scholarly journals Lactobacillus reuteri Protects Epidermal Keratinocytes from Staphylococcus aureus-Induced Cell Death by Competitive Exclusion

2012 ◽  
Vol 78 (15) ◽  
pp. 5119-5126 ◽  
Author(s):  
Tessa Prince ◽  
Andrew J. McBain ◽  
Catherine A. O'Neill
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Protective Effect ◽  
Competitive Exclusion ◽  
Lactobacillus Reuteri ◽  
Lactobacillus Rhamnosus ◽  
Probiotic Bacteria ◽  
Epidermal Keratinocytes ◽  
Protective Mechanism ◽  
Content Type

ABSTRACTRecent studies have suggested that the topical application of probiotic bacteria can improve skin health or combat disease. We have utilized a primary human keratinocyte culture model to investigate whether probiotic bacteria can inhibitStaphylococcus aureusinfection. Evaluation of the candidate probioticsLactobacillus reuteriATCC 55730,Lactobacillus rhamnosusAC413, andLactobacillus salivariusUCC118 demonstrated that bothL. reuteriandL. rhamnosus, but notL. salivarius, reducedS. aureus-induced keratinocyte cell death in both undifferentiated and differentiated keratinocytes. Keratinocyte survival was significantly higher if the probiotic was applied prior to (P< 0.01) or simultaneously with (P< 0.01) infection withS. aureusbut not when added after infection had commenced (P> 0.05). The protective effect ofL. reuteriwas not dependent on the elaboration of inhibitory substances such as lactic acid.L. reuteriinhibited adherence ofS. aureusto keratinocytes by competitive exclusion (P= 0.026).L. salivariusUCC118, however, did not inhibitS. aureusfrom adhering to keratinocytes (P> 0.05) and did not protect keratinocyte viability.S. aureusutilizes the α5β1 integrin to adhere to keratinocytes, and blocking of this integrin resulted in a protective effect similar to that observed with probiotics (P= 0.03). This suggests that the protective mechanism forL. reuteri-mediated protection of keratinocytes was by competitive exclusion of the pathogen from its binding sites on the cells. Our results suggest that use of a topical probiotic prophylactically could inhibit the colonization of skin byS. aureusand thus aid in the prevention of infection.

scholarly journals Lactobacillus rhamnosus GG Inhibits the Toxic Effects of Staphylococcus aureus on Epidermal Keratinocytes

2014 ◽  
Vol 80 (18) ◽  
pp. 5773-5781 ◽  
Author(s):  
Walaa Mohammedsaeed ◽  
Andrew J. McBain ◽  
Sheena M. Cruickshank ◽  
Catherine A. O'Neill
Keyword(s):  
Staphylococcus Aureus ◽  
Lactobacillus Rhamnosus ◽  
Culture Fluid ◽  
Human Keratinocytes ◽  
Probiotic Bacterium ◽  
Epidermal Keratinocytes ◽  
Protective Effects ◽  
Primary Human Keratinocytes ◽  
Content Type ◽  
Viable Bacteria

ABSTRACTFew studies have evaluated the potential benefits of the topical application of probiotic bacteria or material derived from them. We have investigated whether a probiotic bacterium,Lactobacillus rhamnosusGG, can inhibitStaphylococcus aureusinfection of human primary keratinocytes in culture. When primary human keratinocytes were exposed toS. aureus, only 25% of the keratinocytes remained viable following 24 h of incubation. However, in the presence of 108CFU/ml of liveL. rhamnosusGG, the viability of the infected keratinocytes increased to 57% (P= 0.01).L. rhamnosusGG lysates and spent culture fluid also provided significant protection to keratinocytes, with 65% (P= 0.006) and 57% (P= 0.01) of cells, respectively, being viable following 24 h of incubation. Keratinocyte survival was significantly enhanced regardless of whether the probiotic was applied in the viable form or as cell lysates 2 h before or simultaneously with (P= 0.005) or 12 h after (P= 0.01)S. aureusinfection. However, spent culture fluid was protective only if added before or simultaneously withS. aureus. With respect to mechanism, bothL. rhamnosusGG lysate and spent culture fluid apparently inhibited adherence ofS. aureusto keratinocytes by competitive exclusion, but only viable bacteria or the lysate could displaceS. aureus(P= 0.04 and 0.01, respectively). Furthermore, growth ofS. aureuswas inhibited by either live bacteria or lysate but not spent culture fluid. Together, these data suggest at least two separate activities involved in the protective effects ofL. rhamnosusGG againstS. aureus, growth inhibition and reduction of bacterial adhesion.

