Differential Toll-Like Receptor Recognition and Induction of Cytokine Profile by Bifidobacterium breve and Lactobacillus Strains of Probiotics

ABSTRACTThe use of probiotics as a food supplement has gained tremendous interest in the last few years as beneficial effects were reported in gut homeostasis and nutrient absorption but also in immunocompromised patients, supporting protection from colonization or infection with pathogenic bacteria or fungi. As a treatment approach for inflammatory bowel diseases, a suitable probiotic strain would ideally be one with a low immunogenic potential. Insight into the immunogenicities and types of T-cell responses induced by potentially probiotic strains allows a more rational selection of a particular strain. In the present study, the bacterial strainsBifidobacterium breve(NumRes 204),Lactobacillus rhamnosus(NumRes1), andLactobacillus casei(DN-114 001) were compared concerning their capacity to induce inflammatory responses in terms of cytokine production by human and mouse primary immune cells. It was demonstrated that theB. brevestrain induced lower levels of the proinflammatory cytokine gamma interferon (IFN-γ) than the testedL. rhamnosusandL. caseistrains. BothB. breveand lactobacilli induced cytokines in a Toll-like receptor 9 (TLR9)-dependent manner, while the lower inflammatory profile ofB. brevewas due to inhibitory effects of TLR2. No role for TLR4, NOD2, and C-type lectin receptors was apparent. In conclusion, TLR signaling is involved in the differentiation of inflammatory responses between probiotic strains used as food supplements.

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Ecological Importance of Cross-Feeding of the Intermediate Metabolite 1,2-Propanediol between Bacterial Gut Symbionts

Applied and Environmental Microbiology ◽

10.1128/aem.00190-20 ◽

2020 ◽

Vol 86 (11) ◽

Cited By ~ 3

Author(s):

Christopher C. Cheng ◽

Rebbeca M. Duar ◽

Xiaoxi Lin ◽

Maria Elisa Perez-Munoz ◽

Stephanie Tollenaar ◽

...

Keyword(s):

Trophic Interactions ◽

Lactobacillus Reuteri ◽

Trophic Interaction ◽

Bacterial Strains ◽

Content Type ◽

Bifidobacterium Breve ◽

Gut Symbionts ◽

Gnotobiotic Mice ◽

Ecological Importance ◽

Isogenic Mutants

ABSTRACT Cross-feeding based on the metabolite 1,2-propanediol has been proposed to have an important role in the establishment of trophic interactions among gut symbionts, but its ecological importance has not been empirically established. Here, we show that in vitro growth of Lactobacillus reuteri (syn. Limosilactobacillus reuteri) ATCC PTA 6475 is enhanced through 1,2-propanediol produced by Bifidobacterium breve UCC2003 and Escherichia coli MG1655 from the metabolization of fucose and rhamnose, respectively. Work with isogenic mutants showed that the trophic interaction is dependent on the pduCDE operon in L. reuteri, which encodes the ability to use 1,2-propanediol, and the l-fucose permease (fucP) gene in B. breve, which is required for 1,2-propanediol formation from fucose. Experiments in gnotobiotic mice revealed that, although the pduCDE operon bestows a fitness burden on L. reuteri ATCC PTA 6475 in the mouse digestive tract, the ecological performance of the strain was enhanced in the presence of B. breve UCC2003 and the mucus-degrading species Bifidobacterium bifidum. The use of the respective pduCDE and fucP mutants of L. reuteri and B. breve in the mouse experiments indicated that the trophic interaction was specifically based on 1,2-propanediol. Overall, our work established the ecological importance of cross-feeding relationships based on 1,2-propanediol for the fitness of a bacterial symbiont in the vertebrate gut. IMPORTANCE Through experiments in gnotobiotic mice that employed isogenic mutants of bacterial strains that produce (Bifidobacterium breve) and utilize (Lactobacillus reuteri) 1,2-propanediol, this study provides mechanistic insight into the ecological ramifications of a trophic interaction between gut symbionts. The findings improve our understanding on how cross-feeding influences the competitive fitness of L. reuteri in the vertebrate gut and revealed a putative selective force that shaped the evolution of the species. The findings are relevant since they provide a basis to design rational microbial-based strategies to modulate gut ecosystems, which could employ mixtures of bacterial strains that establish trophic interactions or a personalized approach based on the ability of a resident microbiota to provide resources for the incoming microbe.

