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Monday 1 October 2018

Repair of the gut barrier with beta-glucans

In intestinal disorders, L-glutamine is often used to reduce gut permeability. However, a recent study has revealed that there is another therapy that we can use: administration of beta-glucans from mushrooms.

In Asian countries, mushrooms such as shiitake, maitake and oyster, have been valued for centuries for their nutritional and medicinal properties. Beta-glucans are complex fibres, polysaccharides, that are abundant in these mushrooms. Apart from mushrooms, they can also be isolated from (baker’s) yeast and from the cell wall of oats and barley. Lentinan from shiitake is made up entirely from beta-1.3/1.6 glucans. Especially these beta-glucans have an immune-modulating effect. They show positive effects in different syndromes. 

 

Inflammatory bowel diseases 

Earlier in-vitro and in-vivo studies revealed that, by inhibiting inflammatory mediators and inhibiting the NF-κB activity, shiitake, maitake and oyster show an improvement in inflammatory bowel diseases (ulcerative colitis, Crohn’s disease). Furthermore, research had already demonstrated that chronic and acute (psychological) stress can lead to degranulation of mast cells, resulting in weakening of the gut barrier and an increase in gut permeability. In general, increased gut permeability is seen as, in any case, a co-factor for numerous chronic diseases.

 

Recent study

A recent study of inflammatory bowel diseases revealed that gut permeability (leaky gut) can be reduced by a prebiotic dietary fibre containing beta glucan. Beta glucan resulted in improvements in the intestinal barrier function, both in patients with Crohn’s disease and in control groups. 

Whereas mast cell degranulation can increase the permeability of the intestinal cells and the spaces in between, beta glucan weakens this effect. This takes place through the follicle-associated epithelium that lies across the Peyer’s patches and through the villi. Furthermore, it appears that both the Peyer’s patches and the villi can absorb beta-glucan.

 

Mechanism of action of beta glucan

Beta-1.3/1.6 glucans are important for non-specific immune strengthening. Mainly macrophages and neutrophils are stimulated, these belong to the immune system’s first line of defence. Through phagocytosis they can render pathogens harmless. Furthermore, they produce important cytokines, because of which ultimately the humoral immune system can also be set in motion. 

Neutrophil granulocytes are one of the first immune cells to respond to an infection. As well as macrophages, they contain specific receptors (CR3 receptors) for the beta glucan macromolecule. Binding to these receptors improves the damaging effect of these neutrophils and improves the migration to the site of the infection. 

Pre-treatment of the neutrophils with beta-glucans improves their ability, with the help of chemokines, to move quickly through the blood to the site of infection. There are signs that beta-glucans rebalance an immune system mainly dominated by the humoral immunity (guided by Th2 helper cells), by a shift towards a mainly cellular immune response guided more by Th1 helper cells, which increases resistance to bacterial and parasitic infections. It can also rebalance Th2 and reduce Th1 allergic reactions.

 

Possibilities

Not only can beta-glucan offer relief in inflammatory bowel diseases. The effectiveness in improving intestinal permeability in the healthy control groups also offers prospects. Beta-glucan may, for example, be able to counterbalance the aforementioned harmful effect of stress on the intestinal barrier function. 


References

Ganda Mall, J.P. Casado-Bedmar, M. Winberg, M.E.  Brummer, R.J.  Schoultz, I.  Keita, Å.V. “A beta-Glucan-Based Dietary Fiber Reduces Mast Cell-Induced Hyperpermeability in Ileum From Patients With Crohn’s Disease and Control Subjects” Inflammatory Bowel Diseases Volume 24, issue 1, Pages 166–178.

Ashley L. St. John, Gladys W.X. Ang, Abhay P.S. Rathore, Soman N. Abraham. Reprograming Immunity to Food Allergens. Journal of Allergy and Clinical Immunology, 2018; DOI: 10.1016/j.jaci.2018.01.020