scholarly journals Regulator RcsB Controls Prodigiosin Synthesis and Various Cellular Processes in Serratia marcescens JNB5-1

2020 ◽  
Vol 87 (2) ◽  
Author(s):  
Xuewei Pan ◽  
Mi Tang ◽  
Jiajia You ◽  
Fei Liu ◽  
Changhao Sun ◽  
...  
Keyword(s):  
Cell Motility ◽  
Serratia Marcescens ◽  
Biofilm Formation ◽  
Capsular Polysaccharide ◽  
Regulatory Mechanism ◽  
Acid Resistance ◽  
Content Type ◽  
Cellular Processes ◽  
Polysaccharide Production ◽  
Insight Into

ABSTRACT Prodigiosin (PG), a red linear tripyrrole pigment normally secreted by Serratia marcescens, has received attention for its reported immunosuppressive, antimicrobial, and anticancer properties. Although several genes have been shown to be important for prodigiosin synthesis, information on the regulatory mechanisms behind this cellular process remains limited. In this work, we identified that the transcriptional regulator RcsB encoding gene BVG90_13250 (rcsB) negatively controlled prodigiosin biosynthesis in S. marcescens. Disruption of rcsB conferred a remarkably increased production of prodigiosin. This phenotype corresponded to negative control of transcription of the prodigiosin-associated pig operon by RcsB, probably by binding to the promoter region of the prodigiosin synthesis positive regulator FlhDC. Moreover, using transcriptomics and further experiments, we revealed that RcsB also controlled some other important cellular processes, including swimming and swarming motilities, capsular polysaccharide production, biofilm formation, and acid resistance (AR), in S. marcescens. Collectively, this work proposes that RcsB is a prodigiosin synthesis repressor in S. marcescens and provides insight into the regulatory mechanism of RcsB in cell motility, capsular polysaccharide production, and acid resistance in S. marcescens. IMPORTANCE RcsB is a two-component response regulator in the Rcs phosphorelay system, and it plays versatile regulatory functions in Enterobacteriaceae. However, information on the function of the RcsB protein in bacteria, especially in S. marcescens, remains limited. In this work, we illustrated experimentally that the RcsB protein was involved in diverse cellular processes in S. marcescens, including prodigiosin synthesis, cell motility, capsular polysaccharide production, biofilm formation, and acid resistance. Additionally, the regulatory mechanism of the RcsB protein in these cellular processes was investigated. In conclusion, this work indicated that RcsB could be a regulator for prodigiosin synthesis and provides insight into the function of the RcsB protein in S. marcescens.

scholarly journals LysR-Type Transcriptional Regulator MetR Controls Prodigiosin Production, Methionine Biosynthesis, Cell Motility, H2O2 Tolerance, Heat Tolerance, and Exopolysaccharide Synthesis in Serratia marcescens

2019 ◽  
Vol 86 (4) ◽  
Author(s):  
Xuewei Pan ◽  
Changhao Sun ◽  
Mi Tang ◽  
Jiajia You ◽  
Tolbert Osire ◽  
...  
Keyword(s):  
Cell Motility ◽  
Serratia Marcescens ◽  
Heat Tolerance ◽  
Biofilm Formation ◽  
Regulatory Mechanisms ◽  
Ecological Niches ◽  
Methionine Biosynthesis ◽  
Mobility Shift ◽  
Content Type ◽  
Wide Range

ABSTRACT Prodigiosin, a secondary metabolite produced by Serratia marcescens, has attracted attention due to its immunosuppressive, antimicrobial, and anticancer properties. However, information on the regulatory mechanism behind prodigiosin biosynthesis in S. marcescens remains limited. In this work, a prodigiosin-hyperproducing strain with the BVG90_22495 gene disrupted (ZK66) was selected from a collection of Tn5G transposon insertion mutants. Using real-time quantitative PCR (RT-qPCR) analysis, β-galactosidase assays, transcriptomics analysis, and electrophoretic mobility shift assays (EMSAs), the LysR-type regulator MetR encoded by the BVG90_22495 gene was found to affect prodigiosin synthesis, and this correlated with MetR directly binding to the promoter region of the prodigiosin-synthesis positive regulator PigP and hence negatively regulated the expression of the prodigiosin-associated pig operon. More analyses revealed that MetR regulated some other important cellular processes, including methionine biosynthesis, cell motility, H2O2 tolerance, heat tolerance, exopolysaccharide synthesis, and biofilm formation in S. marcescens. Although MetR protein is highly conserved in many bacteria, we report here on the LysR-type regulator MetR exhibiting novel roles in negatively regulating prodigiosin synthesis and positively regulating heat tolerance, exopolysaccharide synthesis, and biofilm formation. IMPORTANCE Serratia marcescens, a Gram-negative bacterium, is found in a wide range of ecological niches and can produce several secondary metabolites, including prodigiosin, althiomycin, and serratamolide. Among them, prodigiosin shows diverse functions as an immunosuppressant, antimicrobial, and anticancer agent. However, the regulatory mechanisms behind prodigiosin synthesis in S. marcescens are not completely understood. Here, we adapted a transposon mutant library to identify the genes related to prodigiosin synthesis, and the BVG90_22495 gene encoding the LysR-type regulator MetR was found to negatively regulate prodigiosin synthesis. The molecular mechanism of the metR mutant hyperproducing prodigiosin was investigated. Additionally, we provided evidence supporting new roles for MetR in regulating methionine biosynthesis, cell motility, heat tolerance, H2O2 tolerance, and exopolysaccharide synthesis in S. marcescens. Collectively, this work provides novel insight into regulatory mechanisms of prodigiosin synthesis and uncovers novel roles for the highly conserved MetR protein in regulating prodigiosin synthesis, heat tolerance, exopolysaccharide (EPS) synthesis, and biofilm formation.

