Collagenous colitis

Griga, Thomas; Tromm, Andreas; Schmiegel, Wolff; Pfisterer, Okka; Müller, K M; Brasch, Frank

doi:10.1097/00042737-200404000-00005

Cited by 35 publications

(5 citation statements)

References 22 publications

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“…VEGF limits the release of TIMP-1 by endothelial cells, thereby increasing MMP-1 activity (16, 45). In the epithelium and in inflammatory cells of the lamina propria, expression of VEGF reflects an important physiological mechanism counteracting the MMP-1/TIMP-1 imbalance in CC; disinhibiting MMP-1 and reducing levels of TIMP-1 leads to an accumulation of immature subepithelial ECM in CC (87). An increased immunostaining for VEGF within the epithelium is also maintained when clinical and histological remission is achieved, suggesting the persistence of the repair mechanism (87).…”

Section: Histological Markersmentioning

confidence: 99%

Biomarkers and Microscopic Colitis: An Unmet Need in Clinical Practice

et al. 2017

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One of the most common causes of chronic diarrhea is ascribed to microscopic colitis (MC). MC is classified in subtypes: collagenous colitis (CC) and lymphocytic colitis (LC). Patients with MC report watery, non-bloody diarrhea of chronic course, abdominal pain, weight loss, and fatigue that may impair patient’s health-related quality of life. A greater awareness, and concomitantly an increasing number of diagnoses over the last years, has demonstrated that the incidence and prevalence of MC are on the rise. To date, colonoscopy with histological analysis on multiple biopsies collected along the colon represents the unique accepted procedure used to assess the diagnosis of active MC and to evaluate the response to medical therapy. Therefore, the emerging need for less-invasive procedures that are also rapid, convenient, standardized, and reproducible, has encouraged scientists to turn their attention to the identification of inflammatory markers and other molecules in blood or feces and within the colonic tissue that can confirm a MC diagnosis. This review gives an update on the biomarkers that are potentially available for the identification of inflammatory activity, related to CC and LC.

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Section: Histological Markersmentioning

confidence: 99%

Biomarkers and Microscopic Colitis: An Unmet Need in Clinical Practice

et al. 2017

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“…The detection of the same cells by the antibody raised specifically against VEGF 165 b, as by an antibody to all VEGF isoforms, concurs with our ELISA findings that in normal colonic mucosa it is the VEGF xxx b isoforms that predominate. This has significant implications for interpretation of all previous studies investigating VEGF expression in the colon, not only for tumour studies (Hurwitz et al , 2004), but also for collagenous (Griga et al , 2004) and ischaemic colitides (Okuda et al , 2005).…”

Section: Discussionmentioning

confidence: 99%

VEGF165b, an antiangiogenic VEGF-A isoform, binds and inhibits bevacizumab treatment in experimental colorectal carcinoma: balance of pro- and antiangiogenic VEGF-A isoforms has implications for therapy

et al. 2008

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Bevacizumab, an anti-vascular endothelial growth factor (VEGF-A) antibody, is used in metastatic colorectal carcinoma (CRC) treatment, but responses are unpredictable. Vascular endothelial growth factor is alternatively spliced to form proangiogenic VEGF 165 and antiangiogenic VEGF 165 b. Using isoform-specific enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, we found that over 90% of the VEGF in normal colonic tissue was VEGF xxx b, but there was a variable upregulation of VEGF xxx and downregulation of VEGF xxx b in paired human CRC samples. Furthermore, cultured colonic adenoma cells expressed predominantly VEGF xxx b, whereas colonic carcinoma cells expressed predominantly VEGF xxx . However, adenoma cells exposed to hypoxia switched their expression from predominantly VEGF xxx b to predominantly VEGF xxx . VEGF 165 b overexpression in LS174t colon cancer cells inhibited colon carcinoma growth in mouse xenograft models. Western blotting and surface plasmon resonance showed that VEGF 165 b bound to bevacizumab with similar affinity as VEGF 165 . However, although bevacizumab effectively inhibited the rapid growth of colon carcinomas expressing VEGF 165 , it did not affect the slower growth of tumours from colonic carcinoma cells expressing VEGF 165 b. Both bevacizumab and anti-VEGF 165 b-specific antibodies were cytotoxic to colonic epithelial cells, but less so to colonic carcinoma cells. These results show that the balance of antiangiogenic to proangiogenic isoforms switches to a variable extent in CRC, regulates tumour growth rates and affects the sensitivity of tumours to bevacizumab by competitive binding. Together with the identification of an autocrine cytoprotective role for VEGF 165 b in colonic epithelial cells, these results indicate that bevacizumab treatment of human CRC may depend upon this balance of VEGF isoforms.

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“…Various studies have demonstrated that VEGF promotes angiogenesis during acute inflammation and ischemia (42,43). VEGF also plays a role in counteracting the local imbalance of fibrogenesis and fibrolysis, leading to an accumulation of immature subepithelial matrix in collagenous colitis (44). Using intravital microscopy of the rat mesenteric microcirculation to measure leukocyte-endothelium interactions, Scalia et al (45) demonstrated that VEGF inhibits leukocyte-epithelial cell adherence and the effects of chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%