ARTICLE IN PRESS

International Journal of Medical Microbiology 300 (2010) 5762

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International Journal of Medical Microbiology

journal homepage: www.elsevier.de/ijmm

Mini Review

Mechanisms of probiotic actions A review

Tobias A. Oelschlaeger 
Institut fur Molekulare Infektionsbiologie, University of Wurzburg, Rontgenring 11, D-97070 Wurzburg, Germany

a r t i c l e in fo abstract

Probiotics are gaining more and more interest as alternatives for antibiotics or anti-inammatory drugs.
Keywords: However, their mode of action is poorly understood. This review will present examples of probiotic
Probiotics actions from three general modes of actions into which probiotic effects can be classied. Probiotics
Mechanisms of action might modulate the hosts immune system, affect other microorganisms directly or act on microbial
products, host products or food components. What kind of effect(s) a certain probiotic executes depends
on its metabolic properties, the molecules presented at its surface or on the components secreted. Even
integral parts of the bacterial cell such as its DNA or peptidoglycan might be of importance for its
probiotic effectiveness. The individual combination of such properties in a certain probiotic strain
determines its specic probiotic action and as a consequence its effective application for the prevention
and/or treatment of a certain disease.
& 2009 Elsevier GmbH. All rights reserved.

Introduction
In this review I will give an overview on the effects of
probiotics. It has to be taken into account, that many reported
mechanisms of probiotic actions are the results of in vitro
experiments. Therefore, these results must be conrmed by in
vivo studies.
The effects of probiotics may be classied in three modes of
action. (i) Probiotics might be able to modulate the hosts defences
including the innate as well as the acquired immune system. This
mode of action is most likely important for the prevention and
therapy of infectious diseases but also for the treatment of
(chronic) inammation of the digestive tract or parts thereof. In
addition, this probiotic action could be important for the
eradication of neoplastic host cells. (ii) Probiotics can also have
a direct effect on other microorganisms, commensal and/or
pathogenic ones. This principle is in many cases of importance
for the prevention and therapy of infections and restoration of the
microbial equilibrium in the gut. (iii) Finally, probiotic effects may
be based on actions affecting microbial products like toxins, host
products e.g. bile salts and food ingredients. Such actions may
result in inactivation of toxins and detoxication of host and food
components in the gut.
All three modes of probiotic action are in all likelihood
involved in infection defence, prevention of cancer and in
stabilising or reconstituting the physiological balance between
the intestinal microbiota and its host. However, it has to be
 Tel.: + 49 931 31 2150; fax: + 49 931 31 2578.
E-mail address: t.oelschlaeger@mail.uni-wuerzburg.de
stressed that there seems not to be one probiotic exhibiting all
three principles, at least not to that extent that it could be a
remedy for prevention or therapy of all mentioned kinds of
disease. It depends on the metabolic properties, the kind of
surface molecules expressed and components to be secreted
which probiotic actions a certain probiotic strain might show. The
era of omics we are living in at this time, will make crucial
contributions because it enables the analysis and comparison of
whole genomes, transcriptomes, proteomes and secretomes (see
also Wohlgemuth et al., 2010). This all will lead to the
identication and characterisation of probiotic properties, distin-
guishing real probiotics from those, which are not.
Immune modulation
Probiotics can inuence the immune system by products like
metabolites, cell wall components and DNA. Obviously, immune
modulatory effects might be even achieved with dead probiotic
bacteria or just probiotics-derived components like peptidoglycan
fragments or DNA. Probiotic products are recognized by host cells
sensitive for these because they are e.g. equipped with recognition
receptors. The main target cells in that context are therefore gut
epithelial and gut-associated immune cells. The interaction of
probiotics with host (epithelial) cells by adhesion itself might
already trigger a signalling cascade leading to immune modula-
tion. Alternatively, release of soluble factors can trigger signalling
cascades in immune cells or in epithelial cells which subsequently
affect immune cells. The direct adhesion of probiotics to host
epithelial cells has been demonstrated in many in vitro experi-
ments. However, probiotic and commensal bacterial adherence to

1438-4221/$ - see front matter & 2009 Elsevier GmbH. All rights reserved.
doi:10.1016/j.ijmm.2009.08.005
 ARTICLE IN PRESS
58 T.A. Oelschlaeger / International Journal of Medical Microbiology 300 (2010) 5762
gut epithelial cells in vivo has not been demonstrated. Rather,
such bacteria adhere just to and invade the outer mucus layer but
do not reach the epithelial cells themselves (Matsuo et al., 1997).
