The VSL# 3 Probiotic Mixture Modifies Microflora but Does Not Heal Chronic Dextran-Sodium Sulfate–Induced Colitis or Reinforce the Mucus Barrier in Mice

Abstract

The mucus layer covering the epithelium is one of the main lines of defense of the colonic barrier. Both mucus gel and mucin expressions are altered during colonic inflammation and could be involved in epithelial repair. We postulated that modulating colonic mucus and mucins by probiotic supplementation could contribute to healing inflammatory mucosa. Our aim in this study was to determine whether probiotics could repair dextran-sodium sulfate (DSS)-induced chronic colitis in mice, and whether modifications of the colonic mucins could be involved. For that purpose, the VSL#3 probiotic mixture of 8 lactic acid bacteria probiotic strains was administered daily for 2 wk to mice with a mucosa impaired by a mild DSS treatment, and to mice with a normal mucosa. Probiotic strains survived in the gastrointestinal tract, increased the cecal concentrations of bifidobacteria, and modified cecal microflora metabolic activity in both DSS-treated and healthy mice. However, probiotic supplementation did not reverse the inflammation induced by DSS at either the macroscopic or histological level. Concurrently, probiotics did not modify the colonic mucus barrier, in terms of either mucin gene expression or adherent mucus layer thickness. In conclusion, the modification of microflora by supplementation with the VSL#3 probiotic mixture did not help to repair the colonic barrier breakdown caused by DSS treatment. The potential healing roles of mucins were neither confirmed nor invalidated by this study.

Lactic Acid Bacteria as Probiotics: Characteristics, Selection Criteria and Role in Immunomodulation of Human GI Muccosal Barrier

“…Conversely, another study showed that L. acidophilus A4 cell extract was sufficient to increase MUC2 expression in HT29 cells, independent of attachment (Kim et al, 2008). Additionally, intestinal trefoil factor 3 (TFF3) is coexpressed with MUC2 by colonic goblet cells and is suggested to promote wound repair (Gaudier et al, 2005 ;Kalabis et al, 2006). However, healthy rats did not display increased colonic TFF3 expression after stimulation by VSL#3 probiotics (Caballero-Franco et al, 2007).…”

Probiotics, prebiotics and synbiotics: A role in chemoprevention for colorectal cancer?

“…15,16 On the basis of previous studies linking commensal bacteria with CRC pathogenesis, manipulation of the intestinal bacterial milieu by administration of probiotics represents a rational therapeutic target. The mechanisms by which probiotics may inhibit colon cancer are not yet fully characterised, however, there is evidence for: a reduction in the inflammatory response to host flora, 17 alterations in the metabolic activities of intestinal bacteria, 18 a reduction in the numbers of bacteria involved in pro-carcinogenic and mutagenic pathways, 19 and the production of anti-tumorigenic and mutagenic substances. [20][21][22] Alteration of the intestinal microflora composition/competition with pathogens.…”

Mechanisms of maintenance of intestinal homeostasis by autochthonic microbiota and probiotics

“…Dodatkowo okazało się, że koekspresji z MUC2 ulega również jelitowy czynnik TFF3 (intestinal trefoil factor) przyczyniający się do regeneracji uszkodzonego nabłonka (25). Niestety, nie udało się udowodnić na tej drodze regeneracji nabłonka po jego celowym uszkodzeniu przez siarczan sodowy dekstranu (DSS) (14).…”