Increase in Lectin Binding Sites on Epithelial Cells by Chronic Bladder Infection in Rats

Abstract

Using lectin histochemistry we assessed whether chronic bladder infection modifies carbohydrate residues of glycoconjugates on uroepithelial cells in rats. The bladder infection was produced by implanting a knotted silk thread with Escherichia coli into the bladder. One or 4 weeks after the implantation the bladder was excised, incubated with sixteen biotinylated lectins and stained. The bladder epithelia as a whole stained more strongly positive for eight lectins in the infected rats than in the control rats having a sterile silk thread in the bladder. In the infected rats, the superficial epithelial layer that stained negative for Arachis hypogaea (PNA) in the controls became strongly positive for PNA, whereas the middle and deep epithelial layers increased in staining for Canavalia ensiformis and six other lectins. These results indicate that chronic bladder infection increases carbohydrate residues on uroepithelial cells and may facilitate bacterial adherence to uroepithelial cells.

Inflammation-Induced Adhesin-Receptor Interaction Provides a Fitness Advantage to Uropathogenic E. coli during Chronic Infection

“…Further, our results (Figure 6) are in agreement with the glycan remodeling seen in a recent study of the mouse bladder transcriptome during chronic cystitis, which revealed the alteration of many glycosyl transferases including 20 involved in modifying the galactose epitopes such as C1GALT, GALNT4, B3GNT3 and GALNT3 that can make or modify Gal(β1-3)GalNAc (Schwartz et al, 2015). Finally, studies looking at specific lectin binding to naïve and inflamed rat bladders chronically exposed to UPEC showed a very similar phenotype to what we observe in mice with increased expression of Gal and GalNAc epitopes (Nakagawa et al, 1996). …”

Lectins as Biomarkers of IC/BPS Disease: A Comparative Study of Glycosylation Patterns in Human Pathologic Urothelium and IC/BPS Experimental Models

“…Glycosylation patterns of healthy human urinary bladders have been previously studied using lectin histochemistry, particularly in comparison to bladder cancer tissue [28][29][30][31][32][33]. In addition, glycoconjugate expression has been analyzed in normal bladders of various species, including rabbit [11,34], donkey [35], rat [36,37], and mouse [38], as well as in various urothelial cell lines [39][40][41]. Lectin binding has also been studied in animal models of bladder cancer [31,38] and chronic bacterial cystitis [37], showing specific binding of some lectins to neoplastic bladder tissue, and increased glycosylation of the urothelium in E. coli-induced bladder inflammation, respectively.…”

“…In addition, glycoconjugate expression has been analyzed in normal bladders of various species, including rabbit [11,34], donkey [35], rat [36,37], and mouse [38], as well as in various urothelial cell lines [39][40][41]. Lectin binding has also been studied in animal models of bladder cancer [31,38] and chronic bacterial cystitis [37], showing specific binding of some lectins to neoplastic bladder tissue, and increased glycosylation of the urothelium in E. coli-induced bladder inflammation, respectively. However, to our knowledge, lectin binding has never been analyzed in in vitro or in vivo models of IC/BPS.…”