One exception is the uptake and transcytosis of bacteria by M-
cells, which collect at a low level luminal gut antigens, here
bacteria, and pass them down to dendritic cells (DCs) in the
subepithelial dome region. Another direct contact between
probiotics and host cells in the gut occurs by internalization of
bacteria by DCs which are localized below the epithelial cells (non
M-cells) (Macpherson and Uhr, 2004). These cells are also able to
collect antigens from the gut lumen with their dendrites by
extending these dendrites through the epithelium into the gut
lumen. Ex vivo studies with human monocyte-derived DCs
matured in the presence of Lactobacillus rhamnosus were used to
instruct naive CD4 + T cells. Such T-cells showed a decreased
proliferation and cytokine production (IL-2, IL-4, IL-10) while
responding normal to IL-2. In vivo oral supplementation of six
patients suffering from Crohns disease with L. rhamnosus for 2
weeks induced a similar hyporesponsiveness including impaired
ex vivo T helper subsets 1 and 2 responses, demonstrating the
important role of DCs in immune modulation by probiotics (Braat
et al., 2004).
Teichoic acid, a component of the Gram-positive cell wall, of L.
plantarum is involved in the anti-inammatory activity of this
probiotic. A mutant with enhanced anti-inammatory capacity
incorporated much less D-ala in its teichoic acids than the wild-
type strain and dramatically reduced secretion of pro-inamma-
tory cytokines by peripheral blood mononuclear cells and
monocytes resulting in signicant increase in IL-10 production.
The effects observed were clearly TLR-2 dependent. This mutant
was also more protective in a murine colitis model than its wild-
type counterpart (Grangette et al., 2005). This study elegantly
demonstrated the involvement of TLR-2 in the probiotic effect of L.
plantarum highlighting the importance of TLRs for probiotic
actions.
However, probiotics are also able to protect the integrity of the
mucosal gut barrier against the destructive action of enteropatho-
genic Escherichia coli in a TLR-independent way. They achieve this
by changing protein kinase C signalling resulting in an amplica-
tion of expression and redistribution of zonula occludens protein
2 (ZO-2) in T84 cells (Zyrek et al., 2007). This makes perfect sense
because ZO-2 is an important factor for the preservation of tight-
junction function in the gut epithelium. Induction by the probiotic
E. coli strain Nissle 1917 (EcN) of ZO-2 as well as ZO-1 expression
in vivo was demonstrated in the mouse model. EcN was even able
to protect mice with dextran sodium sulphate-induced colitis by
reducing the loss of body weight and colon shortening as a
consequence of increasing intestinal barrier function (Ukena et al.,
2007).
A direct anti-inammatory effect of EcN on human gut
epithelial cells (HCT15) could only be demonstrated for live
bacteria but without direct contact. Rather a secreted factor
mediated this effect by suppressing the TNFa-induced IL-8
transactivation by a mechanism independent of NF-kB inhibition
(Kamada et al., 2008).
In general, some probiotics are able to alter cytokine produc-
tion by modulating cellular signal transduction. They can either
block degradation of the inhibitor IkB by inhibiting the ubiqui-
tination of this inhibitor, by interfering with proteasome function
or inuencing RelA localisation via the receptor g-dependent
signal cascade which in turn is activated through a peroxisome
proliferator (Petrof et al., 2004; Kelly et al., 2004).
Two soluble proteins from Lactobacillus rhamnosus GG promote
intestinal epithelial cell survival and growth. These proteins
inhibit TNF-a-mediated apoptosis by activation of the anti-
apoptotic factor Akt and protein kinase B. Furthermore, they
inactivate the pro-apoptotic p38 mitogen-activating protein
kinase signalling pathway in epithelial cells (Yan et al., 2007).
All these effects of probiotics are suitable for strengthening the
gut epithelial barrier. Also the production of butyric acid by
eubacteria and clostridia, which can be boosted by prebiotics,
results in consolidation of the epithelial barrier. Finally, probiotics
were shown in vitro to induce the expression of defensins and
cryptidins. The amplication of defensin/cryptidin expression in
Paneth cells might indeed be part of the reinforcement of the
mucosal barrier by certain probiotics. The induction of a-
defensins in Paneth cells is carried out by activation of the
cytoplasmic receptor NOD2, which recognizes muramyl dipeptide
(Wehkamp et al., 2004).