scholarly journals The Fructose-Specific Phosphotransferase System ofKlebsiella pneumoniaeIs Regulated by Global Regulator CRP and Linked to Virulence and Growth

2018 ◽  
Vol 86 (8) ◽  
Author(s):  
Disi Lin ◽  
JinMing Fan ◽  
Jingjie Wang ◽  
Long Liu ◽  
Li Xu ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Capsular Polysaccharide ◽  
Regulatory Mechanism ◽  
Opportunistic Pathogen ◽  
Receptor Protein ◽  
Global Regulator ◽  
Phosphotransferase System ◽  
Mobility Shift ◽  
Content Type ◽  
Mobility Shift Assay

ABSTRACTKlebsiella pneumoniaeis an opportunistic pathogen, and its hypervirulent variants cause serious invasive community-acquired infections. A genomic view ofK. pneumoniaeNTUH-2044 for the carbohydrate phosphotransferase system (PTS) found a putative fructose PTS, namely, the Frw PTS gene cluster. The deletion mutant and the complemented mutant offrwC(KP1_1992), which encodes the putative fructose-specific enzyme IIC, were constructed, and the phenotypes were characterized. This transmembrane PTS protein is responsible for fructose utilization.frwCdeletion can enhance biofilm formation and capsular polysaccharide (CPS) biosynthesis but decreases the growth rate and lethality in mice.frwC expression was repressed in the cyclic AMP receptor protein (CRP) mutant. Electrophoretic mobility shift assay showed that CRP can directly bind to the promoter offrwC. These results indicated thatfrwCexpression is controlled by CRP directly and that such regulation contributes to bacterial growth, CPS synthesis, and the virulence of theΔcrpstrain. The findings help elucidate fructose metabolism and the CRP regulatory mechanism inK. pneumoniae.

scholarly journals Serratia marcescens ShlA Pore-Forming Toxin Is Responsible for Early Induction of Autophagy in Host Cells and Is Transcriptionally Regulated by RcsB

2014 ◽  
Vol 82 (9) ◽  
pp. 3542-3554 ◽  
Author(s):  
Gisela Di Venanzio ◽  
Tatiana M. Stepanenko ◽  
Eleonora García Véscovi
Keyword(s):  
Serratia Marcescens ◽  
Promoter Region ◽  
Regulatory Mechanism ◽  
Host Cells ◽  
Binding Motif ◽  
Content Type ◽  
Life Threatening ◽  
Opportunistic Human Pathogen ◽  
Flagellar Biogenesis ◽  
Fine Tune

ABSTRACTSerratia marcescensis a Gram-negative bacterium that thrives in a wide variety of ambient niches and interacts with an ample range of hosts. As an opportunistic human pathogen, it has increased its clinical incidence in recent years, being responsible for life-threatening nosocomial infections.S. marcescensproduces numerous exoproteins with toxic effects, including the ShlA pore-forming toxin, which has been catalogued as its most potent cytotoxin. However, the regulatory mechanisms that govern ShlA expression, as well as its action toward the host, have remained unclear. We have shown thatS. marcescenselicits an autophagic response in host nonphagocytic cells. In this work, we determine that the expression of ShlA is responsible for the autophagic response that is promoted prior to bacterial internalization in epithelial cells. We show that a strain unable to express ShlA is no longer able to induce this autophagic mechanism, while heterologous expression of ShlA/ShlB suffices to confer on noninvasiveEscherichia colithe capacity to trigger autophagy. We also demonstrate thatshlBAharbors a binding motif for the RcsB regulator in its promoter region. RcsB-dependent control ofshlBAconstitutes a feed-forward regulatory mechanism that allows interplay with flagellar-biogenesis regulation. At the top of the circuit, activated RcsB downregulates expression of flagella by binding to theflhDCpromoter region, preventing FliA-activated transcription ofshlBA. Simultaneously, RcsB interaction within theshlBApromoter represses ShlA expression. This circuit offers multiple access points to fine-tune ShlA production. These findings also strengthen the case for an RcsB role in orchestrating the expression ofSerratiavirulence factors.

