scholarly journals MogR is a ubiquitous transcriptional repressor affecting motility, biofilm formation and virulence in Bacillus thuringiensis

2020 ◽  
Author(s):  
Veronika Smith ◽  
Malin Josefsen ◽  
Toril Lindbäck ◽  
Ida K. Hegna ◽  
Sarah Finke ◽  
...  
Keyword(s):  
Bacillus Thuringiensis ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Major Gene ◽  
Transcriptional Repressor ◽  
Dependent Manner ◽  
Flagellar Motility ◽  
Independent Manner ◽  
Motile Species ◽  
Group Species

Flagellar motility is considered an important virulence factor in different pathogenic bacteria. In Listeria monocytogenes the transcriptional repressor MogR regulates motility in a temperature-dependent manner, directly repressing flagellar- and chemotaxis genes. The only other bacteria known to carry a mogR homolog are members of the Bacillus cereus group, which includes motile species such as B. cereus and Bacillus thuringiensis as well as the non-motile species Bacillus anthracis, Bacillus mycoides and Bacillus pseudomycoides. Furthermore, the main motility locus in B. cereus group bacteria, carrying the genes for flagellar synthesis, appears to be more closely related to L. monocytogenes than to Bacillus subtilis, which belongs to a separate phylogenetic group of Bacilli and does not carry a mogR ortholog. Here, we show that in B. thuringiensis, MogR overexpression results in non-motile cells devoid of flagella. Global gene expression profiling showed that 110 genes were differentially regulated by MogR overexpression, including flagellar motility genes, but also genes associated with virulence, stress response and biofilm lifestyle. Accordingly, phenotypic assays showed that MogR also affects cytotoxicity and biofilm formation in B. thuringiensis. Overexpression of a MogR variant mutated in two amino acids within the putative DNA binding domain restored phenotypes to those of an empty vector control. In accordance, introduction of these mutations resulted in complete loss in MogR binding to its candidate flagellar locus target site in vitro. In contrast to L. monocytogenes, MogR appears to be regulated in a growth-phase dependent and temperature-independent manner in B. thuringiensis 407. Interestingly, mogR was found to be conserved also in non-motile B. cereus group species such as B. mycoides and B. pseudomycoides, which both carry major gene deletions in the flagellar motility locus and where in B. pseudomycoides mogR is the only gene retained. Furthermore, mogR is expressed in non-motile B. anthracis. Altogether this provides indications of an expanded set of functions for MogR in B. cereus group species, beyond motility regulation. In conclusion, MogR constitutes a novel B. thuringiensis pleiotropic transcriptional regulator, acting as a repressor of motility genes, and affecting the expression of a variety of additional genes involved in biofilm formation and virulence.

scholarly journals MogR Is a Ubiquitous Transcriptional Repressor Affecting Motility, Biofilm Formation and Virulence in Bacillus thuringiensis

2020 ◽  
Vol 11 ◽  
Author(s):  
Veronika Smith ◽  
Malin Josefsen ◽  
Toril Lindbäck ◽  
Ida K. Hegna ◽  
Sarah Finke ◽  
...  
Keyword(s):  
Bacillus Thuringiensis ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Major Gene ◽  
Transcriptional Repressor ◽  
Dependent Manner ◽  
Flagellar Motility ◽  
Independent Manner ◽  
Motile Species ◽  
Group Species