As the inducing agent for human b-defensin 2 the agella of
EcN have been identied (Schlee et al., 2007). This modulation of
the innate immune system is suitable for keeping commensals
and pathogens alike at a distance to the intestinal epithelium. This
mechanism seems to be of importance for keeping patients
suffering from colitis ulcerosa in remission (Kruis et al., 2004).
Even DNA of some probiotics showed a systemic anti-
inammatory effect in contrast to DNA from pathogenic bacteria
which induced an inammatory reaction. Essential for DNA effects
is the Toll-like receptor 9 (TLR9) (Rachmilewitz et al., 2004). The
reason for the differing DNA effects remains unclear.
Besides effects on epithelial cells various immune cells such as
DCs are affected by probiotics. DCs are responsible for collecting
continuously antigens from the gut and present it to naive T cells.
This usually leads to T cell activation and differentiation. In
contrast, contact with certain probiotics results rather in an anti-
inammatory effect which often is the consequence of increased
IL-10 expression in DCs.
Even some regulatory T (Treg) cells are induced by some
probiotics. This might explain how subcutaneously applied
probiotics exert an anti-inammatory effect. This approach was
successful not only in murine colitis but also in arthritis treatment
(Sheil et al., 2004).
In a placebo-controlled cross-over trial the effect of Lactoba-
cillus casei Shirota on natural killer cell (NK) activity in humans
was demonstrated. The activity of NK was increased as a likely
consequence of L. casei Shirota-induced IL-12 production which
was detected in in vitro assays (Takeda et al., 2006).
On one hand all the examples mentioned show probiotics to be
able to modulate the immune system in a strain-specic manner.
On the other hand, it is clear that we just started to understand
the molecular basis of the observed effects.
Direct effects on other microorganisms
Antimicrobial substances produced by probiotics
Bacteriocins. In vitro-studies showed inhibition of pathogen
replication mediated by low-molecular-weight substances. Top of
this list are short chain fatty acids e.g. lactic acid. A similar effect
was observed for hydrogen peroxide. Also low-molecular-weight
bacteriocins (LMWB) and high-molecular-weight bacteriocins
(class III) are produced by lactobacilli. The LMBW are antimicro-
bial peptides. LMWB can be grouped into three classes: (class I)
lantibiotics, posttranslationally modied peptides harbouring
unusual amino acids such as lanthionin, (class II) heat stable
non-lantibiotics, (class IV) cyclic antimicrobial peptides (Maqueda
et al., 2008). The broad-spectrum class II bacteriocin Abp118
produced by Lactobacillus salivarius strain UCC118 is able to
protect mice against infection with the invasive foodborne
pathogen Listeria monocytogenes. Abp118 is obviously the primary
mediator of protection since an Abp118-negative mutant failed to
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T.A. Oelschlaeger / International Journal of Medical Microbiology 300 (2010) 5762
protect the animals (Corr et al., 2007). Besides LMWB probiotics
produce also certain antibiotics. The production of the antibiotic
reuterin (3-hydroxypropionaldehyde) by Lactobacillus reuteri
strain ATCC55730 has been reported. Reuterin is a broad-
spectrum antibiotic active not only against Gram-positive and
Gram-negative bacteria but also against yeast, fungi, protozoa and
viruses (Cleusix et al., 2008). Finally microcines, which are
peptides with a narrow window of activity, have to be mentioned,
because they are also synthesised by many probiotics.
A specic antimicrobial function is the property of proteins
(molecular weight 420 kDa) belonging to the family of bacter-
iocins. These proteins are sometimes termed group III bacteriocins
of Gram-positive bacteria. However, such proteins (bacteriocins)
are also produced by Gram-negative bacteria. Production of
bacteriocins with an antimicrobial effect towards Gram-positive
as well as Gram-negative bacteria could be proven for various
bidobacteria strains (Cheikhyoussef et al., 2008).
Deconjugated bile acids. Probiotic bacteria are able to
produce so-called deconjugated bile acids which are derivatives
of bile salts. Deconjugated bile acids show a stronger antimicro-
bial activity compared to the bile salts synthesized by the host
organism. How the probiotics protect themselves from these
selfmade metabolites or if they are resistant to deconjugated
bile acids at all remains to be elucidated.
