Chemistry Reference
In-Depth Information
forming units (cfu)/mL of
L. rhamnosus
was shown to significantly decrease the cell
apoptosis-to-proliferation ratio in ulcerated rat gastric epithelium.
26
The reduction of
this ratio was hypothesized to occur due to upregulation of ornithine decarboxylase
and B-cell lymphoma 2 (growth factors critical to ulcer healing).
26
Lactobacillus
rhamnosus
GG has been found to increase epithelial cell proliferation in the small
intestine and distal colon of rats,
26
facilitating repair of epithelial damage. This was
most likely the result of polysaccharide fermentation by the probiotic strain, thus
increasing SCFA availability for the epithelial cells.
27
Stimulation of the mucosal
immune system is a further mechanism, with evidence suggesting that some probi-
otics have potential antiinflammatory properties.
14
Lorea-Baroja et al.
14
describe a
number of potential mechanisms for the antiinflammatory effect of probiotics, such
as modulation of the balance between T-helper 1 (Th1), Th2, and regulatory T (T
reg
)
cells; downregulation of proinflammatory cytokine production (e.g., IL-12, TNF-α)
and/or stimulation of antiinflammatory cytokines (e.g., IL-10); enhanced elimina-
tion and permeation of proinflammatory antigens; and as a response to antagonism
against potentially pathogenic or proinflammatory endogenous bacteria.
14
It is likely,
however, that there are further mechanisms of action that have not yet been eluci-
dated, as such, a wide range of candidate strains continue to be screened
in vitro
,
in
vivo,
and in clinical trials.
12.2.1 Probiotics in IbD
12.2.1.1 In Vitro Models
There has been a recent increase in the number of comprehensive cell culture
experiments investigating the effects of probiotics using
in vitro
model systems of
IBD. Miyoshi and colleagues investigated the relationship between mucus adhesion-
promoting protein (MapA) and
L. reuteri
in Caco-2 cells.
46
Lactobacillus reuteri
has been shown to attenuate visceral pain
47
and moderate diarrhea,
48
but the mecha-
nism behind the adhesion of the bacteria to the GI tract was previously unknown.
This study demonstrated that MapA plays a key role in the adhesion of
L. reuteri
as it binds to receptor-like molecules on the Caco-2 cells, as well as revealing the
existence of multiple receptor-like molecules in Caco-2 cells, which may also be
involved.
46
Further studies could involve competitive binding assays between
L. reu-
teri
and pathogenic bacteria to determine whether this is a mechanism by which
L. reuteri
exerts its beneficial effect. In addition to competitive binding, a recent
study has identified production of the potent, broad-spectrum antimicrobial com-
pound reuterin as another mechanism by which
L. reuteri
could exert a beneficial
effect in the GI tract.
41
Four
L. reuteri
strains were investigated, and each produced
different amounts of reuterin. The reuterin derived from each strain was then shown
to inhibit the growth of pathogenic bacteria (enterohemorrhagic and enterotoxigenic
Escherichia coli
,
Salmonella enterica
,
Shigella sonnei,
and
Vibrio cholera
) to a sim-
ilar extent, indicating no strain specificity. Live
L. reuteri
displayed greater patho-
gen-inhibitory activities than reuterin alone, indicating that other microbial factors