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Phosphothreonine Lyase Promotes p65 Degradation in a Mitogen-Activated Protein Kinase/Mitogen- and Stress-Activated Protein Kinase 1-Dependent Manner

Infection and Immunity ◽

10.1128/iai.00508-18 ◽

2018 ◽

Vol 87 (1) ◽

Cited By ~ 1

Author(s):

Mingyu Hou ◽

Wenhui Wang ◽

Feizi Hu ◽

Yuanxing Zhang ◽

Dahai Yang ◽

...

Keyword(s):

Protein Kinase ◽

Pathogenic Bacteria ◽

Critical Role ◽

Nuclear Factor Κb ◽

Mapk Signaling ◽

Mitogen Activated Protein Kinase ◽

Dependent Manner ◽

Content Type ◽

Catalytic Active Site ◽

Mitogen Activated Protein

ABSTRACT Bacterial phosphothreonine lyases have been identified to be type III secretion system (T3SS) effectors that irreversibly dephosphorylate host mitogen-activated protein kinase (MAPK) signaling to promote infection. However, the effects of phosphothreonine lyase on nuclear factor κB (NF-κB) signaling remain largely unknown. In this study, we detected significant phosphothreonine lyase-dependent p65 degradation during Edwardsiella piscicida infection in macrophages, and this degradative effect was blocked by the protease inhibitor MG132. Further analysis revealed that phosphothreonine lyase promotes the dephosphorylation and ubiquitination of p65 by inhibiting the phosphorylation of mitogen- and stress-activated protein kinase-1 (MSK1) and by inhibiting the phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2), p38α, and c-Jun N-terminal kinase (JNK). Moreover, we revealed that the catalytic active site of phosphothreonine lyase plays a critical role in regulating the MAPK-MSK1-p65 signaling axis. Collectively, the mechanism described here expands our understanding of the pathogenic effector in not only regulating MAPK signaling but also regulating p65. These findings uncover a new mechanism by which pathogenic bacteria overcome host innate immunity to promote pathogenesis.

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Toll-Like Receptor Stimulation Induces Nondefensin Protein Expression and Reverses Antibiotic-Induced Gut Defense Impairment

Infection and Immunity ◽

10.1128/iai.01578-14 ◽

2014 ◽

Vol 82 (5) ◽

pp. 1994-2005 ◽

Cited By ~ 15

Author(s):

Ying-Ying Wu ◽

Ching-Mei Hsu ◽

Pei-Hsuan Chen ◽

Chang-Phone Fung ◽

Lee-Wei Chen

Keyword(s):

Dna Binding ◽

Protein Expression ◽

Antibiotic Treatment ◽

Intestinal Mucosa ◽

Pathogenic Bacteria ◽

Binding Activity ◽

Toll Like Receptor ◽

Content Type ◽

Killing Activity ◽

Dna Binding Activity

ABSTRACTPrior antibiotic exposure is associated with increased mortality in Gram-negative bacteria-induced sepsis. However, how antibiotic-mediated changes of commensal bacteria promote the spread of enteric pathogenic bacteria in patients remains unclear. In this study, the effects of systemic antibiotic treatment with or without Toll-like receptor (TLR) stimulation on bacterium-killing activity, antibacterial protein expression in the intestinal mucosa, and bacterial translocation were examined in mice receiving antibiotics with or without oral supplementation of deadEscherichia coliorStaphylococcus aureus. We developed a systemic ampicillin, vancomycin, and metronidazole treatment protocol to simulate the clinical use of antibiotics. Antibiotic treatment decreased the total number of bacteria, including aerobic bacteria belonging to the familyEnterobacteriaceaeand the genusEnterococcusas well as organisms of the anaerobic generaLactococcusandBifidobacteriumin the intestinal mucosa and lumen. Antibiotic treatment significantly decreased the bacterium-killing activity of the intestinal mucosa and the expression of non-defensin-family proteins, such as RegIIIβ, RegIIIγ, C-reactive protein-ductin, and RELMβ, but not the defensin-family proteins, and increasedKlebsiella pneumoniaetranslocation. TLR stimulation after antibiotic treatment increased NF-κB DNA binding activity, nondefensin protein expression, and bacterium-killing activity in the intestinal mucosa and decreasedK. pneumoniaetranslocation. Moreover, germfree mice showed a significant decrease in nondefensin proteins as well as intestinal defense against pathogen translocation. Since TLR stimulation induced NF-κB DNA binding activity, TLR4 expression, and mucosal bacterium-killing activity in germfree mice, we conclude that the commensal microflora is critical in maintaining intestinal nondefensin protein expression and the intestinal barrier. In turn, we suggest that TLR stimulation induces nondefensin protein expression and reverses antibiotic-induced gut defense impairment.