Competition for limiting resources
An important example for a limited substance in the host is
iron. But for almost all bacteria iron is an essential element with
the exception of lactobacilli. They do not need iron in their natural
habitat (Weinberg, 1997). This might be a crucial advantage in
competition with other microorganisms which depend on iron.
Nevertheless L. acidophilus and L. delbrueckii are able to bind ferric
hydroxide at their cell surface, rendering it unavailable to
pathogenic microorganisms (Elli et al., 2000). In contrast to
lactobacilli the probiotic EcN relies on iron and secretes side-
rophores to chelate ferric or ferrous iron and expresses iron
uptake systems to transport it into the bacterial cell. This property
is also common to pathogenic bacteria. However, EcN is able to
compete very effectively for this limited resource because it
encodes at least seven different iron uptake systems (Grozdanov
et al., 2004; Groe et al., 2006).
Anti-adhesive effects
Because probiotic bacteria are able to adhere to epithelial cells
in cell culture assays, thereby blocking adherence of pathogens, it
is extrapolated that this mechanism is important for the probiotic
effect in the host. The anti-adhesive effect might be the result of
competition between probiotic and pathogen for the same
receptor or the induction by probiotics of (increased) mucin
production. Mack et al. (2003) reported indeed induction of MUC3
mucin in HT20-MTX cells when co-cultured with L. plantarum
299v or L. rhamnosus GG. MUC3 mucin inhibited subsequently the
adhesion of enteropathogenic E. coli strain E2348/69. Even
adhesion of pathogenic Salmonella, Clostridium and E. coli strains
to pig intestinal mucus could be reduced in the presence of
probiotic Bidobacterium lactis Bb12 and/or Lactobacillus rhamno-
sus LGG (Collado et al., 2007a). However, the ability to inhibit the
adhesion of pathogens to immobilized human mucus appears to
depend on both the specic probiotic strains and the pathogens.
Furthermore, some commercial probiotic strains even increased
the adhesion of E. coli, L. monocytogenes and Salmonella typhimu-
rium to human mucus (Collado et al., 2007b). The most prominent
adhesins of probiotics are surface proteins of Lactobacillus (e.g.
59
Mub: mucus-binding protein of L. reuteri 1063; Roos and Jonsson,
2002) which share common characteristics such as the presence
of a signal peptide, a C-terminal cell wall-anchoring motif (LPXTG)
and several repeated domains with putative adhesion function
(Sanchez et al., 2008).
Besides competitive exclusion, i.e. competition for the same
receptor by probiotics and pathogens as described above, other
modes of anti-adhesiveness expressed by probiotics could be
degradation of carbohydrate receptors by secreted proteins,
establishing a biolm, production of receptor analogues and the
induction of biosurfactants.
Anti-invasive effects
Not only adhesion to but also invasion of epithelial cells is an
important property for full pathogenicity of many gut pathogens.
This fact led to investigations for probable anti-invasive effects of
probiotics. The standard assay for quantication of invasiveness is
the gentamicin protection assay (Hess et al., 2004). In this cell
culture assay, differentiation between intracellular and extracel-
lular bacteria is achieved by gentamicin, which kills the extra-
cellular bacteria. The number of intracellular bacteria is
enumerated after release of the bacteria by lysis of the epithelial
cells and determination of the colony-forming units. All anti-
microbial substances produced by probiotics result in reduced
numbers of intracellular bacteria although these substances do
not directly inhibit invasion but just kill the pathogens. However,
there are probiotics able to specically interfere with bacterial
host cell invasion. For EcN inhibition of invasion of various gut
epithelial cell lines by S. typhimurium, Yersinia enterocolitica,
Shigella exneri, Legionella pneumophila and L. monocytogenes has
been reported. The extent of inhibition is dependent on the
number of EcN bacteria administered and only observed with live
EcN. A direct contact between EcN and the invasive bacteria or
with the epithelial cells is not necessary and therefore a secreted
not yet identied factor seems to mediate inhibition of invasion
by EcN (Altenhoefer et al., 2004). Secreted factors of some
probiotic lactobacilli and Bidobacterium bidum strain Bb12 are
also interfering with invasion of host epithelial cells by S.
typhimurium (Ingrassia et al., 2005; Botes et al., 2008). For some
Lactobacillus ker strains the component mediating the anti-
invasive effect was identied as an S-layer protein which is also
shed into the culture medium (Golowczyc et al., 2007). The ability
to inhibit bacterial invasion of gut epithelial cells by pathogens is
rather wide spread among probiotics. Whether this in vitro
property has also in vivo relevance must be validated in animal
experiments after identication of the responsible genes with
isogenic mutants and their corresponding complemented strains
in relation to the parental strain.