scholarly journals Complete Genome Sequence of Lactobacillus reuteri Byun-re-01, Isolated from Mouse Small Intestine

2018 ◽  
Vol 7 (17) ◽  
Author(s):  
Dongjun Kim ◽  
Mun-ju Cho ◽  
Seungchan Cho ◽  
Yongjun Lee ◽  
Sung June Byun ◽  
...  
Keyword(s):  
Small Intestine ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Complete Genome ◽  
Lactobacillus Reuteri ◽  
Probiotic Bacteria ◽  
Content Type ◽  
Mouse Small Intestine

Lactic acid bacteria (LAB) are generally recognized as safe (GRAS) and serve as probiotic bacteria when consumed in adequate amounts. Here, we report the complete genome sequence of Lactobacillus reuteri Byun-re-01, isolated from mouse small intestine.

scholarly journals Intracellular Staphylococcus aureus Perturbs the Host Cell Ca2+ Homeostasis To Promote Cell Death

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. e02250-20
Author(s):  
Kathrin Stelzner ◽  
Ann-Cathrin Winkler ◽  
Chunguang Liang ◽  
Aziza Boyny ◽  
Carsten P. Ade ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Host Cell ◽  
Intracellular Bacterium ◽  
Tissue Destruction ◽  
Content Type ◽  
Host Cell Death ◽  
Genome Wide ◽  
A Genome ◽  
Spread Of Infection

ABSTRACTThe opportunistic human pathogen Staphylococcus aureus causes serious infectious diseases that range from superficial skin and soft tissue infections to necrotizing pneumonia and sepsis. While classically regarded as an extracellular pathogen, S. aureus is able to invade and survive within human cells. Host cell exit is associated with cell death, tissue destruction, and the spread of infection. The exact molecular mechanism employed by S. aureus to escape the host cell is still unclear. In this study, we performed a genome-wide small hairpin RNA (shRNA) screen and identified the calcium signaling pathway as being involved in intracellular infection. S. aureus induced a massive cytosolic Ca2+ increase in epithelial host cells after invasion and intracellular replication of the pathogen. This was paralleled by a decrease in endoplasmic reticulum Ca2+ concentration. Additionally, calcium ions from the extracellular space contributed to the cytosolic Ca2+ increase. As a consequence, we observed that the cytoplasmic Ca2+ rise led to an increase in mitochondrial Ca2+ concentration, the activation of calpains and caspases, and eventually to cell lysis of S. aureus-infected cells. Our study therefore suggests that intracellular S. aureus disturbs the host cell Ca2+ homeostasis and induces cytoplasmic Ca2+ overload, which results in both apoptotic and necrotic cell death in parallel or succession.IMPORTANCE Despite being regarded as an extracellular bacterium, the pathogen Staphylococcus aureus can invade and survive within human cells. The intracellular niche is considered a hideout from the host immune system and antibiotic treatment and allows bacterial proliferation. Subsequently, the intracellular bacterium induces host cell death, which may facilitate the spread of infection and tissue destruction. So far, host cell factors exploited by intracellular S. aureus to promote cell death are only poorly characterized. We performed a genome-wide screen and found the calcium signaling pathway to play a role in S. aureus invasion and cytotoxicity. The intracellular bacterium induces a cytoplasmic and mitochondrial Ca2+ overload, which results in host cell death. Thus, this study first showed how an intracellular bacterium perturbs the host cell Ca2+ homeostasis.

scholarly journals Probiotic Bifunctionality of Bacillus subtilis—Rescuing Lactic Acid Bacteria from Desiccation and Antagonizing Pathogenic Staphylococcus aureus

2019 ◽  
Vol 7 (10) ◽  
pp. 407 ◽  
Author(s):  
Hadar Kimelman ◽  
Moshe Shemesh
Keyword(s):  
Staphylococcus Aureus ◽  
Bacillus Subtilis ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Pathogenic Bacteria ◽  
Lactobacillus Rhamnosus ◽  
Probiotic Bacterium ◽  
Probiotic Bacteria ◽  
Mammalian Host ◽  
Beneficial Effects

