scholarly journals Antibiofilm Activity of Lactobacillus plantarum 12 Exopolysaccharides against Shigella flexneri

2020 ◽  
Vol 86 (15) ◽  
Author(s):  
Yinglong Song ◽  
Mengying Sun ◽  
Lu Feng ◽  
Xue Liang ◽  
Xing Song ◽  
...  
Keyword(s):  
Developing Countries ◽  
Lactobacillus Plantarum ◽  
Biofilm Formation ◽  
Glucuronic Acid ◽  
Shigella Flexneri ◽  
Molar Ratio ◽  
Composition Analysis ◽  
Antibiofilm Activity ◽  
Content Type ◽  
Ht 29

ABSTRACT In developing countries, Shigella flexneri is the most common enteric pathogen causing bacillary dysentery. Biofilm formation by S. flexneri can cause the emergence of antibiotic-resistant strains, which poses serious threats to food safety and human health. In this study, the effects of Lactobacillus plantarum 12 exopolysaccharides (L-EPSs) and S. flexneri exopolysaccharides (S-EPSs) on S. flexneri CMCC51574 biofilm formation were investigated. The results showed that L-EPS could decrease polysaccharide production in the extracellular polymeric matrix of S. flexneri and inhibit biofilm formation by S. flexneri. L-EPS could decrease the minimum biofilm elimination concentration (MBEC) of antibiotics against S. flexneri biofilm and inhibit S. flexneri adhesion to and invasion into HT-29 cell monolayers, which might be ascribed to S. flexneri biofilm disturbance by L-EPS. In contrast, S-EPS exhibited the opposite effects compared to L-EPS. The monosaccharide composition analysis showed that L-EPS was composed of mannose, glucuronic acid, galactosamine, glucose, galactose, and xylose, with the molar ratio of 32.26:0.99:1.79:5.63:0.05:4.07, while S-EPS was composed of mannose, glucuronic acid, galactosamine, glucose, and galactose, with the molar ratio of 25.43:2.28:7.13:5.35. L-EPS was separated into the neutral polysaccharide L-EPS 1-1 and the acidic polysaccharide L-EPS 2-1 by ion-exchange chromatography and gel chromatography. L-EPS 2-1 exerted higher antibiofilm activity than L-EPS 1-1. The antibiofilm activity of L-EPS might be associated with its structure. IMPORTANCE S. flexneri is a widespread foodborne pathogen causing food contamination and responsible for food poisoning outbreaks related to various foods in developing countries. Not only has biofilm formation by S. flexneri been difficult to eliminate, but it has also increased the drug resistance of the strain. In the present study, it was demonstrated that L-EPSs secreted by Lactobacillus plantrum 12 could inhibit S. flexneri biofilm formation on, adhesion to, and invasion into HT-29 cells. Also, L-EPSs could decrease the minimum biofilm elimination concentration (MBEC) of the antibiotics used against S. flexneri biofilm. Therefore, L-EPSs were shown to be bioactive macromolecules with the potential ability to act against S. flexneri infections.

scholarly journals Clarithromycin Exerts an Antibiofilm Effect against Salmonella enterica Serovar Typhimurium rdar Biofilm Formation and Transforms the Physiology towards an Apparent Oxygen-Depleted Energy and Carbon Metabolism

2020 ◽  
Vol 88 (11) ◽  
Author(s):  
Munirah Zafar ◽  
Humera Jahan ◽  
Sulman Shafeeq ◽  
Manfred Nimtz ◽  
Lothar Jänsch ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Bacterial Cells ◽  
Content Type ◽  
Regulatory Pathways ◽  
Heat Shock Stress ◽  
Extracellular Matrix Components ◽  
Serovar Typhimurium