Flagellar motility is considered an important virulence factor in different pathogenic bacteria. In Listeria monocytogenes the transcriptional repressor MogR regulates motility in a temperature-dependent manner, directly repressing flagellar- and chemotaxis genes. The only other bacteria known to carry a mogR homolog are members of the Bacillus cereus group, which includes motile species such as B. cereus and Bacillus thuringiensis as well as the non-motile species Bacillus anthracis, Bacillus mycoides and Bacillus pseudomycoides. Furthermore, the main motility locus in B. cereus group bacteria, carrying the genes for flagellar synthesis, appears to be more closely related to L. monocytogenes than to Bacillus subtilis, which belongs to a separate phylogenetic group of Bacilli and does not carry a mogR ortholog. Here, we show that in B. thuringiensis, MogR overexpression results in non-motile cells devoid of flagella. Global gene expression profiling showed that 110 genes were differentially regulated by MogR overexpression, including flagellar motility genes, but also genes associated with virulence, stress response and biofilm lifestyle. Accordingly, phenotypic assays showed that MogR also affects cytotoxicity and biofilm formation in B. thuringiensis. Overexpression of a MogR variant mutated in two amino acids within the putative DNA binding domain restored phenotypes to those of an empty vector control. In accordance, introduction of these mutations resulted in complete loss in MogR binding to its candidate flagellar locus target site in vitro. In contrast to L. monocytogenes, MogR appears to be regulated in a growth-phase dependent and temperature-independent manner in B. thuringiensis 407. Interestingly, mogR was found to be conserved also in non-motile B. cereus group species such as B. mycoides and B. pseudomycoides, which both carry major gene deletions in the flagellar motility locus and where in B. pseudomycoides mogR is the only gene retained. Furthermore, mogR is expressed in non-motile B. anthracis. Altogether this provides indications of an expanded set of functions for MogR in B. cereus group species, beyond motility regulation. In conclusion, MogR constitutes a novel B. thuringiensis pleiotropic transcriptional regulator, acting as a repressor of motility genes, and affecting the expression of a variety of additional genes involved in biofilm formation and virulence.

Identification of ica-dependent biofilm production by Staphylococcus aureus clinical isolates and antibiofilm effects of ascorbic acid against biofilm production

2020 ◽  
Vol 73 (5) ◽  
pp. 261-266
Author(s):  
Sahra Kırmusaoğlu ◽  
Havva Kaşıkçı
Keyword(s):  
Staphylococcus Aureus ◽  
Ascorbic Acid ◽  
Biofilm Formation ◽  
Surface Proteins ◽  
Clinical Isolates ◽  
High Morbidity ◽  
Dependent Manner ◽  
Independent Manner ◽  
Biofilm Production ◽  
Life Threatening

AimsStaphylococcus aureus (S. aureus) is a life-threatening pathogen with high morbidity and mortality rates which causes nosocomial and community-acquired infections. Biofilm, considered to be a common virulence factor for pathogens, plays a significant role in recurrent and untreatable infections. Biofilm formation of S. aureus is mediated by synthesis of either poly-N-acetylglucosamine in an ica-dependent manner or surface proteins in an ica-independent manner. In some cases treatment is impossible and recurrent. In this study, ica-dependent biofilm-producing S. aureus isolates were detected and the anti-biofilm effect of ascorbic acid against biofilm formation of isolates was investigated.MethodsA total of 21 methicillin-sensitive S. aureus (MSSA) clinical isolates stored in our bacterial stock were used to detect ica-dependent biofilm-producing MSSA isolates. The anti-biofilm study was undertaken with three ica-dependent biofilm-producing isolates (MSSA2–4) and ATCC 29213 (MSSA1). Biofilms and the anti-biofilm effect of ascorbic acid were detected using the microtitre plate (MtP) method. 16S-rRNA, nuc, icaA and icaD genes and expression levels of icaA and icaD of isolates were detected by RT-PCR.ResultsThe minimum inhibitory concentrations (MICs) of ascorbic acid prevented biofilm formation of MSSA1 and MSSA3. Also, 1/2 MIC of ascorbic acid prevented biofilm formation of MSSA3. It was observed that biofilm formation decreased with increased concentration. There was no significant increase in ica gene expression of MSSA1 and MSSA2. Expression of icaA and icaD of MSSA3 decreased 13% and 38%, respectively. Expression of icaA in MSSA4 decreased 12%.ConclusionThe results of our study show that ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation of S. aureus and thus biofilm-related infections.

scholarly journals Antibacterial Effects of Bicarbonate in Media Modified to Mimic Cystic Fibrosis Sputum