Antitoxin effects
May be the most important group of bacterial virulence factors
are toxins. The effectiveness of certain probiotics in diarrhoea is
most likely based on their ability to protect the host against
toxins. This protection can result from inhibition of toxin
expression in pathogens. For Bidobacterium breve Yakult and
Bidobacterium pseudocatenulatum DSM20439 inhibition of shiga
toxin expression in E. coli (STEC) O157:H7 strains in vitro as well
as in mice was demonstrated in contrast to other Bidobacterium
isolates. Thus all animals treated with B. breve strain Yakult
survived whereas 90% of the mice in the control group died after
challenge with STEC. In vitro studies imply the high concentration
of acetic acid produced by strain Yakult to be responsible for
inhibition of Shiga toxin expression (Asahara et al., 2004).
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Similarly, probiotic Clostridium butyricum strain MIYAIRI protected
gnotobiotic mice against an infection with enterohaemorrhagic E.
coli (EHEC) O157:H7. Strain MIYAIRI inhibits in vitro and in vivo
not only shiga toxin expression by production of butyric and lactic
acid but butyric acid also reduces viability of EHEC after
neutralization (pH 7) (Takahashi et al., 2004). Real-time PCR
conrmed that in vitro 15 different probiotic lactobacilli strains
inhibited shiga toxin 2A expression via production of organic acids
at subbactericidal concentrations for EHEC O157:H7 (Carey et al.,
2008).
The probiotic yeast Saccharomyces boulardii, actually a strain of
Saccharomyces cerevisiae, shows effective protection against
Clostridium difcile toxin A in the murine ileal loop model and in
cell culture assays. This protection results from interference of S.
boulardii with the toxin A-induced inammatory signal cascade
activating Erk1/2 and JNK/SAPK pathways (Chen et al., 2006).
Additionally, S. boulardii is able to induce a specic anti-toxin A
IgA immune response and secretes a protease which can destroy
this toxin (Qamar et al., 2001; Castagliuolo et al., 1996).
Certain probiotics are even able to protect against cyanobac-
terial and fungal toxins. The basis of the observed protective effect
is rather physicochemical interaction between toxin and probiotic
than metabolic inactivation. The mycotoxin deoxynivalenol as a
contaminant of cereal crops can cause gastroenteritis. Lactoba-
cillus rhamnosus GG dead or alive can bind deoxynivalenol and
therefore potentially restricts bioavailability of this toxin (Turner
et al., 2008). The same strain and L. rhamnosus strain LC-705 are
able to bind other mycotoxins including aatoxins. In the rat
model L. rhamnosus strain GG was able to modulate intestinal
absorption and increased faecal excretion of aatoxin resulting in
lowered toxicity expressed as alleviated liver injury. All this was
the result of aatoxin binding to this probiotic (Gratz et al., 2006).
In vitro data indicate, that strain GG reduces aatoxin B1 uptake
and protects against both membrane and DNA damage (Gratz et
al., 2007).
Finally the same L. rhamnosus strains but also certain
Bidobacterium lactis and B. longum strains were shown to bind
in addition cyanobacterial peptide toxins such as microcystin LR.
This toxin is the most frequent and toxic variant of the liver toxic
microcystins and can be found in drinking water after contam-
ination with cyanobacteria. Such toxins could be removed from
aqueous solutions by binding to the mentioned probiotics to a
varying degree depending on the strain employed (Nybom et al.,
2008).
Designer probiotics
The identication of toxin receptors paved the way for
recombinant E. coli expressing receptor structures at their surface
identical with the receptor for a certain toxin. Such designer
probiotics bind very efciently e.g. shiga toxin 1 (Stx1) and 2
(Stx2). One mg bacterial dry weight is able to bind more than
100 mg Stx1 or Stx2. This was achieved by replacing the O-side
chains of the original LPS by Gb3, the receptor for these toxins.