Live probiotic bacteria obtained with food are thought to have beneficial effects on a mammalian host, including their ability to reduce intestinal colonization by pathogens. To ensure the beneficial effects, the probiotic cells must survive processing and storage of food, its passage through the upper gastrointestinal tract (GIT), and subsequent chemical ingestion processes until they reach their target organ. However, there is considerable loss of viability of the probiotic bacteria during the drying process, in the acidic conditions of the stomach, and in the high bile concentration in the small intestine. Bacillus subtilis, a spore-forming probiotic bacterium, can effectively maintain a favorable balance of microflora in the GIT. B. subtilis produces a protective extracellular matrix (ECM), which is shared with other probiotic bacteria; thus, it was suggested that this ECM could potentially protect an entire community of probiotic cells against unfavorable environmental conditions. Consequently, a biofilm-based bio-coating system was developed that would enable a mutual growth of B. subtilis with different lactic acid bacteria (LAB) through increasing the ECM production. Results of the study demonstrate a significant increase in the survivability of the bio-coated LAB cells during the desiccation process and passage through the acidic environment. Thus, it provides evidence about the ability of B. subtilis in rescuing the desiccation-sensitive LAB, for instance, Lactobacillus rhamnosus, from complete eradication. Furthermore, this study demonstrates the antagonistic potential of the mutual probiotic system against pathogenic bacteria such as Staphylococcus aureus. The data show that the cells of B. subtilis possess robust anti-biofilm activity against S. aureus through activating the antimicrobial lipopeptide production pathway.

scholarly journals Interleukin-10 (IL-10) Produced by Mutant Toxic Shock Syndrome Toxin 1 Vaccine-Induced Memory T Cells Downregulates IL-17 Production and Abrogates the Protective Effect against Staphylococcus aureus Infection

2019 ◽  
Vol 87 (10) ◽  
Author(s):  
Kouji Narita ◽  
Dong-Liang Hu ◽  
Krisana Asano ◽  
Akio Nakane
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Infectious Diseases ◽  
Protective Effect ◽  
Toxic Shock Syndrome ◽  
Long Term Memory ◽  
Toxic Shock ◽  
Content Type ◽  
Memory Phase ◽  
Toxic Shock Syndrome Toxin

ABSTRACT Development of long-term memory is crucial for vaccine-induced adaptive immunity against infectious diseases such as Staphylococcus aureus infection. Toxic shock syndrome toxin 1 (TSST-1), one of the superantigens produced by S. aureus, is a possible vaccine candidate against infectious diseases caused by this pathogen. We previously reported that vaccination with less toxic mutant TSST-1 (mTSST-1) induced T helper 17 (Th17) cells and elicited interleukin-17A (IL-17A)-mediated protection against S. aureus infection 1 week after vaccination. In the present study, we investigated the host immune response induced by mTSST-1 vaccination in the memory phase, 12 weeks after the final vaccination. The protective effect and IL-17A production after vaccination with mTSST-1 were eliminated because of IL-10 production. In the presence of IL-10-neutralizing monoclonal antibody (mAb), IL-17A production was restored in culture supernatants of CD4+ T cells and macrophages sorted from the spleens of vaccinated mice. Vaccinated mice treated with anti-IL-10 mAb were protected against systemic S. aureus infection in the memory phase. From these results, it was suggested that IL-10 produced in the memory phase suppresses the IL-17A-dependent vaccine effect through downregulation of IL-17A production.

scholarly journals Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

2015 ◽  
Vol 83 (6) ◽  
pp. 2531-2541 ◽  
Author(s):  
Abdul G. Lone ◽  
Erhan Atci ◽  
Ryan Renslow ◽  
Haluk Beyenal ◽  
Susan Noh ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Effective Diffusion ◽  
Oxygen Demand ◽  
Shotgun Proteomics ◽  
Cellular Damage ◽  
Label Free ◽  
Content Type ◽  
Dermal Tissue ◽  
The Difference

We developed a porcine dermal explant model to determine the extent to whichStaphylococcus aureusbiofilm communities deplete oxygen, change pH, and produce damage in underlying tissue. Microelectrode measurements demonstrated that dissolved oxygen (DO) in biofilm-free dermal tissue was 4.45 ± 1.17 mg/liter, while DO levels for biofilm-infected tissue declined sharply from the surface, with no measurable oxygen detectable in the underlying dermal tissue. Magnetic resonance imaging demonstrated that biofilm-free dermal tissue had a significantly lower relative effective diffusion coefficient (0.26 ± 0.09 to 0.30 ± 0.12) than biofilm-infected dermal tissue (0.40 ± 0.12 to 0.48 ± 0.12;P< 0.0001). Thus, the difference in DO level was attributable to biofilm-induced oxygen demand rather than changes in oxygen diffusivity. Microelectrode measures showed that pH within biofilm-infected explants was more alkaline than in biofilm-free explants (8.0 ± 0.17 versus 7.5 ± 0.15, respectively;P< 0.002). Cellular and nuclear details were lost in the infected explants, consistent with cell death. Quantitative label-free shotgun proteomics demonstrated that both proapoptotic programmed cell death protein 5 and antiapoptotic macrophage migration inhibitory factor accumulated in the infected-explant spent medium, compared with uninfected-explant spent media (1,351-fold and 58-fold, respectively), consistent with the cooccurrence of apoptosis and necrosis in the explants. Biofilm-origin proteins reflected an extracellular matrix-adapted lifestyle ofS. aureus. S. aureusbiofilms deplete oxygen, increase pH, and induce cell death, all factors that contribute to impede wound healing.

