scholarly journals Fibrinogen-InducedStreptococcus mutansBiofilm Formation and Adherence to Endothelial Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Telma Blanca Lombardo Bedran ◽  
Jabrane Azelmat ◽  
Denise Palomari Spolidorio ◽  
Daniel Grenier

Streptococcus mutans, the predominant bacterial species associated with dental caries, can enter the bloodstream and cause infective endocarditis. The aim of this study was to investigateS. mutansbiofilm formation and adherence to endothelial cells induced by human fibrinogen. The putative mechanism by which biofilm formation is induced as well as the impact of fibrinogen onS. mutansresistance to penicillin was also evaluated. Bovine plasma dose dependently induced biofilm formation byS. mutans. Of the various plasma proteins tested, only fibrinogen promoted the formation of biofilm in a dose-dependent manner. Scanning electron microscopy observations revealed the presence of complex aggregates of bacterial cells firmly attached to the polystyrene support.S. mutansin biofilms induced by the presence of fibrinogen was markedly resistant to the bactericidal effect of penicillin. Fibrinogen also significantly increased the adherence ofS. mutansto endothelial cells. NeitherS. mutanscells nor culture supernatants converted fibrinogen into fibrin. However, fibrinogen is specifically bound to the cell surface ofS. mutansand may act as a bridging molecule to mediate biofilm formation. In conclusion, our study identified a new mechanism promotingS. mutansbiofilm formation and adherence to endothelial cells which may contribute to infective endocarditis.

2020 ◽  
Vol 17 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Pavan K. Mujawdiya ◽  
Suman Kapur

: Quorum Sensing (QS) is a phenomenon in which bacterial cells communicate with each other with the help of several low molecular weight compounds. QS is largely dependent on population density, and it triggers when the concentration of quorum sensing molecules accumulate in the environment and crosses a particular threshold. Once a certain population density is achieved and the concentration of molecules crosses a threshold, the bacterial cells show a collective behavior in response to various chemical stimuli referred to as “auto-inducers”. The QS signaling is crucial for several phenotypic characteristics responsible for bacterial survival such as motility, virulence, and biofilm formation. Biofilm formation is also responsible for making bacterial cells resistant to antibiotics. : The human gut is home to trillions of bacterial cells collectively called “gut microbiota” or “gut microbes”. Gut microbes are a consortium of more than 15,000 bacterial species and play a very crucial role in several body functions such as metabolism, development and maturation of the immune system, and the synthesis of several essential vitamins. Due to its critical role in shaping human survival and its modulating impact on body metabolisms, the gut microbial community has been referred to as “the forgotten organ” by O`Hara et al. (2006) [1]. Several studies have demonstrated that chemical interaction between the members of bacterial cells in the gut is responsible for shaping the overall microbial community. : Recent advances in phytochemical research have generated a lot of interest in finding new, effective, and safer alternatives to modern chemical-based medicines. In the context of antimicrobial research various plant extracts have been identified with Quorum Sensing Inhibitory (QSI) activities among bacterial cells. This review focuses on the mechanism of quorum sensing and quorum sensing inhibitors isolated from natural sources.


2021 ◽  
Vol 9 (5) ◽  
pp. 1037
Author(s):  
Craig Resch ◽  
Mihir Parikh ◽  
J. Alejandro Austria ◽  
Spencer D. Proctor ◽  
Thomas Netticadan ◽  
...  