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Dectin-1 Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Trained Macrophages via an Indirect Cell-Autonomous Mechanism

mBio ◽

10.1128/mbio.00781-20 ◽

2020 ◽

Vol 11 (3) ◽

Cited By ~ 1

Author(s):

Cristina Bono ◽

Alba Martínez ◽

Javier Megías ◽

Daniel Gozalbo ◽

Alberto Yáñez ◽

...

Keyword(s):

Bone Marrow ◽

Candida Albicans ◽

Progenitor Cells ◽

Recipient Mouse ◽

Dependent Manner ◽

Toll Like Receptor ◽

Hematopoietic Stem ◽

Content Type ◽

Stem And Progenitor Cells

ABSTRACT Toll-like receptor (TLR) agonists drive hematopoietic stem and progenitor cells (HSPCs) to differentiate along the myeloid lineage. In this study, we used an HSPC transplantation model to investigate the possible direct interaction of β-glucan and its receptor (dectin-1) on HSPCs in vivo. Purified HSPCs from bone marrow of B6Ly5.1 mice (CD45.1 alloantigen) were transplanted into dectin-1−/− mice (CD45.2 alloantigen), which were then injected with β-glucan (depleted zymosan). As recipient mouse cells do not recognize the dectin-1 agonist injected, interference by soluble mediators secreted by recipient cells is negligible. Transplanted HSPCs differentiated into macrophages in response to depleted zymosan in the spleens and bone marrow of recipient mice. Functionally, macrophages derived from HSPCs exposed to depleted zymosan in vivo produced higher levels of inflammatory cytokines (tumor necrosis factor alpha [TNF-α] and interleukin 6 [IL-6]). These results demonstrate that trained immune responses, already described for monocytes and macrophages, also take place in HSPCs. Using a similar in vivo model of HSPC transplantation, we demonstrated that inactivated yeasts of Candida albicans induce differentiation of HSPCs through a dectin-1- and MyD88-dependent pathway. Soluble factors produced following exposure of HSPCs to dectin-1 agonists acted in a paracrine manner to induce myeloid differentiation and to influence the function of macrophages derived from dectin-1-unresponsive or β-glucan-unexposed HSPCs. Finally, we demonstrated that an in vitro transient exposure of HSPCs to live C. albicans cells, prior to differentiation, is sufficient to induce a trained phenotype of the macrophages they produce in a dectin-1- and Toll-like receptor 2 (TLR2)-dependent manner. IMPORTANCE Invasive candidiasis is an increasingly frequent cause of serious and often fatal infections. Understanding host defense is essential to design novel therapeutic strategies to boost immune protection against Candida albicans. In this article, we delve into two new concepts that have arisen over the last years: (i) the delivery of myelopoiesis-inducing signals by microbial components directly sensed by hematopoietic stem and progenitor cells (HSPCs) and (ii) the concept of “trained innate immunity” that may also apply to HSPCs. We demonstrate that dectin-1 ligation in vivo activates HSPCs and induces their differentiation to trained macrophages by a cell-autonomous indirect mechanism. This points to new mechanisms by which pathogen detection by HSPCs may modulate hematopoiesis in real time to generate myeloid cells better prepared to deal with the infection. Manipulation of this process may help to boost the innate immune response during candidiasis.