ABSTRACT Upon biofilm formation, production of extracellular matrix components and alteration in physiology and metabolism allows bacteria to build up multicellular communities which can facilitate nutrient acquisition during unfavorable conditions and provide protection toward various forms of environmental stresses to individual cells. Thus, bacterial cells within biofilms become tolerant against antimicrobials and the immune system. In the present study, we evaluated the antibiofilm activity of the macrolides clarithromycin and azithromycin. Clarithromycin showed antibiofilm activity against rdar (red, dry, and rough) biofilm formation of the gastrointestinal pathogen Salmonella enterica serovar Typhimurium ATCC 14028 (Nalr) at a 1.56 μM subinhibitory concentration in standing culture and dissolved cell aggregates at 15 μM in a microaerophilic environment, suggesting that the oxygen level affects the activity of the drug. Treatment with clarithromycin significantly decreased transcription and production of the rdar biofilm activator CsgD, with biofilm genes such as csgB and adrA to be concomitantly downregulated. Although fliA and other flagellar regulon genes were upregulated, apparent motility was downregulated. RNA sequencing showed a holistic cell response upon clarithromycin exposure, whereby not only genes involved in the biofilm-related regulatory pathways but also genes that likely contribute to intrinsic antimicrobial resistance, and the heat shock stress response were differentially regulated. Most significantly, clarithromycin exposure shifted the cells toward an apparent oxygen- and energy-depleted status, whereby the metabolism that channels into oxidative phosphorylation was downregulated, and energy gain by degradation of propane 1,2-diol, ethanolamine and l-arginine catabolism, potentially also to prevent cytosolic acidification, was upregulated. This analysis will allow the subsequent identification of novel intrinsic antimicrobial resistance determinants.

scholarly journals Shigella Vaccine Development: Finding the Path of Least Resistance

2016 ◽  
Vol 23 (12) ◽  
pp. 904-907 ◽  
Author(s):  
Wilbur H. Chen ◽  
Karen L. Kotloff
Keyword(s):  
Public Health ◽  
Developing Countries ◽  
Phase I ◽  
Phase I Study ◽  
Vaccine Development ◽  
Shigella Flexneri ◽  
Health Concern ◽  
Childhood Diarrhea ◽  
Public Health Concern ◽  
Content Type

ABSTRACTShigellaspp. represent the second most common etiologic pathogen causing childhood diarrhea in developing countries. There are no licensedShigellavaccines, and progress for such vaccines has been limited. In this issue ofClinical and Vaccine Immunology, Riddle and colleagues (M. S. Riddle, R. W. Kaminski, C. Di Paolo, C. K. Porter, R. L. Gutierrez, et al., Clin Vaccine Immunol 23:908–917, 2016,http://dx.doi.org/10.1128/CVI.00224-16) report results from a phase I study of a parenterally administered monovalent O-polysaccharide “bioconjugate” directed againstShigella flexneri2a. Ultimately, the goal is to develop a broad-spectrumShigellavaccine to address this public health concern. A parenteralShigellavaccine capable of eliciting protection in children of developing countries would be an important tool to reach this goal.

scholarly journals Effects of a Novel Probiotic Combination on Pathogenic Bacterial-Fungal Polymicrobial Biofilms

mBio ◽  
2019 ◽  
Vol 10 (2) ◽  
Author(s):  
Christopher L. Hager ◽  
Nancy Isham ◽  
Kory P. Schrom ◽  
Jyotsna Chandra ◽  
Thomas McCormick ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Gut Microbiome ◽  
Biofilm Formation ◽  
Bacterial Species ◽  
Bacterial Flora ◽  
Confocal Scanning Laser Microscopy ◽  
Antibiofilm Activity ◽  
Content Type ◽  
Bowel Diseases ◽  
Inflammatory Bowel

