Colitis and the GI mucosal lining

The inflammatory response of UC is primarily located in the colonic mucosa and submucosa. The distal colon is always affected, with the condition expressing itself in acute attacks followed by periods of symptom‐free remission. The disease almost invariably appears first in the rectum and distal colon, and over time, it usually progresses up the colon towards the proximal bowel. 

Microbial involvement has been proposed in both the initiation and maintenance stages of UC   [Cummings et al] While we cannot narrow it down to a single microbe in every case, some of the microbes commonly associated with UC include Desulfovibrio, E-coli, Shigella and Bacteroides. And now that PCR testing can identify microbes at the species level, we are finding that Instead of there being a diverse array of species within a single genus, there is a tendency for one species to dominate. For example, one species of E-coli or one species of Bacteroides will dominate that genus within Colitis. [Masseret et al] 

The gut flora seems to communicate with the host’s epithelial cells and intestinal immune factors—thus contributing to the development of inflammation through a variety of ways including: 

. secretion of quorum-sensing molecules

. through direct damage to the epithelium through definable virulence properties of the bacteria 

. Bacterial DNA can be an immuno-modulatory component of healthy gut flora or can lead to persistent inflammation of the intestine. 

. Gut bacteria can bind to the mucosa by microbial polysaccharides and polynucleotides, which are also recognized by TLRs, thus contributing to the inflammatory response

On this note, research has concluded It is likely that the mucosal-associated bacterial flora is more important than the luminal flora in IBD. [DuPont et al]

Considering the make-up of the intestinal mucosal layer and what research has shown in regards to microbial and immune modulation, we are starting to see that a mucosal/microbial/immune centred approach can be beneficial for UC patients.

An investigation by Langlands et al found that even small dietary changes could have profound effects on the mucosal microbiota, which opens up the possibility that new therapeutic strategies can be developed for tackling bacteria‐associated gut diseases.

We know that UC patients tend to be deficient in bifidobacteria, and that some bifidobacteria strains are modulators of the mucosa. So it is only intuitive that researchers are looking at using targeted prebiotics, probiotics and other compounds to modify the microbiota; starting with bifidobacteria. For example, certain bifidobacteria probiotic strains are being used to reduce inflammatory cytokines and modulate the mucosa. 

Although bifidobacteria modulate mucus levels, several well characterized Bifidobacterium species harbor glycosyl hydrolases which can extensively degrade mucin glycans. While these mucin-degrading enzymes are likely important in GI niche development, the ability of select bifidobacteria species to degrade mucin glycans may be unfavorable when there is diminished mucin production, such as during colitis. Thus, it becomes important to select your strains carefully.

Among the better combinations studied thus far has been Bifidobacteria longum and oligofructose enriched inulin.

This is all well and fine, but in stubborn UC patients what about supporting other aspects of mucosal lining health? 

Patients might be missing the necessary compounds for the body to create mucus, such as the amino acids serine, proline and threonine. Or, perhaps even promoting rehydration, which is necessary for healthy mucus turnover; and water making up 90% of mucus.

Besides growing and using bifidobacteria, there are other microbes associated with mucosal health: Akkermansia being the keystone species of mucosal health. This would fit with the researchers suggestion to use a ratio of mucus builders to degraders to determine chance of relapse. 

To our clients I usually suggest nervous system support, which research has found to be a contributor to mucosal homeostasis. 

Microbe-friendly improvements to oral hygiene practices, which have a downstream impact on the gut microbiome.

And using nutrition and lifestyle to increase IL-10, which UC patients are often lacking due to genetic predispositions.

If you would like to learn more about your microbiome schedule your free discovery call with microbiome analyst Kristina. OR, sign up for our email newsletter to be notified about our next webinar on the gut mucosal layer.


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