There is an increased interest in the gut microbiota as it relates to health and obesity. The impact of diet and sex on the gut microbiota in conjunction with obesity also demands extensive systemic investigation. Thus, the influence of sex, diet, and flaxseed supplementation on the gut microbiota was examined in the JCR:LA-cp rat model of genetic obesity. Male and female obese rats were randomized into four groups (n = 8) to receive, for 12 weeks, either (a) control diet (Con), (b) control diet supplemented with 10% ground flaxseed (CFlax), (c) a high-fat, high sucrose (HFHS) diet, or (d) HFHS supplemented with 10% ground flaxseed (HFlax). Male and female JCR:LA-cp lean rats served as genetic controls and received similar dietary interventions. Illumine MiSeq sequencing revealed a richer microbiota in rats fed control diets rather than HFHS diets. Obese female rats had lower alpha-diversity than lean female; however, both sexes of obese and lean JCR rats differed significantly in β-diversity, as their gut microbiota was composed of different abundances of bacterial types. The feeding of an HFHS diet affected the diversity by increasing the phylum Bacteroidetes and reducing bacterial species from phylum Firmicutes. Fecal short-chain fatty acids such as acetate, propionate, and butyrate-producing bacterial species were correspondingly impacted by the HFHS diet. Flax supplementation improved the gut microbiota by decreasing the abundance of Blautia and Eubacterium dolichum. Collectively, our data show that an HFHS diet results in gut microbiota dysbiosis in a sex-dependent manner. Flaxseed supplementation to the diet had a significant impact on gut microbiota diversity under both flax control and HFHS dietary conditions.


2021 ◽  
Vol 12 ◽  
Author(s):  
Florencia Ferrara ◽  
Analía Rial ◽  
Norma Suárez ◽  
José Alejandro Chabalgoity

Polyvalent bacterial lysates have been in use for decades for prevention and treatment of respiratory infections with reported clinical benefits. However, besides claims of broad immune activation, the mode of action is still a matter of debate. The lysates, formulated with the main bacterial species involved in respiratory infections, are commonly prepared by chemical or mechanical disruption of bacterial cells, what is believed influences the biological activity of the product. Here, we prepared two polyvalent lysates with the same composition but different method of bacterial cell disruption and evaluated their biological activity in a comparative fashion. We found that both bacterial lysates induce NF-kB activation in a MyD88 dependent manner, suggesting they work as TLR agonists. Further, we found that a single intranasal dose of any of the two lysates, is sufficient to protect against pneumococcal pneumonia, suggesting that they exert similar biological activity. We have previously shown that protection against pneumococcal pneumonia can also be induced by prior S. pneumoniae sub lethal infection or therapeutic treatment with a TLR5 agonist. Protection in those cases depends on neutrophil recruitment to the lungs, and can be associated with increased local expression of IL-17A. Here, we show that bacterial lysates exert protection against pneumococcal pneumonia independently of neutrophils, IL-17A or Caspase-1/11 activation, suggesting the existence of redundant mechanisms of protection. Trypsin-treated lysates afford protection to the same extent, suggesting that just small peptides suffice to exert the protective effect or that the molecules responsible for the protective effect are not proteins. Understanding the mechanism of action of bacterial lysates and deciphering the active components shall allow redesigning them with more precisely defined formulations and expanding their range of action.


Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 767
Author(s):  
Assmaa Anter ◽  
Mohamed Abd El-Ghany ◽  
Marwa Abou El Dahab ◽  
Noha Mahana

There is strong correlation between changes in abundance of specific bacterial species and several diseases including schistosomiasis. Several studies have described therapeutic effects of curcumin (CUR) which may arise from its regulative effects on intestinal microbiota. Thus, we examined the impact of CUR on the diversity of intestinal microbiota with/without infection by Schistosoma mansoni cercariae for 56 days. Enterobacteriaceae was dominating in a naive and S. mansoni infected mice group without CUR treatment, the most predominant species was Escherichia coli with relative density (R.D%) = 80.66% and the least one was Pseudomonas sp. (0.52%). The influence of CUR on murine microbiota composition was examined one week after oral administration of high (40) and low (20 mg/kg b.w.) CUR doses were administered three times, with two day intervals. CUR induced high variation in the Enterobacteriaceae family, characterized by a significant (p < 0.001) reduction in E. coli and asignificant (p < 0.001) increase in Pseudomonas sp. in both naïve and S. mansoni-infected mice, compared to untreated mice, in a dose-dependent manner. Additionally, our study showed the effects of high CUR doses on S. mansoni infection immunological and parasitological parameters. These data support CUR’s ability to promote Pseudomonas sp. known to produce schistosomicidal toxins and offset the sequelae of murine schistosomiasis.