2020 ◽  
Vol 21 (22) ◽  
pp. 8614
Author(s):  
Pongsiri Jaikumpun ◽  
Kasidid Ruksakiet ◽  
Balázs Stercz ◽  
Éva Pállinger ◽  
Martin Steward ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Culture Media ◽  
Anion Channel ◽  
Ambient Air ◽  
Hereditary Disease ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cell Counts

Cystic fibrosis (CF) is a hereditary disease caused by mutations in the gene encoding an epithelial anion channel. In CF, Cl− and HCO3− hyposecretion, together with mucin hypersecretion, leads to airway dehydration and production of viscous mucus. This habitat is ideal for colonization by pathogenic bacteria. We have recently demonstrated that HCO3− inhibits the growth and biofilm formation of Pseudomonas aeruginosa and Staphylococcus aureus when tested in laboratory culture media. Using the same bacteria our aim was to investigate the effects of HCO3− in artificial sputum medium (ASM), whose composition resembles CF mucus. Control ASM containing no NaHCO3 was incubated in ambient air (pH 7.4 or 8.0). ASM containing NaHCO3 (25 and 100 mM) was incubated in 5% CO2 (pH 7.4 and 8.0, respectively). Viable P. aeruginosa and S. aureus cells were counted by colony-forming unit assay and flow cytometry after 6 h and 17 h of incubation. Biofilm formation was assessed after 48 h. The data show that HCO3− significantly decreased viable cell counts and biofilm formation in a concentration-dependent manner. These effects were due neither to extracellular alkalinization nor to altered osmolarity. These results show that HCO3− exerts direct antibacterial and antibiofilm effects on prevalent CF bacteria.

scholarly journals Cyclic di-GMP Increases Catalase Production and Hydrogen Peroxide Tolerance inVibrio cholerae

2019 ◽  
Author(s):  
Nicolas L. Fernandez ◽  
Christopher M. Waters
Keyword(s):  
Catalase Activity ◽  
Biofilm Formation ◽  
Salt Water ◽  
Bacterial Pathogen ◽  
Second Messenger ◽  
Signaling Network ◽  
Guanosine Monophosphate ◽  
Dependent Manner ◽  
Flagellar Motility ◽  
Environmental Persistence

AbstractVibrio choleraeis a Gram-negative bacterial pathogen that causes the disease cholera, which affects nearly 1 million people each year. In between outbreaks,V. choleraeresides in fresh and salt water environments where it is able to persist through changes in temperature, oxygen, and salinity. One key characteristic that promotes environmental persistence ofV. choleraeis the ability to form multicellular communities, called biofilms, that often adhere to biotic and abiotic sources. Biofilm formation inV. choleraeis positively regulated by the dinucleotide second messenger cyclic dimeric guanosine monophosphate (c-di-GMP). While most research on the c-di-GMP regulon has focused on biofilm formation or motility, we hypothesized the c-di-GMP signaling network encompassed a larger set of effector functions than reported. We found that high intracellular c-di-GMP increased catalase activity approximately 4-fold relative to strains with unaltered c-di-GMP. Genetic studies demonstrated that c-di-GMP mediated catalase activity was due to increased expression of the catalase encoding genekatB. Moreover, c-di-GMP mediated regulation of catalase activity andkatBexpression required the c-di-GMP dependent transcription factors VpsT and VpsR. Lastly, we found that high c-di-GMP increased survival after H2O2challenge in akatB, vpsR, andvpsTdependent manner. Our results indicate antioxidant production is regulated by c-di-GMP inV. choleraeuncovering a new node in the growing VpsT and VpsR c-di-GMP signaling network.ImportanceAs a result of infection withV. cholerae, patients become dehydrated leading to death if not properly treated. The marine environment is the natural reservoir forV. choleraewhere it can survive alterations in temperature, salinity, and oxygen. The second messenger molecule c-di-GMP is an important signal regulating host and marine environmental persistence because it controls whetherV. choleraewill form a biofilm or disperse through flagellar motility. In this work, we demonstrate another function of c-di-GMP inV. choleraebiology: promoting tolerance to the reactive oxygen species H2O2through differential regulation of catalase expression. Our results suggest a mechanism where c-di-GMP simultaneously controls biofilm formation and antioxidant production, which could promote persistence in human and marine environments.