The resulting recombinant strain protected all mice after
challenge with a toxin dose killing all animals in the control
group. Similar designer probiotics carrying the receptor for the
heat-labile enterotoxin of enterotoxigenic E. coli (ETEC) or the
receptor for cholera toxin very efciently bound the respective
toxin and showed good protection in animal models after ETEC or
Vibrio cholerae challenge. For some constructs formaldehyde-
killed bacteria mediated also efcient protection as long as the
frequency of application was increased (Paton et al., 2006).
Inhibitory activity against genotoxins
There are claims for anti-cancer activity of probiotics. If such a
protection occurs in humans who consume the appropriate
probiotic is unknown. However, the repression of putrefactive
bacteria such as Clostridium, coliforms or Bacteroides species and
an increase in numbers of lactobacilli and bidobacteria might at
least reduce the probability of incidence for colorectal cancer. The
incidence of adenocarcinoma in the colon of IL-10 knockout mice
was factually reduced in mice treated with probiotic Lactobacillus
salivarius ssp. salivarius (OMahony et al., 2001). Treatment with
probiotics able to interfere with chronic recurrent inammation of
the gut might also be helpful in preventing colon carcinoma,
because chronic inammation promotes the appearance of this
disease. An example of an anti-inammatory active probiotic is
Streptococcus thermophilus strain TH-4 which also produces high
amounts of folate important for DNA repair in epithelial cells (Van
Guelpen et al., 2006; Tooley et al., 2006).
Many lactobacilli, some bidobacteria strains and EcN show a
marked anti-mutagenic activity in in vitro systems. The ability of
these probiotics to metabolically inactivate mutagenic substances
might be responsible for this property. In addition, it was shown
that certain probiotics bind N-nitroso compounds and hetero-
cyclic aromatic amines. This can lead to reducing the levels of
carcinogenic compounds and reducing DNA damage (Geier et al.,
2006).
Similarly, binding of certain mycotoxins and cyanobacterial
toxins, which are viewed as tumour promoters or even carcino-
gens, to probiotics correlates with reduced mutagenicity of these
toxins in the presence of appropriate probiotics.
Another way for anti-tumour activity of probiotics is their
ability to amplify the immune response to tumour tissue. This
boosted immune response is achieved by modulation of cytokine
production and T cell function (Hirayama and Rafter, 2000).
Reduction of tumour cell proliferation in vitro and increased
survival rate of mice, injected with tumour cells, was indeed based
on an increased cellular immune response as a result of
administration of the cytoplasmic fraction of L. acidophilus SNUL,
L. casei YIT9092 and B. longum HY8001 (Lee et al., 2004). Another
evidence of anti-carcinogenic property of cell fractions is a study
with peptidoglycan from Lactobacillus species. In this study
peptidoglycan reduced in a dose-dependent manner growth of
CT26 cancer cells originating from the colon of BALB/C mice by
increasing apoptosis (Sun et al., 2005). Lactobacillus reuteri ATCC
PTA 6475 secretes factors that potentiate apoptosis in myeloid
leukemia-derived cells induced by tumour necrosis factor. This
involves inhibition of IkBa ubiquitination and enhancing pro-
apoptotic MAPK signalling (Chandra et al., 2008).
Final remarks
Taken into account the low number of probiotic bacteria
administered with a daily dose of 109 or 1010 bacteria compared to
up to 1014 bacteria in the colon it is to some extent surprising that
there are probiotic effects observable at all. Still this minority is
able to kill pathogens, inhibit probably adhesion and invasion of
pathogens, inactivate toxins and compete for limited resources
successfully. This might be explained by colonization of the same
gut compartment by probiotics and pathogens (e.g. the colon
epithelium), by an amplication like the production of human b-
defensins induced by the EcN agella or the inactivation of
clostridial toxins A and B by a protease secreted by S. boulardii. The
biggest boost might be achieved by the modulation of the
immune system. This can be effective in ghting pathogens and
is important for anti-carcinogenic effects. Furthermore, modula-
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T.A. Oelschlaeger / International Journal of Medical Microbiology 300 (2010) 5762
tion of the immune system might have a long-range effect on the
complete mucosal immune system of the host not just affecting
the mucosal immune system of the gut.
The molecular elucidation of the probiotics actions in vivo will
help to identify true probiotics and select the most suitable ones
for the prevention and/or treatment of a certain illness. Even
though it is still a long way to go to reach this goal, it is worth the
efforts to develop more probiotics into medication (and not just
food additives) to increase our arsenal to ght old and new
diseases.
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