2015 ◽  
Vol 60 (2) ◽  
pp. 818-826 ◽  
Author(s):  
Eun-Young Jang ◽  
Minjung Kim ◽  
Mi Hee Noh ◽  
Ji-Hoi Moon ◽  
Jin-Yong Lee

ABSTRACTPolyphosphate (polyP) has gained a wide interest in the food industry due to its potential as a decontaminating agent. In this study, we examined the effect of sodium tripolyphosphate (polyP3; Na5P3O10) against planktonic and biofilm cells ofPrevotella intermedia, a major oral pathogen. The MIC of polyP3 againstP. intermediaATCC 49046 determined by agar dilution method was 0.075%, while 0.05% polyP3 was bactericidal againstP. intermediain time-kill analysis performed using liquid medium. A crystal violet binding assay for the assessment of biofilm formation byP. intermediashowed that sub-MICs of polyP3 significantly decreased biofilm formation. Under the scanning electron microscope, decreased numbers ofP. intermediacells forming the biofilms were observed when the bacterial cells were incubated with 0.025% or higher concentrations of polyP3. Assessment of biofilm viability with LIVE/DEAD staining and viable cell count methods showed that 0.05% or higher concentrations of polyP3 significantly decreased the viability of the preformed biofilms in a concentration-dependent manner. The zone sizes of alpha-hemolysis formed on horse blood agar produced byP. intermediawere decreased in the presence of polyP3. The expression of the genes encoding hemolysins and the genes of the hemin uptake (hmu) locus was downregulated by polyP3. Collectively, our results show that polyP is an effective antimicrobial agent againstP. intermediain biofilms as well as planktonic phase, interfering with the process of hemin acquisition by the bacterium.


2020 ◽  
Author(s):  
Judith Kikhney ◽  
Laura Kursawe ◽  
Swb Eichinger ◽  
Walter Eichinger ◽  
Julia Schmidt ◽  
...  

&lt;p&gt;&lt;strong&gt;Introduction&lt;/strong&gt;&lt;/p&gt; &lt;p&gt;In Infective Endocarditis (IE), early diagnosis of the causative microorganism is crucial for correct antibiotic therapy, which improves the patients&amp;#8217; outcome.&lt;/p&gt; &lt;p&gt;&lt;strong&gt;Objectives&lt;/strong&gt;&lt;/p&gt; &lt;p&gt;We studies the impact of biofilm formation in IE samples.&lt;/p&gt; &lt;p&gt;&lt;strong&gt;Materials &amp; methods&lt;/strong&gt;&lt;/p&gt; &lt;p&gt;We used Fluorescence in situ Hybridization (FISH) combined with 16S rRNA-gene PCR and sequencing to visualize and identify the infectious agents in native as well as prosthetic valves and to study any biofilm formation. The signal intensity of the fluorescence-labelled FISH probes correlates to a high ribosome content of the bacteria indicating metabolic activity at the time point of surgery. We developed a spacer FISH assay for the detection of the 16S-23S intergenic spacer region that is only present in actively transcribing cells to detect the activity of bacterial cells more precisely on a single cell level.&lt;/p&gt; &lt;p&gt;&lt;strong&gt;Results&lt;/strong&gt;&lt;/p&gt; &lt;p&gt;FISH visualized bacteria in the heart valves ranging from single cells to highly organized biofilms. Interestingly, we found FISH positive bacteria in culture negative samples and samples from patients under antibiotic therapy. Using the spacer FISH, we visualized positive microbial cells in heart valves of patients under adequate therapy. Preliminary data point to a correlation between the biofilm state and treatment inefficiency.&lt;/p&gt; &lt;p&gt;&lt;strong&gt;Conclusion&lt;/strong&gt;&lt;/p&gt; &lt;p&gt;FISH/PCR not only allows timely identification of the pathogens in IE, but also biofilm-staging and visualization of the effect of antimicrobial therapy at time of surgery. The technique provides crucial information for successful targeted antibiotic therapy, and it might guide therapeutical decisions in relation to biofilm state in the future.&lt;/p&gt;


2015 ◽  
Vol 197 (13) ◽  
pp. 2104-2111 ◽  
Author(s):  
Izumi Mashima ◽  
Futoshi Nakazawa