scholarly journals Cigarette Smoke Increases Staphylococcus aureus Biofilm Formation via Oxidative Stress

2012 ◽  
Vol 80 (11) ◽  
pp. 3804-3811 ◽  
Author(s):  
Ritwij Kulkarni ◽  
Swati Antala ◽  
Alice Wang ◽  
Fábio E. Amaral ◽  
Ryan Rampersaud ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cigarette Smoke ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Protein A ◽  
Model Organism ◽  
Human Cells ◽  
Dependent Manner ◽  
Content Type ◽  
Tract Infections

ABSTRACTThe strong epidemiological association between cigarette smoke (CS) exposure and respiratory tract infections is conventionally attributed to immunosuppressive and irritant effects of CS on human cells. Since pathogenic bacteria such asStaphylococcus aureusare members of the normal microbiota and reside in close proximity to human nasopharyngeal cells, we hypothesized that bioactive components of CS might affect these organisms and potentiate their virulence. UsingStaphylococcus aureusas a model organism, we observed that the presence of CS increased both biofilm formation and host cell adherence. Analysis of putative molecular pathways revealed that CS exposure decreased expression of the quorum-sensingagrsystem, which is involved in biofilm dispersal, and increased transcription of biofilm inducers such assarAandrbf. CS contains bioactive compounds, including free radicals and reactive oxygen species, and we observed transcriptional induction of bacterial oxidoreductases, including superoxide dismutase, following exposure. Moreover, pretreatment of CS with an antioxidant abrogated CS-mediated enhancement of biofilms. Exposure of bacteria to hydrogen peroxide alone increased biofilm formation. These observations are consistent with the hypothesis that CS induces staphylococcal biofilm formation in an oxidant-dependent manner. CS treatment induced transcription offnbA(encoding fibronectin binding protein A), leading to increased binding of CS-treated staphylococci to immobilized fibronectin and increased adherence to human cells. These observations indicate that the bioactive effects of CS may extend to the resident microbiota of the nasopharynx, with implications for the pathogenesis of respiratory infection in CS-exposed humans.

scholarly journals Lactobacillus plantarum Lipoteichoic Acids Possess Strain-Specific Regulatory Effects on the Biofilm Formation of Dental Pathogenic Bacteria

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongwook Lee ◽  
Jintaek Im ◽  
Dong Hyun Park ◽  
Sungho Jeong ◽  
Miri Park ◽  
...  
Keyword(s):  
Lactobacillus Plantarum ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Lipoteichoic Acid ◽  
Molecular Structures ◽  
Bacterial Biofilm ◽  
Infection Model ◽  
Dependent Manner ◽  
Regulatory Effects ◽  
Different Strains

Bacterial biofilm residing in the oral cavity is closely related to the initiation and persistence of various dental diseases. Previously, we reported the anti-biofilm activity of Lactobacillus plantarum lipoteichoic acid (Lp.LTA) on a representative dental cariogenic pathogen, Streptococcus mutans. Since LTA structure varies in a bacterial strain-specific manner, LTAs from various L. plantarum strains may have differential anti-biofilm activity due to their distinct molecular structures. In the present study, we isolated Lp.LTAs from four different strains of L. plantarum (LRCC 5193, 5194, 5195, and 5310) and compared their anti-biofilm effects on the dental pathogens, including S. mutans, Enterococcus faecalis, and Streptococcus gordonii. All Lp.LTAs similarly inhibited E. faecalis biofilm formation in a dose-dependent manner. However, their effects on S. gordonii and S. mutans biofilm formation were different: LRCC 5310 Lp.LTA most effectively suppressed the biofilm formation of all strains of dental pathogens, while Lp.LTAs from LRCC 5193 and 5194 hardly inhibited or even enhanced the biofilm formation. Furthermore, LRCC 5310 Lp.LTA dramatically reduced the biofilm formation of the dental pathogens on the human dentin slice infection model. Collectively, these results suggest that Lp.LTAs have strain-specific regulatory effects on biofilm formation of dental pathogens and LRCC 5310 Lp.LTA can be used as an effective anti-biofilm agent for the prevention of dental infectious diseases.