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SalmonellaFimbrial Protein FimH Is Involved in Expression of Proinflammatory Cytokines in a Toll-Like Receptor 4-Dependent Manner

Infection and Immunity ◽

10.1128/iai.00881-18 ◽

2019 ◽

Vol 87 (3) ◽

Cited By ~ 3

Author(s):

Kei-ichi Uchiya ◽

Yurie Kamimura ◽

Ayumi Jusakon ◽

Toshiaki Nikai

Keyword(s):

Proinflammatory Cytokines ◽

Mitogen Activated Protein Kinase ◽

Hek293 Cells ◽

Dependent Manner ◽

Toll Like Receptor ◽

Toll Like Receptor 4 ◽

Content Type ◽

Type 1 Fimbriae ◽

Serovar Typhimurium

ABSTRACTType 1 fimbriae are proteinaceous filamentous structures present on bacterial surfaces and are mainly composed of the major fimbrial protein subunit FimA and the adhesive protein FimH, which is located at the tip of the fimbrial shaft. Here, we investigated the involvement of type 1 fimbriae in the expression of proinflammatory cytokines in macrophages infected withSalmonella entericaserovar Typhimurium. The level of interleukin-1β (IL-1β) mRNA was lower in macrophages infected withfimAorfimHmutant strains than in those infected with wild-typeSalmonella. Treatment of macrophages with purified recombinant FimH protein, but not FimA, resulted in the activation of the mitogen-activated protein kinase and nuclear factor κB signaling pathways, leading to the expression of not only IL-1β but also other proinflammatory cytokines, such as IL-6 and tumor necrosis factor alpha. However, FimH carrying an N-terminal region deletion or heat-treated FimH did not show such effects. The expression of FimH-induced IL-1β was inhibited by treatment with the Toll-like receptor 4 (TLR4) inhibitor TAK-242 but not by treatment with polymyxin B, a lipopolysaccharide antagonist. Furthermore, FimH treatment stimulated HEK293 cells expressing TLR4 and MD-2/CD14 but did not stimulate HEK293 cells expressing only TLR4. Collectively, FimH is a pathogen-associated molecular pattern ofS. entericaserovar Typhimurium that is recognized by TLR4 in the presence of MD-2 and CD14 and plays a significant role in the expression of proinflammatory cytokines inSalmonella-infected macrophages.

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A Toll-Like Receptor 5 Agonist Improves the Efficacy of Antibiotics in Treatment of Primary and Influenza Virus-Associated Pneumococcal Mouse Infections

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01210-15 ◽

2015 ◽

Vol 59 (10) ◽

pp. 6064-6072 ◽

Cited By ~ 21

Author(s):

Rémi Porte ◽

Delphine Fougeron ◽

Natalia Muñoz-Wolf ◽

Julien Tabareau ◽

Anne-France Georgel ◽

...

Keyword(s):

Influenza Virus ◽

Combination Treatment ◽

Intranasal Administration ◽

Pathogenic Bacteria ◽

Bacterial Load ◽

Pneumococcal Infection ◽

Toll Like Receptor ◽

Content Type ◽

Toll Like Receptor 5 ◽

Stimulation Of

ABSTRACTProphylactic intranasal administration of the Toll-like receptor 5 (TLR5) agonist flagellin protects mice against respiratory pathogenic bacteria. We hypothesized that TLR5-mediated stimulation of lung immunity might improve the therapeutic index of antibiotics for the treatment ofStreptococcus pneumoniaerespiratory infections in mice. Intranasal administration of flagellin was combined with either oral administration of amoxicillin or intraperitoneal injection of trimethoprim-sulfamethoxazole to treatS. pneumoniae-infected animals. Compared with standalone treatments, the combination of antibiotic and flagellin resulted in a lower bacterial load in the lungs and greater protection againstS. pneumoniaedissemination and was associated with an early increase in neutrophil infiltration in the airways. The antibiotic-flagellin combination treatment was, however, not associated with any exacerbation of inflammation. Moreover, combination treatment was more efficacious than standalone antibiotic treatments in the context of post-influenza virus pneumococcal infection. Lastly, TLR5 signaling was shown to be mandatory for the efficacy of the combined antibacterial therapy. This report is the first to show that combining antibiotic treatment with the stimulation of mucosal innate immunity is a potent antibacterial strategy against pneumonia.

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Toll-Like Receptor 4 Agonistic Antibody Promotes Host Defense against Chronic Pseudomonas aeruginosa Lung Infection in Mice

Infection and Immunity ◽

10.1128/iai.01384-15 ◽

2016 ◽

Vol 84 (7) ◽

pp. 1986-1993 ◽

Cited By ~ 8

Author(s):

Shigeki Nakamura ◽

Naoki Iwanaga ◽

Masafumi Seki ◽

Kenji Fukudome ◽

Kazuhiro Oshima ◽

...