Dental plaque is a multispecies oral biofilm, the development of which is initiated by adherence of the pioneerStreptococcusspp. OralVeillonellaspp., includingV. atypica,V. denticariosi,V. dispar,V. parvula,V. rogosae, andV. tobetsuensis, are known as early colonizers in oral biofilm formation. These species have been reported to coaggregate withStreptococcusspp. in a metabolic cooperation-dependent manner to form biofilms in human oral cavities, especially in the early stages of biofilm formation. However, in our previous study,Streptococcus gordoniishowed biofilm formation to the greatest extent in the presence ofV. tobetsuensis, without coaggregation between species. These results suggest thatV. tobetsuensisproduces signaling molecules that promote the proliferation ofS. gordoniiin biofilm formation. It is well known in many bacterial species that the quorum-sensing (QS) system regulates diverse functions such as biofilm formation. However, little is known about the QS system with autoinducers (AIs) with respect toVeillonella and Streptococcusspp. Recently, autoinducer 1 (AI-1) and AI-2 were detected and identified in the culture supernatants ofV. tobetsuensisas strong signaling molecules in biofilm formation withS. gordonii. In particular, the supernatant fromV. tobetsuensisshowed the highest AI-2 activity among 6 oralVeillonellaspecies, indicating that AIs, mainly AI-2, produced byV. tobetsuensismay be important factors and may facilitate biofilm formation ofS. gordonii. Clarifying the mechanism that underlies the QS system betweenS. gordoniiandV. tobetsuensismay lead to the development of novel methods for the prevention of oral infectious diseases caused by oral biofilms.


2020 ◽  
Author(s):  
Meztlli O. Gaytán ◽  
Anirudh K. Singh ◽  
Shireen A. Woodiga ◽  
Surina A. Patel ◽  
Seon-Sook An ◽  
...  

AbstractBacterial binding to platelets is a key step in the development of infective endocarditis (IE). Sialic acid, a common terminal carbohydrate on host glycans, is the major receptor for streptococci on platelets. So far, all defined interactions between streptococci and sialic acid on platelets are mediated by serine rich repeat proteins (SRRPs). However, we identified Streptococcus oralis subsp. oralis IE-isolates that bind sialic acid but lack SRRPs. In addition to binding sialic acid, some SRRP-negative isolates also bind the cryptic receptor β-1,4-linked galactose through a yet unknown mechanism. Using comparative genomics, we identified a novel sialic acid-binding adhesin, here named AsaA (associated with sialic acid adhesion A), present in IE-isolates lacking SRRPs. We demonstrated that S. oralis subsp. oralis AsaA is required for binding to platelets in a sialic acid-dependent manner. AsaA comprises a non-repeat region (NRR), consisting of a FIVAR/CBM and two Siglec-like and Unique domains, followed by 31 DUF1542 domains. When recombinantly expressed, Siglec-like and Unique domains competitively inhibited binding of S. oralis subsp. oralis and directly interacted with sialic acid on platelets. We further demonstrated that AsaA impacts the pathogenesis of S. oralis subsp. oralis in a rabbit model of IE. Additionally, we found AsaA orthologues in other IE-causing species and demonstrated that the NRR of AsaA from Gemella haemolysans blocked binding of S. oralis subsp. oralis, suggesting that AsaA contributes to the pathogenesis of multiple IE-causing species. Finally, our findings provide evidence that sialic acid is a key factor for bacterial-platelets interactions in a broader range of species than previously appreciated, highlighting its potential as a therapeutic target.Authors summaryInfective endocarditis (IE) is typically a bacterial infection of the heart valves that causes high mortality. Infective endocarditis can affect people with preexisting lesions on their heart valves (Subacute-IE). These lesions contain platelets and other host factors to which bacteria can bind. Growth of bacteria and accumulation of host factors results in heart failure. Therefore, the ability of bacteria to bind platelets is key to the development of IE. Here, we identified a novel bacterial protein, AsaA, which helps bacteria bind to platelets and contributes to the development of disease. Although this virulence factor was characterized in Streptococcus oralis, a leading cause of IE, we demonstrated that AsaA is also present in several other IE-causing bacterial species and is likely relevant to their ability to cause disease. We showed that AsaA binds to sialic acid, a terminal sugar present on platelets, thereby demonstrating that sialic acid serves as a receptor for a wider range of IE-causing bacteria than previously appreciated, highlighting its potential as a therapeutic target.


