Role of Intestinal Microbiota in Ulcerative Colitis

difference from the luminal microbiota, it is crucial to apply an in vitro model that accounts for the
study of the mucosal microbiota.
We have demonstrated that the ability to colonize the mucus was significantly lower for
bifidobacteria and lactobacilli originating from UC patients when compared to those derived from
healthy subjects (Table 3). In consistence with our observations, lower levels of bifidobacteria in
the mucus layer of biopsy specimens from UC patients have previously been described [39,43].
Bifidobacteria and lactobacilli are believed to play an important role in promoting intestinal
health, due to their ability to inhibit colonization of pathogenic bacteria by lowering of colonic pH
[15], produce antimicrobial compounds [34,54], and compete for adhesion sites [7,9,35,54].
Additionally, they have shown to stimulate immune regulatory responses [21,66]. Hence, a
depletion of bifidobacteria and lactobacilli in UC patients could have a consequence for colonic
health and favor inflammation. Stimulation of these groups through pre‐ or probiotics could be an
approach in prevention of flare ups in UC.
In previous literature, the glycosylation patterns in UC patients in relapse has shown to differ
compared to control subjects and UC patients in remission, however, the aberrant profile is
reversible upon remission [33] and the microbiota has shown to be altered in UC patients in
relapse compared to controls but only to some extent in UC patients in remission [57,58,64]. It is
not well understood how changes in mucus composition can affect adhesion and colonization of
gut microorganisms, however, a changed mucus niche in UC patients in relapse may select a
different microbiota community and upon remission the level may not be reversed for all bacteria,
even though the mucus structure is back to “normal” [33].
Species or strain specific mucus adhesion promoting proteins have been found in several
bifidobacteria and lactobacilli. This includes among others fimbriae (L. rhamnosus GG, L. Johnsonii
NCC533, B. animalis subsp. lactis, B. bifidum)[17,24,50], Msa, mannose‐specific adhesin protein (L.
plantarum) [49], MucBP domain containing proteins (lactic acid bacteria) [26], and adhesion‐like
factor EF‐Tu (L. plantarum, B. animalis subsp. lactis) [17,63]. The expression of adhesion
molecules may be changed in the lactic acid bacteria from UC patients, hence their inability to
colonize the mucus in vitro, however, to our knowledge, no species of bifidobacteria or lactobacilli
have be isolated from UC patients to identify adhesion molecules.
11