scholarly journals SrrAB Modulates Staphylococcus aureus Cell Death through Regulation ofcidABCTranscription

2016 ◽  
Vol 198 (7) ◽  
pp. 1114-1122 ◽  
Author(s):  
Ian H. Windham ◽  
Sujata S. Chaudhari ◽  
Jeffrey L. Bose ◽  
Vinai C. Thomas ◽  
Kenneth W. Bayles
Keyword(s):  
Reactive Oxygen Species ◽  
Staphylococcus Aureus ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Extracellular Dna ◽  
Death Process ◽  
Oxygen Species ◽  
Content Type ◽  
Biofilm Development

ABSTRACTThe death and lysis of a subpopulation inStaphylococcus aureusbiofilm cells are thought to benefit the surviving population by releasing extracellular DNA, a critical component of the biofilm extracellular matrix. Although the means by whichS. aureuscontrols cell death and lysis is not understood, studies implicate the role of thecidABCandlrgABoperons in this process. Recently, disruption of thesrrABregulatory locus was found to cause increased cell death during biofilm development, likely as a result of the sensitivity of this mutant to hypoxic growth. In the current study, we extended these findings by demonstrating that cell death in the ΔsrrABmutant is dependent on expression of thecidABCoperon. The effect ofcidABCexpression resulted in the generation of increased reactive oxygen species (ROS) accumulation and was independent of acetate production. Interestingly, consistently with previous studies,cidC-encoded pyruvate oxidase was found to be important for the generation of acetic acid, which initiates the cell death process. However, these studies also revealed for the first time an important role of thecidBgene in cell death, as disruption ofcidBin the ΔsrrABmutant background decreased ROS generation and cell death in acidC-independent manner. ThecidBmutation also caused decreased sensitivity to hydrogen peroxide, which suggests a complex role for this system in ROS metabolism. Overall, the results of this study provide further insight into the function of thecidABCoperon in cell death and reveal its contribution to the oxidative stress response.IMPORTANCEThe manuscript focuses on cell death mechanisms inStaphylococcus aureusand provides important new insights into the genes involved in this ill-defined process. By exploring the cause of increased stationary-phase death in anS. aureusΔsrrABregulatory mutant, we found that the decreased viability of this mutant was a consequence of the overexpression of thecidABCoperon, previously shown to be a key mediator of cell death. These investigations highlight the role of thecidBgene in the death process and the accumulation of reactive oxygen species. Overall, the results of this study are the first to demonstrate a positive role for CidB in cell death and to provide an important paradigm for understanding this process in all bacteria.

scholarly journals Study on the Mechanism of Lactobacillus Rhamnosus Probio-M9 Combined With Antibiotics on Staphylococcus Aureus Mastitis in Rat

2021 ◽  
Author(s):  
Xu Rui Bo ◽  
Heping Zhang
Keyword(s):  
Staphylococcus Aureus ◽  
Lactobacillus Reuteri ◽  
Lactobacillus Rhamnosus ◽  
Intestinal Bacteria ◽  
Probiotic Strain ◽  
Protective Role ◽  
The Body ◽  
Metagenomic Sequencing ◽  
Illumina Hiseq ◽  
New Research

Abstract This study aims to investigate the potential anti-inflammatory mechanism of Lactobacillus rhamnosus Probio-M9 (Probio-M9) combined with antibiotics. Probio-M9, a probiotic strain previously isolated from the milk of healthy women. The Illumina Hiseq platform performs metagenomic sequencing on faeces samples at various time points; UPLC-Q-TOF/MS is used to detect a large number of endogenous metabolites in the serum of rats with mastitis induced by Staphylococcus aureus. The results show that the Probio-M9 combined with antibiotics increases beneficial intestinal bacteria (Lactobacillus murinus, Lactobacillus reuteri) and positively regulates metabolites (linoleic acid, glycerophospholipids, arachidonic acid, Sphingolipids. etc.), reduce inflammation in the body to play a protective role against mastitis. This research provides a new research method to relieve mastitis, and also provides a theoretical basis for the development and utilization of Probio-M9.

