Enhancement of the intestinal barrier

The lumen of the intestine contains bacteria, bacterial products, and dietary antigens capable of initiating and sustaining inflammation. The normal intestinal epithelium provides a relatively imperme­able barrier to these luminal constituents. From the findings of a study done by Isolauri et al. (39), Madsen et al. (72) described an increase in the intestinal permeability in IL-1 0 gene-deficient mice.

These models showed an increase in ileal and colonic permeability that is absent in mice raised under germ-free conditions. This suggests that the intestinal permeability defect in IL-10 gene-deficient mice is caused by a dysregulated immune response to normal enteric microflora and, furthermore, this permeability defect exists prior to the development of mucosal inflammation.

VSL3 treatment reduced colonic permeability in both IL-10 gene-deficient mice and control mice, suggesting that the type and quantity of bacterial species in the colon modulate intestinal permeability.

Adhesion and receptor competition

According to Madsen et al. (74), the intestinal permeability was reduced by VSL#3 treatment, partially as a result of probiotic bacterial-induced reduction in pro-inflammatory cytokine release. To determine the effect of VSL3 on epithelial function, Madsen et al. exposed T84 monolayers to bacteria for different periods of time and placed them in Ussing chambers for measurement of Isc, PO, and mannitol permeability. Staphylococcus dublin invasion was reduced after exposure to the VSL#3.

The results indicated that epithelial cells may also respond directly to certain probiotic bacteria or to a secreted bacterial factor. This supports the idea of a surface-acting proteinaceous component being released by a bacteria found in the VSL#3 mixture (74).

In this respect, Heinemann et al. (75) have demonstrated that a certain strain of Lactobacillus bacteria, Lactobacillus fermentum RC-14, releases surface-active components that may inhibit adhesion of bacteria. The results suggest that this Lactobacillus anti adhesive cell surface protein might protect against pathogens by preventing their adhesion.

Another beneficial mechanism described by Madsen et al. (74) was the receptor competition. Probiotics compete with microbial pathogens for a limited number of receptors on the surface epithelium. Almost certainly this competition contributes to the beneficial effects of the VSL#3 probiotic compound in vivo, since their data showed a substantial increase in levels of adherent bacteria.

However, the findings with T 84 cells showed the following:

  1. that conditioned media had the same effect as live bacteria on monolayer permeability, and
  2. that removal of VSL#3 bacteria before the invasion by S. dublin still resulted in protection from bacterial invasion.
These observations indicated that some secreted factor is responsible for additional direct effects on epithelium.


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