Role of Intestinal Microbiota in Ulcerative Colitis

Theoretical part
Figure 4: Location of UC in the different colon regions (Longstreth et al., 2010)
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3. Inflammatory Bowel disease
The factors responsible for the initiation and perpetuation of UC are unknown (Loftus,
2004;Sartor, 2006). However, evidence suggests that the colonic host‐bacterial interaction and
microbial composition play a pivotal role in the pathogenesis of UC. Firstly, the colon is the area of
the gut with the highest bacterial concentrations (section 1.1) and is also the site where
inflammation occurs in UC patients. Secondly, genetically engineered germ‐free mice, rats, and
guinea pigs completely lack enterocolitis but develop intestinal inflammation within 1 – 4 weeks if
they are colonized with conventional gut bacteria (Himmel et al., 2008;Sartor, 2008). Thirdly,
clinical studies have revealed that some PRRs have gene mutations (e.g. TRL9) or an increased
expression on IECs (e.g. TLR2 and TLR4) in UC patients (De Jager et al., 2007;Frolova et al.,
2008;Fuse et al., 2010), and finally, studies have shown that UC patients in relapse have a colonic
mucus layer that has an altered O‐glycan profile and is significantly thinner compared to healthy
subjects (Pullan et al., 1994;Larsson et al., 2011). Thus, gut host‐bacterial interaction seems to be
disturbed in UC, which may have consequences for the composition of the gut commensal
bacteria.
3.2. Alteration in the bacterial community of ulcerative colitis patients
Compositional changes in the colonic microbiota have been observed when comparing fecal and
mucosal samples from UC patients to that of healthy subjects (Lepage et al., 2005;Frank et al.,
2007;Takaishi et al., 2008;Sokol et al., 2009;Qin et al., 2010). Studies have demonstrated that the
fecal and mucosal amount of Firmicutes was significantly lower in UC patients than in healthy
subjects (Frank et al., 2007;Sokol et al., 2009). This was also applicable for the two dominant