scholarly journals Protective effect of probiotic bacteria against cadmium-induced genotoxicity in rat hepatocytes in vivo and in vitro

2012 ◽  
Vol 64 (3) ◽  
pp. 1197-1206 ◽  
Author(s):  
Adel Jama ◽  
Dragana Mitic-Culafic ◽  
S. Kolarevic ◽  
Sinisa Djurasevic ◽  
Jelena Knezevic-Vukcevic
Keyword(s):  
Protective Effect ◽  
Rattus Norvegicus ◽  
Single Cells ◽  
Lactobacillus Rhamnosus ◽  
Rat Hepatocytes ◽  
Probiotic Bacteria ◽  
Protection Mechanism ◽  
Male Wistar Rats

The protective effect of probiotic bacteria against cadmium (Cd)-induced genotoxicity was studied in rat hepatocytes in vivo and in vitro. Male Wistar rats, Rattus norvegicus, were treated for five weeks with (i) CdCl2 (70 ppm in the drinking water), (ii) a mixture of lyophilized probiotic bacteria Lactobacillus rhamnosus, L. acidophilus and Bifido-bacterium longum (5?108 cfu/g of food), or (iii) CdCl2 and probiotic bacteria. In addition, single cells obtained from the untreated rat liver were exposed to CdCl2 (70 ppm), probiotic bacteria (1.28 mg/ml), or CdCl2 and probiotic bacteria, for 15 min at 22?C in the dark. The level of Cd-induced DNA damage in hepatocytes was determined by the comet assay. The obtained results show that probiotic bacteria significantly reduced Cd-induced genotoxicity, both in vivo and in vitro (20% and 48%, respectively). Moreover, the toxicity of Cd to lactobacilli in the gastrointestinal tracts of rats was significantly decreased in the probiotic-treated animals. The binding of Cd2+ to probiotic bacteria was proposed as the most probable protection mechanism.

scholarly journals Functional Dynamics of the Gut Microbiome in Elderly People during Probiotic Consumption

mBio ◽  
2015 ◽  
Vol 6 (2) ◽  
Author(s):  
Emiley A. Eloe-Fadrosh ◽  
Arthur Brady ◽  
Jonathan Crabtree ◽  
Elliott F. Drabek ◽  
Bing Ma ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lactobacillus Rhamnosus ◽  
Probiotic Bacteria ◽  
Healthy Human ◽  
Content Type ◽  
Treatment Comparison ◽  
Functional Dynamics ◽  
Single Organism ◽  
Probiotic Treatment ◽  
The Impact

ABSTRACT A mechanistic understanding of the purported health benefits conferred by consumption of probiotic bacteria has been limited by our knowledge of the resident gut microbiota and its interaction with the host. Here, we detail the impact of a single-organism probiotic, Lactobacillus rhamnosus GG ATCC 53103 (LGG), on the structure and functional dynamics (gene expression) of the gut microbiota in a study of 12 healthy individuals, 65 to 80 years old. The analysis revealed that while the overall community composition was stable as assessed by 16S rRNA profiling, the transcriptional response of the gut microbiota was modulated by probiotic treatment. Comparison of transcriptional profiles based on taxonomic composition yielded three distinct transcriptome groups that displayed considerable differences in functional dynamics. The transcriptional profile of LGG in vivo was remarkably concordant across study subjects despite the considerable interindividual nature of the gut microbiota. However, we identified genes involved in flagellar motility, chemotaxis, and adhesion from Bifidobacterium and the dominant butyrate producers Roseburia and Eubacterium whose expression was increased during probiotic consumption, suggesting that LGG may promote interactions between key constituents of the microbiota and the host epithelium. These results provide evidence for the discrete functional effects imparted by a specific single-organism probiotic and challenge the prevailing notion that probiotics substantially modify the resident microbiota within nondiseased individuals in an appreciable fashion. IMPORTANCE Probiotic bacteria have been used for over a century to promote digestive health. Many individuals report that probiotics alleviate a number of digestive issues, yet little evidence links how probiotic microbes influence human health. Here, we show how the resident microbes that inhabit the healthy human gut respond to a probiotic. The well-studied probiotic Lactobacillus rhamnosus GG ATCC 53103 (LGG) was administered in a clinical trial, and a suite of measurements of the resident microbes were taken to evaluate potential changes over the course of probiotic consumption. We found that LGG transiently enriches for functions to potentially promote anti-inflammatory pathways in the resident microbes.

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