Abstract
Up to date several authors discussed interactions between cells forming inflammatory infiltrates in the course of inflammatory bowel disease (IBD), mainly dealing with endoscopic biopsy specimens. These usually contain only mucosa. We have evaluated full bowel wall sections, which seems to be especially important in patients with Crohn's disease (CD). The purpose of our study was to evaluate the relationship between vascular density and expression of thrombospondin-1 (TSP-1) and vascular endothelial growth factor receptor 1 (VEGFR-1) in full-thickness tissue fragments of intestinal wall taken from patients after colectomy, comparing those with IBD to non-IBD control group. Histological sections were immunostained with antibodies against CD-31, TSP-1, and VEGFR-1 and analyzed by pathologists with the use of computer-assisted morphometrics. Our research showed significantly higher vascular density and vascular area percentage in all layers of bowel wall in patients with CD when compared to control. We have also demonstrated differences in vascular density distribution between ulcerative colitis (CU) and CD and between CU and control. However we have not found statistically significant correlation between those findings and VEGFR-1 or TSP-1 expression. Our results might suggest existence of different, TSP-1 independent pathways of antiangiogenesis in IBD.
Highlights
Ulcerative colitis (CU) and Crohn’s disease (CD) are known as chronic inflammatory bowel diseases (IBD)
We have revealed significantly increased number of blood vessels in almost all of the four layers of bowel wall while comparing Crohn’s disease and ulcerative colitis with normal bowel wall
We believe that a better marker of angiogenesis could be the expression of another vascular endothelial growth factor (VEGF) receptor-VEGFR2 (KDR/Flk-1), which was studied by the same authors
Summary
Ulcerative colitis (CU) and Crohn’s disease (CD) are known as chronic inflammatory bowel diseases (IBD). Among factors associated with inflammatory bowel disease, angiogenesis plays important role in development of clinical symptoms. It has been shown that exacerbation of IBD increases angiogenesis especially in ulcerative colitis [1, 2]. This finding produced a concept of antiangiogenic therapy in IBD, as presented by Danese et al [3]. It was reported that anti-angiogenesis in the development of IBD can be measured by detection of thrombospondin [4, 5]. Since anti-angiogenesis is almost always associated with angiogenesis, numerous angiogenic factors have been indicated as possible counterparts to thrombospondin. Thrombospondin is one of the extracellular matrix adhesive molecules, including laminin, fibronectin, fibrinogen, and von Willebrand
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