Keyword(s):

Immune Response ◽

Pseudomonas Aeruginosa ◽

Neutrophil Recruitment ◽

Dependent Manner ◽

Bacterial Clearance ◽

Toll Like Receptor ◽

Toll Like Receptor 4 ◽

Content Type ◽

Opsonophagocytic Killing

Chronic lower respiratory tract infection withPseudomonas aeruginosais difficult to treat due to enhanced antibiotic resistance and decreased efficacy of drug delivery to destroyed lung tissue. To determine the potential for restorative immunomodulation therapies, we evaluated the effect of Toll-like receptor 4 (TLR4) stimulation on the host immune response toPseudomonasinfection in mice. We implanted sterile plastic tubes precoated withP. aeruginosain the bronchi of mice, administered the TLR4/MD2 agonistic monoclonal antibody UT12 intraperitoneally every week, and subsequently analyzed the numbers of viable bacteria and inflammatory cells and the levels of cytokines. We also performed flow cytometry-based phagocytosis and opsonophagocytic killing assaysin vitrousing UT12-treated murine peritoneal neutrophils. UT12-treated mice showed significantly enhanced bacterial clearance, increased numbers of Ly6G+neutrophils, and increased concentrations of macrophage inflammatory protein 2 (MIP-2) in the lungs (P< 0.05). Depletion of CD4+T cells eliminated the ability of the UT12 treatment to improve bacterial clearance and promote neutrophil recruitment and MIP-2 production. Additionally, UT12-pretreated peritoneal neutrophils exhibited increased opsonophagocytic killing activity via activation of the serine protease pathway, specifically neutrophil elastase activity, in a TLR4-dependent manner. These data indicated that UT12 administration significantly augmented the innate immune response against chronic bacterial infection, in part by promoting neutrophil recruitment and bactericidal function.

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Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner

Infection and Immunity ◽

10.1128/iai.01012-16 ◽

2017 ◽

Vol 85 (4) ◽

Cited By ~ 10

Author(s):

Hua Yao ◽

Hong Zhang ◽

Kai Lan ◽

Hong Wang ◽

Yufeng Su ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Streptococcus Pneumoniae ◽

Host Defense ◽

Defense Response ◽

Dependent Manner ◽

Toll Like Receptor ◽

Content Type ◽

Host Defense Response ◽

Toll Like Receptor 2 ◽

In Cells

ABSTRACT Insights into the host-microbial virulence factor interaction, especially the immune signaling mechanisms, could provide novel prevention and treatment options for pneumococcal diseases. Streptococcus pneumoniae endopeptidase O (PepO) is a newly discovered and ubiquitously expressed pneumococcal virulence protein. A PepO-mutant strain showed impaired adherence to and invasion of host cells compared with the isogenic wild-type strain. It is still unknown whether PepO is involved in the host defense response to pneumococcal infection. Here, we demonstrated that PepO could enhance phagocytosis of Streptococcus pneumoniae and Staphylococcus aureus by peritoneal exudate macrophages (PEMs). Further studies showed that PepO stimulation upregulated the expression of microRNA-155 (miR-155) in PEMs in a time- and dose-dependent manner. PepO-induced enhanced phagocytosis was decreased in cells transfected with an inhibitor of miR-155, while it was increased in cells transfected with a mimic of miR-155. We also revealed that PepO-induced upregulation of miR-155 in PEMs was mediated by Toll-like receptor 2 (TLR2)–NF-κB signaling and that the increased expression of miR-155 downregulated expression of SHIP1. Taken together, these results indicate that PepO induces upregulation of miR-155 in PEMs, contributing to enhanced phagocytosis and host defense response to pneumococci and Staphylococcus aureus.