ABSTRACTDysbiosis of the gut microbiome has been implicated in inflammatory bowel diseases. We have shown that levels ofCandida tropicalis, along with those ofEscherichia coliandSerratia marcescens, are significantly elevated in Crohn’s disease (CD) patients. Here, we evaluated the ability of a novel probiotic to prevent and treat polymicrobial biofilms (PMB) formed byC. tropicaliswithE. coliandS. marcescens. SinceCandida albicanshas been reported to be elevated in CD patients, we investigated the interactions ofC. albicanswith these bacterial species in biofilm formation. We determined whether the interaction betweenCandidaspp. and bacteria is specific by usingTrichosporon inkinandSaccharomyces fibuligeraas comparators. Additionally, the effects of probiotics onC. albicansgermination and biofilm formation were determined. To determine the ability of the probiotic to prevent or treat mature biofilms, probiotic filtrate was added to the PMB at early (prevention) and mature (treatment) phases. Biofilm thickness and architecture were assessed by confocal scanning laser microscopy. The effects of the probiotic on germination were evaluated in the presence of serum. Exposure ofC. tropicalisPMB to probiotic filtrate reduced biofilm matrix, decreased thickness, and inhibited hyphal formation. We showed thatC. albicansorC. tropicalisformed significantly thicker PMB than control biofilms, indicating that this interaction isCandidaspecific. Treatment with probiotic filtrate inhibitedC. albicansgermination and prevented/treatedC. albicansPMB. The designed probiotic may have utility in the management of biofilm-associated gastrointestinal diseases such as Crohn’s and colorectal cancer.IMPORTANCEThe effects of diversity of the gut microbiome on inflammation have centered mainly on bacterial flora. Recent research has implicated fungal species and their interactions with other organisms in the inflammatory process. New ways to restore microbial balance in the gut are being explored. Our goal was to identify beneficial probiotic strains that would antagonize these fungal and bacterial pathogens that are elevated in the inflamed gut, and which also have antibiofilm activity. Fungus-bacterium correlation analysis allowed us to identify candidate probiotic species that can antagonize microbial pathogens, which we subsequently incorporated into a novel probiotic formulation. Amylase, which is known to have some antibiofilm activity, was also added to the probiotic mixture. This novel probiotic may have utility for the management of inflammatory bowel diseases by disrupting polymicrobial biofilm formation.

scholarly journals The Emerging Pathogen Candida auris: Growth Phenotype, Virulence Factors, Activity of Antifungals, and Effect of SCY-078, a Novel Glucan Synthesis Inhibitor, on Growth Morphology and Biofilm Formation

2017 ◽  
Vol 61 (5) ◽  
Author(s):  
Emily Larkin ◽  
Christopher Hager ◽  
Jyotsna Chandra ◽  
Pranab K. Mukherjee ◽  
Mauricio Retuerto ◽  
...  
Keyword(s):  
Amphotericin B ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Invasive Infection ◽  
Dependent Manner ◽  
Synthesis Inhibitor ◽  
Content Type ◽  
Orally Bioavailable ◽  
Glucan Synthesis

ABSTRACT Candida auris, a new multidrug-resistant Candida spp. which is associated with invasive infection and high rates of mortality, has recently emerged. Here, we determined the virulence factors (germination, adherence, biofilm formation, phospholipase and proteinase production) of 16 C. auris isolates and their susceptibilities to 11 drugs belonging to different antifungal classes, including a novel orally bioavailable 1,3-β-d-glucan synthesis inhibitor (SCY-078). We also examined the effect of SCY-078 on the growth, ultrastructure, and biofilm-forming abilities of C. auris. Our data showed that while the tested strains did not germinate, they did produce phospholipase and proteinase in a strain-dependent manner and had a significantly reduced ability to adhere and form biofilms compared to that of Candida albicans (P = 0.01). C. auris isolates demonstrated reduced susceptibility to fluconazole and amphotericin B, while, in general, they were susceptible to the remaining drugs tested. SCY-078 had an MIC90 of 1 mg/liter against C. auris and caused complete inhibition of the growth of C. auris and C. albicans. Scanning electron microscopy analysis showed that SCY-078 interrupted C. auris cell division, with the organism forming abnormal fused fungal cells. Additionally, SCY-078 possessed potent antibiofilm activity, wherein treated biofilms demonstrated significantly reduced metabolic activity and a significantly reduced thickness compared to the untreated control (P < 0.05 for both comparisons). Our study shows that C. auris expresses several virulence determinants (albeit to a lesser extent than C. albicans) and is resistant to fluconazole and amphotericin B. SCY-078, the new orally bioavailable antifungal, had potent antifungal/antibiofilm activity against C. auris, indicating that further evaluation of this antifungal is warranted.

scholarly journals Tannic Acid Inhibits Staphylococcus aureus Surface Colonization in an IsaA-Dependent Manner

