Galectin-3 expression in pouchitis in patients with ulcerative colitis who underwent ileal pouch-anal anastomosis (IPAA)

Brazowski, Eli; Dotan, Iris; Tulchinsky, Hagit; Filip, Irina; Eisenthal, Avi

doi:10.1016/j.prp.2009.02.001

Cited by 15 publications

(16 citation statements)

References 31 publications

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“…Our observation is in agreement with previous findings in humans showing that gal-3 was reduced in active colitis while being elevated in patients with no clinical manifestations confirming a protective role of gal-3 in intestinal inflammation [36] . In active CD, gal-3 expression is decreased in the inflamed epithelium [37] .…”

Section: Discussionsupporting

confidence: 93%

Galectin-3 Modulates Experimental Colitis

et al. 2015

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Background: We recently identified galectin-3 (gal-3) as a new and strong fibroblast activator produced by colonic epithelial cells. Very little is known about the influence of gal-3 in inflammatory bowel disease. We, therefore, investigated the impact of gal-3 on dextran sodium sulfate (DSS)-induced colitis in a mouse model. Methods: Colonic lamina propria fibroblasts of healthy controls were used for co-incubation studies of gal-3 with gal-1, TGF-β1, IFNγ, IL-4 and IL-10. Acute and chronic DSS colitis was induced by 3% DSS in drinking water in female Balb/c mice weighing 20-22 g. Recombinant gal-3 was expressed by the pET vector system and used for a 5-day treatment in different concentrations intraperitoneally. The distal third of the colon was used for histologic analysis. Colonic cytokine expression was determined by quantitative RT-PCR. Results: In vitro, gal-3 induced IL-8 secretion was significantly reduced by co-incubation with IL-10 (5 ng/ml) and IL-4 (10 ng/ml). Acute DSS-induced colitis was ameliorated by gal-3 treatment as indicated by increased colonic length and reduced weight loss compared to that of controls. In acute and chronic colitis, gal-3 treatment resulted in a significant suppression of colonic IL-6. Conclusion: Gal-3 significantly reduces inflammation in acute and chronic DSS colitis in mice indicating a potential role in intestinal inflammation.

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Section: Discussionsupporting

confidence: 93%

Galectin-3 Modulates Experimental Colitis

et al. 2015

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“…Interestingly, loss of Gal3 protein (54,55) and Gal3 autoantibodies (56) have been observed in patients with ulcerative colitis, a pathologic state associated with chronic active mucosal inflammation (57,58). Furthermore, changes in glycosylation of proteins have been reported in patients with chronic inflammatory disorders such as ulcerative colitis and Crohn disease (58,59).…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

Jiang

Rankin

Nava

et al. 2014

Journal of Biological Chemistry

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Background: Desmoglein-2 mediates intestinal epithelial intercellular adhesion. Results: Galectin-3 was identified to associate with the ectodomain of desmoglein-2 and inhibit the degradation of desmoglein-2 and enhance intercellular adhesion. Conclusion: Galectin-3 lattices stabilize desmoglein-2 at the cell surface to regulate intercellular adhesion in intestinal epithelial cells. Significance: This study identifies a novel role of galectin-3 in controlling desmosome structure and function.

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“…No. RM-9116-S, Neomarkers, Fremont, Calif., USA) diluted 1: 100 were employed for immunohistostaining [25] .…”

Section: Antibodiesmentioning

confidence: 99%

FOXP3 Expression in Duodenal Mucosa in Pediatric Patients with Celiac Disease

Brazowski

Cohen²,

Yaron³

et al. 2010

Pathobiology

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Objective: It was the aim of this study to evaluate the number of 2 lymphoid subpopulations, CD8⁺ cells and FOXP3⁺, in the duodenum mucosa from pediatric celiac patients. Methods: Tissue sections prepared from paraffin-embedded biopsies of the descending duodenum of 61 celiac patients with Marsh grade 1 (M1), M2 and M3 disease and biopsies from 21 age-matched non-celiac (NC) patients were immunohistostained with anti-CD8 or FOXP3 antibodies. Results: The histological Marsh grade correlated with the mean number of FOXP3⁺ cells in the lamina propria (LP) mucosa (8.9 ± 1.1, 6.8 ± 2.4, 24.5 ± 2.6 and 31.1 ± 2.8 for NC, M1, M2 and M3 biopsies, respectively; p < 0.001). Using a cutoff point of 15 cells, 95% of NC and 88% of M1 biopsies had a mean of <15 FOXP3⁺ cells compared with 14% for M2 and 13% for M3 biopsies. The number of FOXP3⁺ cells in the epithelial mucosa also correlated with transglutaminase type 2 serum levels from the celiac patients. Unlike the FOXP3⁺ cells, CD8⁺ lymphocytes were present in both LP and surface epithelial mucosa and significantly different only in the LP mucosa of the M2 and M3 groups. Conclusion: The number of FOXP3⁺ cells is substantially increased in the mucosa of celiac patients at advanced stages. Characterization of the activity of these cells in celiac and in other inflammatory bowel diseases will enable us to understand the significance of these cells in celiac disease.

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Galectin-3 expression in pouchitis in patients with ulcerative colitis who underwent ileal pouch-anal anastomosis (IPAA)

Cited by 15 publications

References 31 publications

Galectin-3 Modulates Experimental Colitis

Galectin-3 Modulates Experimental Colitis

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

FOXP3 Expression in Duodenal Mucosa in Pediatric Patients with Celiac Disease

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