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Searching Algorithm for Type IV Effector proteins (S4TE) 2.0: improved tools for type IV effector prediction, analysis and comparison

10.1101/301150 ◽

2018 ◽

Author(s):

Christophe Noroy ◽

Thierry Lefrançois ◽

Damien F. Meyer

Keyword(s):

Pathogenic Bacteria ◽

Wide Spectrum ◽

Bacterial Genome ◽

Effector Proteins ◽

Venn Diagram ◽

Dependent Manner ◽

Bacterial Strains ◽

Cellular Processes ◽

Type Iv ◽

User Friendly

ABSTRACTBacterial pathogens have evolved numerous strategies to corrupt, hijack or mimic cellular processes in order to survive and proliferate. Among those strategies, Type IV effectors (T4Es) are proteins secreted by pathogenic bacteria to manipulate host cell processes during infection. They are delivered into eukaryotic cells in an ATP-dependent manner via the type IV secretion system, a specialized multiprotein complex. T4Es contain a wide spectrum of features including eukaryotic-like domains, localization signals or a C-terminal translocation signal. A combination of these features enables prediction of T4Es in a given bacterial genome. In this study, we developed a web-based comprehensive suite of tools with a user-friendly graphical interface. This version 2.0 of S4TE (Searching Algorithm for Type IV Effector Proteins; http://sate.cirad.fr) enables accurate prediction and comparison of T4Es. Search parameters and threshold can be customized by the user to work with any genome sequence, whether publicly available or not. Applications range from characterizing effector features and identifying potential T4Es to analyzing the effectors based on the genome G+C composition and local gene density. S4TE 2.0 allows the comparison of putative T4E repertoires of up to four bacterial strains at the same time. The software identifies T4E orthologs among strains and provides a Venn diagram and lists of genes for each intersection. New interactive features offer the best visualization of the location of candidate T4Es and hyperlinks to NCBI and Pfam databases. S4TE 2.0 is designed to evolve rapidly with the publication of new experimentally validated T4Es, which will reinforce the predictive power of the algorithm. The computational methodology can be used to identify a wide spectrum of candidate bacterial effectors that lack sequence conservation but have similar amino acid characteristics. This approach will provide very valuable information about bacterial host-specificity and virulence factors, and help identify host targets for the development of new anti-bacterial molecules.

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In-vitro pathogen inhibition: Comparing the inhibitory effects of a complex multistrain synbiotic with simple probiotics containing the yeast Saccharomyces boulardii or Lactobacillus rhamnosus bacteria

10.1101/543819 ◽

2019 ◽

Author(s):

Jacek Piatek ◽

Henning Sommermeyer ◽

Arleta Ciechelska-Rybarczyk ◽

Malgorzata Bernatek

Keyword(s):

Bacterial Infections ◽

Pathogenic Bacteria ◽

Lactobacillus Rhamnosus ◽

Saccharomyces Boulardii ◽

Human Pathogens ◽

Inhibitory Effects ◽

Probiotic Strains ◽

Pathogen Inhibition ◽

Different Strains

AbstractSupplementation with probiotics is considered as alternative treatment or adjuvant therapy for a number of bacterial infections for which the use of antibiotics is either not recommended or emerging antibiotic resistance is a major concern. Inhibition of the growth of pathogenic bacteria has been related to a number of different activities of probiotic bacteria or yeasts, some of which are very specific for particular strains of probiotics. As the different inhibition activities might act additively or even synergistically, probiotic multistrain products are discussed as potentially being more effective in pathogen inhibition than products containing one or a small number of probiotic strains. The present study investigated the in vitro inhibition of Escherichia (E.) coli, Shigella spp., Salmonella (S.) typhimurium and Clostridum (Cl.) difficile, all being human pathogens of significant worldwide healthcare concerns. The probiotic containing the yeast Sacharomyces (S.) boulardii inhibited all four pathogens. Similar inhibitions were observed with a bacterial probiotic containing three different strains (Pen, E/N and Oxy) of Lactobacillus (Lc.) rhamnosus. Compared to the inhibition found for these probiotics, the inhibitory effects of a complex multistrain synbiotic, containing nine different probiotic strains (6 Lactobacilli and 3 Bifidobacteria) and the prebiotic fructooligosaccharide (FOS), were significantly stronger. The stronger inhibition by the complex multistrain synbiotic was observed for all four tested pathogens. Our findings support a hypothesis that complex synbiotic products containing a larger number of different strains combined with a prebiotic component might be more attractive candidates for further clinical characterization than simpler probiotics containing one or only few probiotic strains.

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