2012 ◽  
Vol 81 (2) ◽  
pp. 496-504 ◽  
Author(s):  
David E. Payne ◽  
Nicholas R. Martin ◽  
Katherine R. Parzych ◽  
Alex H. Rickard ◽  
Adam Underwood ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Tannic Acid ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Host Immune System ◽  
Dependent Manner ◽  
Content Type ◽  
Surface Colonization ◽  
Biofilm Development ◽  
Insight Into

ABSTRACTStaphylococcus aureusis a human commensal and pathogen that is capable of forming biofilms on a variety of host tissues and implanted medical devices. Biofilm-associated infections resist antimicrobial chemotherapy and attack from the host immune system, making these infections particularly difficult to treat. In order to gain insight into environmental conditions that influenceS. aureusbiofilm development, we screened a library of small molecules for the ability to inhibitS. aureusbiofilm formation. This led to the finding that the polyphenolic compound tannic acid inhibitsS. aureusbiofilm formation in multiple biofilm models without inhibiting bacterial growth. We present evidence that tannic acid inhibitsS. aureusbiofilm formation via a mechanism dependent upon the putative transglycosylase IsaA. Tannic acid did not inhibit biofilm formation of anisaAmutant. Overexpression of wild-type IsaA inhibited biofilm formation, whereas overexpression of a catalytically dead IsaA had no effect. Tannin-containing drinks like tea have been found to reduce methicillin-resistantS. aureusnasal colonization. We found that black tea inhibitedS. aureusbiofilm development and that anisaAmutant resisted this inhibition. Antibiofilm activity was eliminated from tea when milk was added to precipitate the tannic acid. Finally, we developed a rodent model forS. aureusthroat colonization and found that tea consumption reducedS. aureusthroat colonization via anisaA-dependent mechanism. These findings provide insight into a molecular mechanism by which commonly consumed polyphenolic compounds, such as tannins, influenceS. aureussurface colonization.

scholarly journals Bruton's Tyrosine Kinase Regulates Shigella flexneri Dissemination in HT-29 Intestinal Cells

2012 ◽  
Vol 81 (2) ◽  
pp. 598-607 ◽  
Author(s):  
Ana-Maria Dragoi ◽  
Arthur M. Talman ◽  
Hervé Agaisse
Keyword(s):  
Tyrosine Kinase ◽  
Cell Lines ◽  
Tyrosine Kinases ◽  
Shigella Flexneri ◽  
Intestinal Cells ◽  
Bruton’S Tyrosine Kinase ◽  
Bruton's Tyrosine Kinase ◽  
Content Type ◽  
Bacterial Surface ◽  
Ht 29

ABSTRACTShigella flexneriis a Gram-negative intracellular pathogen that infects the intestinal epithelium and utilizes actin-based motility to spread from cell to cell.S. flexneriactin-based motility has been characterized in various cell lines, but studies in intestinal cells are limited. Here we characterizedS. flexneriactin-based motility in HT-29 intestinal cells. In agreement with studies conducted in various cell lines, we showed thatS. flexnerirelies on neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells. We tested the potential role of various tyrosine kinases involved in N-WASP activation and uncovered a previously unappreciated role for Bruton's tyrosine kinase (Btk) in actin tail formation in intestinal cells. We showed that Btk depletion led to a decrease in N-WASP phosphorylation which affected N-WASP recruitment to the bacterial surface, decreased the number of bacteria displaying actin-based motility, and ultimately affected the efficiency of spread from cell to cell. Finally, we showed that the levels of N-WASP phosphorylation and Btk expression were increased in response to infection, which suggests thatS. flexneriinfection not only triggers the production of proinflammatory factors as previously described but also manipulates cellular processes required for dissemination in intestinal cells.

scholarly journals Structure-Activity Relationship Study of the Plant-Derived Decapeptide OSIP108 Inhibiting Candida albicans Biofilm Formation

2014 ◽  
Vol 58 (8) ◽  
pp. 4974-4977 ◽  
Author(s):  
Nicolas Delattin ◽  
Katrijn De Brucker ◽  
David J. Craik ◽  
Olivier Cheneval ◽  
Barbara De Coninck ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Structure Activity Relationship ◽  
Activity Relationship ◽  
Antibiofilm Activity ◽  
Content Type ◽  
Charged Amino Acids ◽  
Structure Activity ◽  
Relationship Study ◽  
Positively Charged

