Literature DB >> 11923606

Increased adhesion molecule expression in serosal fibroblasts isolated from patients with inflammatory bowel disease is secondary to inflammation.

Ann E Brannigan1, R William G Watson, David Beddy, Hilary Hurley, John M Fitzpatrick, P Ronan O'Connell.   

Abstract

OBJECTIVE: To examine the expression of adhesion molecules by serosal and dermal fibroblasts in patients with inflammatory bowel disease. SUMMARY BACKGROUND DATA: The pathophysiologic process that leads to stricture formation in Crohn's disease (CD) is unknown. Serosal fibroblasts in these patients have an enhanced ability to contract collagen. This property may be reflected in fibroblast adhesion molecule expression, which in turn may be constitutive or secondary to the inflammatory process in patients with CD.
METHODS: Fibroblasts were isolated from inflamed and macroscopically normal serosa of patients with CD or ulcerative colitis (UC) and from normal serosa of patients with colon cancer. Dermal fibroblasts were also isolated from the wound edge. Cell surface and whole cell expression of ICAM-1 were evaluated by flow cytometry and Western blot analysis, respectively. NFkappaB was measured by mobility shift assay in parallel experiments. Interleukin 1beta was added to the culture medium.
RESULTS: Expression of ICAM-1 and NFkappaB, increased in patients with both CD and UC, was unaltered by interleukin 1beta. The whole cell concentration of ICAM-1 was greater in patients with CD than in patients with UC. Dermal fibroblasts did not display these features.
CONCLUSIONS: Patients with inflammatory bowel disease display enhanced ICAM-1 expression in serosal fibroblasts but not dermal fibroblasts, indicating a secondary response to inflammation.

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Year:  2002        PMID: 11923606      PMCID: PMC1422465          DOI: 10.1097/00000658-200204000-00008

Source DB:  PubMed          Journal:  Ann Surg        ISSN: 0003-4932            Impact factor:   12.969


  25 in total

1.  Stricture formation in Crohn's disease: the role of intestinal fibroblasts.

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Journal:  Ann Surg       Date:  2000-01       Impact factor: 12.969

2.  Infliximab for the treatment of fistulas in patients with Crohn's disease.

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5.  Scleroderma fibroblasts show increased responsiveness to endothelial cell-derived IL-1 and bFGF.

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7.  Absence of efficacy of subcutaneous antisense ICAM-1 treatment of chronic active Crohn's disease.

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8.  A placebo-controlled trial of ICAM-1 antisense oligonucleotide in the treatment of Crohn's disease.

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9.  Regulation of Fas antibody induced neutrophil apoptosis is both caspase and mitochondrial dependent.

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  6 in total

1.  Transforming growth factor-beta promotes pro-fibrotic behavior by serosal fibroblasts via PKC and ERK1/2 mitogen activated protein kinase cell signaling.

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Review 2.  Fibrogenesis and fibrosis in inflammatory bowel diseases: Good and bad side of same coin?

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Review 3.  Prof Ronan O'Connell Festschrift: Stricture pathogenesis in Crohn's disease-the role of intestinal fibroblasts.

Authors:  Jürgen Mulsow
Journal:  Ir J Med Sci       Date:  2018-07-18       Impact factor: 1.568

4.  Apigenin inhibits the expression of IL-6, IL-8, and ICAM-1 in DEHP-stimulated human umbilical vein endothelial cells and in vivo.

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Journal:  Inflammation       Date:  2012-08       Impact factor: 4.092

5.  Human subperitoneal fibroblast and cancer cell interaction creates microenvironment that enhances tumor progression and metastasis.

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Review 6.  The Role of Cytokines in the Fibrotic Responses in Crohn's Disease.

Authors:  Renata Curciarello; Guillermo H Docena; Thomas T MacDonald
Journal:  Front Med (Lausanne)       Date:  2017-08-07
  6 in total

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