-associated fibrosis results from chronic transmural inflammation and a complex interplay among intestinal mesenchymal cells, cytokines, and local inflammatory cells. The fibroblast is the key cell type mediating stricture formation. The cytoarchitecure of the bowel wall is altered with disruption of the muscularis mucosa, thickening of the muscularis propria, and deposition of collagen throughout. The cytokine TGF-beta appears critical in this process, acting to increase growth factor and extracellular matrix (ECM) production and dysregulate ECM turnover. Potential therapeutic interventions are likely to concentrate on modulating down-stream targets of TGF-beta.CONCLUSIONSGreater understanding of the biology of fibrostenosis is likely to yield significant advances in our ability to care for patients with stricturing CD. Potential dividends of this approach include identification of novel therapeutic targets and biomarkers useful for prognostication and therapeutic monitoring.
Author BURKE, John P
DOCHERTY, Neil G
RONAN O'CONNELL, P
O'KEANE, Conor
MULSOW, Jurgen J
WATSON, R. William G
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  givenname: Jurgen J
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  fullname: MULSOW, Jurgen J
  organization: Department of Surgery, Mater Misericordiae University Hospital and UCD School of Medicine and Medical Science, United States
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  givenname: Conor
  surname: O'KEANE
  fullname: O'KEANE, Conor
  organization: Department of Pathology, Mater Misericordiae University Hospital and UCD School of Medicine and Medical Science, United States
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  givenname: Neil G
  surname: DOCHERTY
  fullname: DOCHERTY, Neil G
  organization: Conway Institute, University College Dublin, Dublin, Ireland
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  fullname: RONAN O'CONNELL, P
  organization: Department of Surgery, Mater Misericordiae University Hospital and UCD School of Medicine and Medical Science, United States
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Snippet Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical...
INTRODUCTION:Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least...
INTRODUCTIONOver one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one...
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pascalfrancis
nature
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StartPage 439
SubjectTerms Biological and medical sciences
Crohn Disease - complications
Crohn Disease - pathology
Disease Progression
Fibrosis - complications
Fibrosis - pathology
Gastroenterology
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Intestinal Obstruction - etiology
Intestinal Obstruction - pathology
Medical sciences
Other diseases. Semiology
Prognosis
Retrospective Studies
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Title Fibrogenesis in Crohn's Disease
URI http://dx.doi.org/10.1111/j.1572-0241.2006.01010.x
https://www.ncbi.nlm.nih.gov/pubmed/17156147
https://www.proquest.com/docview/1783694158
https://search.proquest.com/docview/69029098
Volume 102
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