scholarly journals Oxantel Disrupts Polymicrobial Biofilm Development of Periodontal Pathogens

2013 ◽  
Vol 58 (1) ◽  
pp. 378-385 ◽  
Author(s):  
Stuart Dashper ◽  
Neil O'Brien-Simpson ◽  
Sze Wei Liu ◽  
Rita Paolini ◽  
Helen Mitchell ◽  
...  
Keyword(s):  
Bone Loss ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Large Scale ◽  
Alveolar Bone ◽  
Similar Degree ◽  
Dependent Manner ◽  
Gene Products ◽  
Content Type ◽  
Biofilm Development

ABSTRACTBacterial pathogens commonly associated with chronic periodontitis are the spirocheteTreponema denticolaand the Gram-negative, proteolytic speciesPorphyromonas gingivalisandTannerella forsythia. These species rely on complex anaerobic respiration of amino acids, and the anthelmintic drug oxantel has been shown to inhibit fumarate reductase (Frd) activity in some pathogenic bacteria and inhibitP. gingivalishomotypic biofilm formation. Here, we demonstrate that oxantel inhibitedP. gingivalisFrd activity with a 50% inhibitory concentration (IC50) of 2.2 μM and planktonic growth ofT. forsythiawith a MIC of 295 μM, but it had no effect on the growth ofT. denticola. Oxantel treatment caused the downregulation of sixP. gingivalisgene products and the upregulation of 22 gene products. All of these genes are part of a regulon controlled by heme availability. There was no large-scale change in the expression of genes encoding metabolic enzymes, indicating thatP. gingivalismay be unable to overcome Frd inhibition. Oxantel disrupted the development of polymicrobial biofilms composed ofP. gingivalis,T. forsythia, andT. denticolain a concentration-dependent manner. In these biofilms, all three species were inhibited to a similar degree, demonstrating the synergistic nature of biofilm formation by these species and the dependence ofT. denticolaon the other two species. In a murine alveolar bone loss model of periodontitis oxantel addition to the drinking water ofP. gingivalis-infected mice reduced bone loss to the same level as the uninfected control.

Antibiotics Application Strategies to Control Biofilm Formation in Pathogenic Bacteria

2020 ◽  
Vol 21 (4) ◽  
pp. 270-286 ◽  
Author(s):  
Fazlurrahman Khan ◽  
Dung T.N. Pham ◽  
Sandra F. Oloketuyi ◽  
Young-Mog Kim
Keyword(s):  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Extracellular Polymeric Substances ◽  
Quorum Quenching ◽  
Resistance Mechanisms ◽  
Bacterial Biofilm ◽  
Bacterial Cells ◽  
High Concentration ◽  
Biofilm Inhibition ◽  
Abiotic Surfaces

Background: The establishment of a biofilm by most pathogenic bacteria has been known as one of the resistance mechanisms against antibiotics. A biofilm is a structural component where the bacterial community adheres to the biotic or abiotic surfaces by the help of Extracellular Polymeric Substances (EPS) produced by bacterial cells. The biofilm matrix possesses the ability to resist several adverse environmental factors, including the effect of antibiotics. Therefore, the resistance of bacterial biofilm-forming cells could be increased up to 1000 times than the planktonic cells, hence requiring a significantly high concentration of antibiotics for treatment. Methods: Up to the present, several methodologies employing antibiotics as an anti-biofilm, antivirulence or quorum quenching agent have been developed for biofilm inhibition and eradication of a pre-formed mature biofilm. Results: Among the anti-biofilm strategies being tested, the sub-minimal inhibitory concentration of several antibiotics either alone or in combination has been shown to inhibit biofilm formation and down-regulate the production of virulence factors. The combinatorial strategies include (1) combination of multiple antibiotics, (2) combination of antibiotics with non-antibiotic agents and (3) loading of antibiotics onto a carrier. Conclusion: The present review paper describes the role of several antibiotics as biofilm inhibitors and also the alternative strategies adopted for applications in eradicating and inhibiting the formation of biofilm by pathogenic bacteria.