2015 ◽  
Vol 83 (12) ◽  
pp. 4682-4692 ◽  
Author(s):  
Nithya Babu Rajendran ◽  
Julian Eikmeier ◽  
Karsten Becker ◽  
Muzaffar Hussain ◽  
Georg Peters ◽  
...  

The coagulase-negative speciesStaphylococcus lugdunensisis an emerging cause of serious and potentially life-threatening infections, such as infective endocarditis. The pathogenesis of these infections is characterized by the ability ofS. lugdunensisto form biofilms on either biotic or abiotic surfaces. To elucidate the genetic basis of biofilm formation inS. lugdunensis, we performed transposon (Tn917) mutagenesis. One mutant had a significantly reduced biofilm-forming capacity and carried a Tn917insertion within the competence genecomEB. Site-directed mutagenesis and subsequent complementation with a functional copy ofcomEBverified the importance ofcomEBin biofilm formation. In several bacterial species, natural competence stimulates DNA release via lysis-dependent or -independent mechanisms. Extracellular DNA (eDNA) has been demonstrated to be an important structural component of many bacterial biofilms. Therefore, we quantified the eDNA in the biofilms and found diminished eDNA amounts in thecomEBmutant biofilm. High-resolution images and three-dimensional data obtained via confocal laser scanning microscopy (CSLM) visualized the impact of thecomEBmutation on biofilm integrity. ThecomEBmutant did not show reduced expression of autolysin genes, decreased autolytic activities, or increased cell viability, suggesting a cell lysis-independent mechanism of DNA release. Furthermore, reduced amounts of eDNA in thecomEBmutant biofilms did not result from elevated levels or activity of theS. lugdunensisthermonuclease NucI. In conclusion, we defined here, for the first time, a role for the competence genecomEBin staphylococcal biofilm formation. Our findings indicate thatcomEBstimulates biofilm formation via a lysis-independent mechanism of DNA release.


2018 ◽  
Author(s):  
Miriam Khider ◽  
Hilde Hansen ◽  
Jostein A. Johansen ◽  
Erik Hjerde ◽  
Nils Peder Willassen

Background. The marine bacterium A. salmonicida uses the quorum sensing (QS) systems, AinS/R and LuxI/R to produce eight acyl-homoserine lactones (AHLs) in a cell density dependent manner. Biofilm formation is one of the QS regulated phenotypes, which requires the expression of exopolysaccharides (EPS).We previously demonstrated that inactivation of LitR, the master regulator of QS in A. salmonicida resulted in biofilm formation, which was, similar to the biofilm formed by the AHL deficient mutant ΔainSluxI-.In this work, we have identified genes regulated by AinS and LuxI using RNA sequensing (RNA-Seq), and studied their role in biofilm formation, colony morphology and motility. We have also studied the effect of two AHLs on the biofilm formation. Results.The transcriptome profiling of ΔainS and luxI- mutants allowed us to identify essential genes regulated by QS in A. salmonicida. Relative to the wild-type, the ΔainS and luxI- mutants revealed 40 and 500 differentially expressed genes (DEGs), respectively. The functional analysis demonstrated that the most pronounced DEGs were involved in bacterial motility and chemotaxis, exopolysaccharide production, and surface structures related to adhesion. Inactivation of luxI but not ainS genes resulted in wrinkled colony morphology. While inactivation of both genes (ΔainSluxI-) resulted in strains able to form wrinkled colonies and mushroom structured biofilm. Moreover, when the ΔainSluxI- mutant was supplemented with N-3-oxo-hexanoyl-L- homoserine lactone (3OC6-HSL) and N-3-hydroxy-decanoyl-L-homoserine lactone(3OHC10-HSL), the biofilm did not develop. We also show that LuxI is needed for motility and repression for EPS production, where repression of EPS is likely operated through the RpoQ-sigma factor. Conclusion.These findings imply that LuxI and AinS synthases have a critical contribution to the QS-dependent regulation on gene expression and the phenotypic traits related to it.


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