Volume 23 • Issue 01 • 2019
in gut microbiota homeostasis. It has been
shown that EcN can stimulate the production
of human β-defensin 2, which can protect the
mucosal barrier against adhesion and invasion
by pathogenic commensals [68, 69]. In addition,
several in vivo and in vitro studies have shown
that EcN has a protective function against
Salmonella, Shigella, Candida, and some other
invasive commensals and may restore damaged
epithelium by modulation of tightjunction and
zonula occludens proteins [70]. However, outer
membrane vesicles (OMVs) released by gram-
negative bacteria play a vital role in the signalling
process of the intestinal gut mucosa. The release
of OMVs begins a mechanism to deliver some
active compounds and microbial proteins to
the host body without intercellular contact. It
was recently demonstrated that OMVs trigger
the host immune and defense responses of the
probiotic strain EcN, which entered intestinal
cells via clathrin-mediated endocytosis. In fact,
in vitro and ex vivo studies have demonstrated
expression of antimicrobial peptides and
modulation of the cytokine/chemokine response
of gut epithelial and gut immune cells when the
probiotic strain EcN induced OMVs. Moreover,
these OMVs promote the upregulation of the
tight-junction proteins of zonula occludens and
claudin-14, but down-regulation of claudin-2
reduces gut permeability and supports intestinal
barrier functions in intestinal epithelial cell
lines [71, 72]. Finally, the probiotic strain EcN
is also involved in the intestinal microbiota
immune response, including macrophages,
epithelial cells, dendritic cells, and upregulation
of proinflammatory cytokines (IL-6, IL-8, and
IL-1β) [71]. Enterococcus are gram-positive
bacteria in the lactic acid bacteria family. Some
strains of Enterococcus exert antibioticinduced
dysbiosis and act as antitumor or anticancer
agents and modulate the immune system. It
has been found that culture of E. faecium strain
from human intestinal epithelium increased the
bactericidal effects against enteroaggregative E.
coli, membrane damage, and cell lysis [73, 74].
Fusco et al. [74] characterized intestinal cytokine
expression in epithelia cells and reported that
intestinal cytokines play a key role in the host
inflammatory response to damage by Salmonella
typhimurium. It has been revealed that E. faecium
increases the expression of proinflammatory and
anti-inflammatory cytokines without appearing
as a pathogen. Furthermore, E. hirae exerts the
gut epithelial barrier function by inducing T17
[30].
Saccharomyces is well-known nonpathogenic
selective probiotic yeast that has been used
commercially in the production of probiotic
foods. Over the past few decades, S. cerevisiae
and S. boulardii have demonstrated extensive
promise as a probiotic treatment [28]. Several
studies have demonstrated that S. cerevisiae and
S. boulardii were associated with an increased
proportion of Bacteroidetes in the gut microbiota
composition and decreased the relative
abundance of Firmicutes and Proteobacteria.
In addition, this yeast has ability to prevent
infammation by promoting proinflammatory
immune function and increasing the production
of short-chain fatty acids [28, 29, 75, 76].
5. Conclusions
Probiotic bacteria species form a reproducible
gut microbiota population in various host bodies
and diseases. Various probiotic species have been
reported to prevent many degenerative diseases,
including obesity, diabetes, cancer, cardiovascular
disease, malignancy, liver diseases, and IBD. An
imbalance of the gut microbiota composition can
lead to several diseases. Probiotics have been
proved to modulate gut microbiota composition
imbalance by increasing bacteria population,
gut epithelium barrier function, and cytokine
production. Meanwhile, diets and different
nutrients have been reported to productively
and markedly shape gut microbiota communities
[77–83], further studies should be performed to
elucidate the metagenomic relationship between
alteration of the gut microbiota composition
and probiotic species under different diets or
nutrients. A well-designed and appropriate
experimental model (in vivo, in vitro, or ex
vivo) is suggested to provide insights into the
gut microbiota composition and potential
commensals for host health. Furthermore, the
identification of new probiotics and isolation
from microbiome and mixture of probiotic
species would be a key pathway for future studies
to promote host health.
Abbreviations
GIT: Gastrointestinal tract
CVD: Cardiovascular disease
LAB: Lactic acid bacteria
HFD: High-fat diet
LPS: Lipopolysaccharide
Treg: T regulatory cell
IL: Interleukin
T: T helper cell
DC: Dendritic cell
IBD: Intestinal bowel disease
WSD: Western-style diet
EcN: Escherichia coli Nissle
OMVs: Outer membrane vessels.
References available online: www.vetlink.co.za
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