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Abstract
Psychological stress can cause dysfunction of the gastrointestinal tract by regulating its interaction with central nervous system (brain-gut axis). Chronic social defeat stress (CSDS) is widely used to produce a rodent model of stress-induced human mood disorders and depression. We previously showed that CSDS significantly affects the intestinal ecosystem including cecal and fecal microbiota, intestinal gene expression profiles and cecal metabolite profiles. Here, we investigated whether the glycosylation pattern in the intestinal epithelium was affected in C57BL/6 mice exposed to CSDS (hereinafter referred to as CSDS mice). A lectin microarray analysis revealed that CSDS significantly reduced the reactivity of fucose-specific lectins (rAOL, TJA-II, rAAL, rGC2, AOL, AAL, rPAIIL and rRSIIL) with distal intestinal mucosa, but not with mucosa from proximal intestine and colon. Flow cytometric analysis confirmed the reduced TJA-II reactivity with intestinal epithelial cells in CSDS mice. In addition, distal intestine expression levels of the genes encoding fucosyltransferase 1 and 2 (Fut1 and Fut2) were downregulated in CSDS mice. These findings suggest that CSDS alters the fucosylation pattern in the distal intestinal epithelium, which could be used as a sensitive marker for CSDS exposure.
Highlights
Psychological stress causes gastrointestinal dysfunction, including impairment of the intestinal barrier and perturbations of the neuroendocrine system and the intestinal immune system[1,2,3]
In a previous study using microarray analysis, we reported that the expression of Fut[2], a gene encoding fucosyltransferase 2 (FUT2), was significantly decreased in the terminal ileum of mice subjected to CSDS8
We found that the reactivity of distal intestinal mucosa with fucose-specific lectins was diminished in Chronic social defeat stress (CSDS) mice
Summary
Psychological stress causes gastrointestinal dysfunction, including impairment of the intestinal barrier and perturbations of the neuroendocrine system and the intestinal immune system[1,2,3]. We previously demonstrated that CSDS has a significant effect on the population of cecal and fecal microbiota and on cecal metabolites[8]. These changes were accompanied by the suppression of genes involved in immune responses in the terminal ileum (distal small intestine)[8]. We found that the reactivity of distal intestinal mucosa with fucose-specific lectins was diminished in CSDS mice. To confirm the results of our lectin microarray analysis, we performed flow cytometry and found that the CSDS mice displayed reduced reactivity with TJA-II, which binds Fucα1-2Galβ1-4GlcNAc (H type 2)
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