scholarly journals In VitroAnalyses of the Effects of Heparin and Parabens on Candida albicans Biofilms and Planktonic Cells

2011 ◽  
Vol 56 (1) ◽  
pp. 148-153 ◽  
Author(s):  
Marisa H. Miceli ◽  
Stella M. Bernardo ◽  
T. S. Neil Ku ◽  
Carla Walraven ◽  
Samuel A. Lee
Keyword(s):  
Candida Albicans ◽  
Metabolic Activity ◽  
Biofilm Formation ◽  
High Dose ◽  
Dependent Manner ◽  
Planktonic Cells ◽  
Content Type ◽  
Heparin Sodium ◽  
The Individual

ABSTRACTInfections and thromboses are the most common complications associated with central venous catheters. Suggested strategies for prevention and management of these complications include the use of heparin-coated catheters, heparin locks, and antimicrobial lock therapy. However, the effects of heparin onCandida albicansbiofilms and planktonic cells have not been previously studied. Therefore, we sought to determine thein vitroeffect of a heparin sodium preparation (HP) on biofilms and planktonic cells ofC. albicans. Because HP contains two preservatives, methyl paraben (MP) and propyl paraben (PP), these compounds and heparin sodium without preservatives (Pure-H) were also tested individually. The metabolic activity of the mature biofilm after treatment was assessed using XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction and microscopy. Pure-H, MP, and PP caused up to 75, 85, and 60% reductions of metabolic activity of the mature preformedC. albicansbiofilms, respectively. Maximal efficacy against the mature biofilm was observed with HP (up to 90%) compared to the individual compounds (P< 0.0001). Pure-H, MP, and PP each inhibitedC. albicansbiofilm formation up to 90%. A complete inhibition of biofilm formation was observed with HP at 5,000 U/ml and higher. When tested against planktonic cells, each compound inhibited growth in a dose-dependent manner. These data indicated that HP, MP, PP, and Pure-H havein vitroantifungal activity againstC. albicansmature biofilms, formation of biofilms, and planktonic cells. Investigation of high-dose heparin-based strategies (e.g., heparin locks) in combination with traditional antifungal agents for the treatment and/or prevention ofC. albicansbiofilms is warranted.

scholarly journals Extract from phyllosphere bacteria with antibiofilm and quorum quenching activity to control several fish pathogenic bacteria

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Olivia Nathalia ◽  
Diana Elizabeth Waturangi
Keyword(s):  
Streptococcus Agalactiae ◽  
Aeromonas Hydrophila ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Vibrio Harveyi ◽  
Quorum Quenching ◽  
Indicator Bacteria ◽  
Antibiofilm Activity ◽  
Fish Pathogen ◽  
Phyllosphere Bacteria

Abstract Objective The objective of this research were to screen quorum quenching activity compound from phyllosphere bacteria as well as antibiofilm activity against several fish pathogen bacteria such as Aeromonas hydrophila, Streptococcus agalactiae, and Vibrio harveyi. Results We found eight phyllosphere bacteria isolates with potential quorum quenching activity to inhibit Chromobacterium violaceum as indicator bacteria. Crude extracts (20 mg/mL) showed various antibiofilm activity against fish pathogenic bacteria used in this study. Isolate JB 17B showed the highest activity to inhibit biofilm formation of A. hydrophila and V. harveyi, meanwhile isolate JB 3B showed the highest activity to inhibit biofilm of S. agalactiae. From destruction assay, isolate JB 8F showed the highest activity to disrupt biofilm of A. hydrophila isolate JB 20B showed the highest activity to disrupt biofilm of V. harveyi, isolate JB 17B also showed the highest activity to disrupt biofilm of S. agalactiae.

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