ABSTRACTWe performed a structure-activity relationship study of the antibiofilm plant-derived decapeptide OSIP108. Introduction of positively charged amino acids R, H, and K resulted in an up-to-5-fold-increased antibiofilm activity againstCandida albicanscompared to native OSIP108, whereas replacement of R9 resulted in complete abolishment of its antibiofilm activity. By combining the most promising amino acid substitutions, we found that the double-substituted OSIP108 analogue Q6R/G7K had an 8-fold-increased antibiofilm activity.

scholarly journals Derivatives of the Mouse Cathelicidin-Related Antimicrobial Peptide (CRAMP) Inhibit Fungal and Bacterial Biofilm Formation

2014 ◽  
Vol 58 (9) ◽  
pp. 5395-5404 ◽  
Author(s):  
Katrijn De Brucker ◽  
Nicolas Delattin ◽  
Stijn Robijns ◽  
Hans Steenackers ◽  
Natalie Verstraeten ◽  
...  
Keyword(s):  
Amino Acid ◽  
Antimicrobial Peptide ◽  
Inhibitory Activity ◽  
Biofilm Formation ◽  
Specific Activity ◽  
Cell Types ◽  
Bacterial Biofilm ◽  
Antibiofilm Activity ◽  
Content Type ◽  
Derivatives Of

ABSTRACTWe identified a 26-amino-acid truncated form of the 34-amino-acid cathelicidin-related antimicrobial peptide (CRAMP) in the islets of Langerhans of the murine pancreas. This peptide, P318, shares 67% identity with the LL-37 human antimicrobial peptide. As LL-37 displays antimicrobial and antibiofilm activity, we tested antifungal and antibiofilm activity of P318 against the fungal pathogenCandida albicans. P318 shows biofilm-specific activity as it inhibitsC. albicansbiofilm formation at 0.15 μM without affecting planktonic survival at that concentration. Next, we tested theC. albicansbiofilm-inhibitory activity of a series of truncated and alanine-substituted derivatives of P318. Based on the biofilm-inhibitory activity of these derivatives and the length of the peptides, we decided to synthesize the shortened alanine-substituted peptide at position 10 (AS10; KLKKIAQKIKNFFQKLVP). AS10 inhibitedC. albicansbiofilm formation at 0.22 μM and acted synergistically with amphotericin B and caspofungin against mature biofilms. AS10 also inhibited biofilm formation of different bacteria as well as of fungi and bacteria in a mixed biofilm. In addition, AS10 does not affect the viability or functionality of different cell types involved in osseointegration of an implant, pointing to the potential of AS10 for further development as a lead peptide to coat implants.

scholarly journals Shigella flexneri Adherence Factor Expression in In Vivo-Like Conditions

mSphere ◽  
2019 ◽  
Vol 4 (6) ◽  
Author(s):  
Rachael B. Chanin ◽  
Kourtney P. Nickerson ◽  
Alejandro Llanos-Chea ◽  
Jeticia R. Sistrunk ◽  
David A. Rasko ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Biofilm Formation ◽  
Bile Salts ◽  
Vaccine Development ◽  
Shigella Flexneri ◽  
Colonic Epithelium ◽  
Structural Genes ◽  
Content Type ◽  
Factor Expression

