Chemistry Reference
In-Depth Information
to 60 g/day) of lactulose is effective in eliminating salmonella from the
intestinal tract of chronic human carriers and it is used as a pharmaceutical
for this purpose in some countries (Schumann, 2002). The mode of action is
speculated to be acidification of the gut that prevents the growth of this acid-
sensitive pathogen. In a placebo-controlled study, Chen et al. (2007) reported
that feeding lactitol significantly reduced plasma levels of endotoxin in a
group of patients with chronic viral hepatitis. Endotoxaemia is closely corre-
lated with the disturbance of the gut flora and the decline of colonization
resistance in these patients. Consuming lactitol significantly increased popu-
lations
of
bifidobacteria
and
lactobacilli,
perhaps
contributing
to
an
improved intestinal barrier.
Another mechanism by which oligosaccharides may provide protection
against enteric infections is through competitive inhibition of pathogen
adherence to the mucosa. Oligosaccharides can act as structural mimics of
the pathogen-binding sites, which are often carbohydrate epitopes. HMOs
act in this way to block the initial binding of a range of pathogens to inhibit
colonization (Gibson et al., 2005; Shoaf et al., 2006). In vitro experiments
using epithelial cell culture models (Tzortzis et al., 2005b; Shoaf et al., 2006)
and in vivo monkey challenge experiments (Gibson et al., 2005) have shown
that GOSs and lactulose have the ability to interfere with the adhesion of
enteropathogenic E. coli. The ability rapidly to install or restore colonization
resistance where the intestinal microbiota has been perturbed may prove to
be an effective use of lactose derivatives in the future. Possible mechanisms
by which prebiotics may increase colonization resistance are illustrated in
Figure 5.12.
5.9.4.7.
Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) describes a group of chronic, severe,
relapsing inflammatory conditions of the gut that includes Crohn's disease
and ulcerative colitis. A genetic predisposition to develop an over-zealous
inflammatory immune response to components of the intestinal microbiota
has been implicated in its aetiology (Schultz et al., 2004). Elimination of
specific bacterial antigens, immunomodulation and trophic effects of SCFA
on the intestinal epithelium have all been proposed as mechanisms by which
prebiotics could alleviate symptoms (Figure 5.9). The size of the intestinal
Bifidobacterium population has been shown to be relatively small (Favier
et al., 1997; Linskens et al., 2001) in subjects afflicted with IBD, although
cause and effect links between disease and a diminished intestinal Bifidobac-
terium population remain to be established. Using different rodent models of
IBD, Rumi et al. (2004) and Camuesco et al. (2005) ameliorated inflamma-
tion by feeding lactulose. Camuesco et al. (2005) noted that the improvement