ABSTRACT The Shigella species are Gram-negative, facultative intracellular pathogens that invade the colonic epithelium and cause significant diarrheal disease. Despite extensive research on the pathogen, a comprehensive understanding of how Shigella initiates contact with epithelial cells remains unknown. Shigella maintains many of the same Escherichia coli adherence gene operons; however, at least one critical gene component in each operon is currently annotated as a pseudogene in reference genomes. These annotations, coupled with a lack of structures upon microscopic analysis following growth in laboratory media, have led the field to hypothesize that Shigella is unable to produce fimbriae or other traditional adherence factors. Nevertheless, our previous analyses have demonstrated that a combination of bile salts and glucose induces both biofilm formation and adherence to colonic epithelial cells. The goal of this study was to perform transcriptomic and genetic analyses to demonstrate that adherence gene operons in Shigella flexneri strain 2457T are functional, despite the gene annotations. Our results demonstrate that at least three structural genes facilitate S. flexneri 2457T adherence for epithelial cell contact and biofilm formation. Furthermore, our results demonstrate that host factors, namely, glucose and bile salts at their physiological concentrations in the small intestine, offer key environmental stimuli required for adherence factor expression in S. flexneri. This research may have a significant impact on Shigella vaccine development and further highlights the importance of utilizing in vivo-like conditions to study bacterial pathogenesis. IMPORTANCE Bacterial pathogens have evolved to regulate virulence gene expression at critical points in the colonization and infection processes to successfully cause disease. The Shigella species infect the epithelial cells lining the colon to result in millions of cases of diarrhea and a significant global health burden. As antibiotic resistance rates increase, understanding the mechanisms of infection is vital to ensure successful vaccine development. Despite significant gains in our understanding of Shigella infection, it remains unknown how the bacteria initiate contact with the colonic epithelium. Most pathogens harbor multiple adherence factors to facilitate this process, but Shigella was thought to have lost the ability to produce these factors. Interestingly, we have identified conditions that mimic some features of gastrointestinal transit and that enable Shigella to express adherence structural genes. This work highlights aspects of genetic regulation for Shigella adherence factors and may have a significant impact on future vaccine development.

scholarly journals Small Molecules Produced by Commensal Staphylococcus epidermidis Disrupt Formation of Biofilms by Staphylococcus aureus

2019 ◽  
Vol 86 (5) ◽  
Author(s):  
Thaís Glatthardt ◽  
Juliana Curityba de Mello Campos ◽  
Raiane Cardoso Chamon ◽  
Thiago Freitas de Sá Coimbra ◽  
Giulia de Almeida Rocha ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Proteinase K ◽  
Antibiofilm Activity ◽  
Skin Microbiome ◽  
Chronic Infections ◽  
Content Type ◽  
Treatment And Prevention

ABSTRACT The microbiota influences host health through several mechanisms, including protecting it from pathogen colonization. Staphylococcus epidermidis is one of the most frequently found species in the skin microbiota, and its presence can limit the development of pathogens such as Staphylococcus aureus. S. aureus causes diverse types of infections ranging from skin abscesses to bloodstream infections. Given the increasing prevalence of S. aureus drug-resistant strains, it is imperative to search for new strategies for treatment and prevention. Thus, we investigated the activity of molecules produced by a commensal S. epidermidis isolate against S. aureus biofilms. We showed that molecules present in S. epidermidis cell-free conditioned media (CFCM) caused a significant reduction in biofilm formation in most S. aureus clinical isolates, including all 4 agr types and agr-defective strains, without any impact on growth. S. epidermidis molecules also disrupted established S. aureus biofilms and reduced the antibiotic concentration required to eliminate them. Preliminary characterization of the active compound showed that its activity is resistant to heat, protease inhibitors, trypsin, proteinase K, and sodium periodate treatments, suggesting that it is not proteinaceous. RNA sequencing revealed that S. epidermidis-secreted molecules modulate the expression of hundreds of S. aureus genes, some of which are associated with biofilm production. Biofilm formation is one of the main virulence factors of S. aureus and has been associated with chronic infections and antimicrobial resistance. Therefore, molecules that can counteract this virulence factor may be promising alternatives as novel therapeutic agents to control S. aureus infections. IMPORTANCE S. aureus is a leading agent of infections worldwide, and its main virulence characteristic is the ability to produce biofilms on surfaces such as medical devices. Biofilms are known to confer increased resistance to antimicrobials and to the host immune responses, requiring aggressive antibiotic treatment and removal of the infected surface. Here, we investigated a new source of antibiofilm compounds, the skin microbiome. Specifically, we found that a commensal strain of S. epidermidis produces molecules with antibiofilm activity, leading to a significant decrease of S. aureus biofilm formation and to a reduction of previously established biofilms. The molecules potentiated the activity of antibiotics and affected the expression of hundreds of S. aureus genes, including those associated with biofilm formation. Our research highlights the search for compounds that can aid us in the fight against S. aureus infections.

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