scholarly journals EDTA Inhibits Biofilm Formation, Extracellular Vesicular Secretion, and Shedding of the Capsular Polysaccharide Glucuronoxylomannan by Cryptococcus neoformans

2012 ◽  
Vol 78 (22) ◽  
pp. 7977-7984 ◽  
Author(s):  
Emma J. Robertson ◽  
Julie M. Wolf ◽  
Arturo Casadevall
Keyword(s):  
Cryptococcus Neoformans ◽  
Biofilm Formation ◽  
Capsular Polysaccharide ◽  
Inhibitory Effect ◽  
Antifungal Drugs ◽  
Biofilm Growth ◽  
Content Type ◽  
Sublethal Concentrations ◽  
Vesicular Secretion

ABSTRACTThe fungal pathogenCryptococcus neoformanscan grow as a biofilm on a range of synthetic and prosthetic materials. Cryptococcal biofilm formation can complicate the placement of shunts used to relieve increased intracranial pressure in cryptococcal meningitis and can serve as a nidus for chronic infection. Biofilms are generally advantageous to pathogensin vivo, as they can confer resistance to antimicrobial compounds, including fluconazole and voriconazole in the case ofC. neoformans. EDTA can inhibit biofilm formation by several microbes and enhances the susceptibility of biofilms to antifungal drugs. In this study, we evaluated the effect of sublethal concentrations of EDTA on the growth of cryptococcal biofilms. EDTA inhibited biofilm growth byC. neoformans, and the inhibition could be reversed by the addition of magnesium or calcium, implying that the inhibitory effect was by divalent cation starvation. EDTA also reduced the amount of the capsular polysaccharide glucuronoxylomannan shed into the biofilm matrix and decreased vesicular secretion from the cell, thus providing a potential mechanism for the inhibitory effect of this cation-chelating compound. Our data imply that the growth ofC. neoformansbiofilms requires the presence of divalent metals in the growth medium and suggest that cations are required for the export of materials needed for biofilm formation, possibly including extracellular vesicles.

scholarly journals The interplay of the type II TA system with other processes

2019 ◽  
Author(s):  
Wei Wen-ping ◽  
Jia Wan Zhong ◽  
Yang Min
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Environmental Stress ◽  
Regulatory Mechanism ◽  
Phage Infection ◽  
Type Ii ◽  
System Research ◽  
Cellular Processes ◽  
The Stability ◽  
And Function ◽  
Insight Into

The type II toxin antitoxin (TA) system is the most well-studied TA system and is widely distributed in bacteria, especially pathogens such as Mycobacterium tuberculosis. Type II TA system plays an important role in many cellular processes, including maintaining the stability of mobile genetic elements, and bacterial altruistic suicide in response to nutritional starvation, environmental stress and phage infection. Interactions between toxin proteins and antitoxin proteins are critical for the regulation and function of type II TA systems; indeed, the understanding of their function is mainly derived from interaction and regulation of paired TA system proteins. Nonetheless, investigating interaction between unpaired TA system proteins, and the interaction between TA system proteins and other functional proteins, are becoming more common and have provided new insight into the complexity of its regulatory mechanism. In this review, we outlined the cross-interaction between TA system proteins, and the interaction between TA system proteins and other functional proteins, and we are trying to explain novel mechanism of TA system in the regulation of cellular activities. On this basis, we further discussed the knowledge and physiological implications of the relevant aspects of TA system research.

scholarly journals Evidence for Cyclic Di-GMP-Mediated Signaling in Bacillus subtilis

2012 ◽  
Vol 194 (18) ◽  
pp. 5080-5090 ◽  
Author(s):  
Yun Chen ◽  
Yunrong Chai ◽  
Jian-hua Guo ◽  
Richard Losick
Keyword(s):  
Bacillus Subtilis ◽  
Biofilm Formation ◽  
Second Messenger ◽  
Negative Control ◽  
Gram Negative Bacteria ◽  
Flagellar Motor ◽  
Positive Bacterium ◽  
Content Type ◽  
Deletion Mutations ◽  
Cellular Processes

ABSTRACTCyclic di-GMP (c-di-GMP) is a second messenger that regulates diverse cellular processes in bacteria, including motility, biofilm formation, cell-cell signaling, and host colonization. Studies of c-di-GMP signaling have chiefly focused on Gram-negative bacteria. Here, we investigated c-di-GMP signaling in the Gram-positive bacteriumBacillus subtilisby constructing deletion mutations in genes predicted to be involved in the synthesis, breakdown, or response to the second messenger. We found that a putative c-di-GMP-degrading phosphodiesterase, YuxH, and a putative c-di-GMP receptor, YpfA, had strong influences on motility and that these effects depended on sequences similar to canonical EAL and RxxxR—D/NxSxxG motifs, respectively. Evidence indicates that YpfA inhibits motility by interacting with the flagellar motor protein MotA and thatyuxHis under the negative control of the master regulator Spo0A∼P. Based on these findings, we propose that YpfA inhibits motility in response to rising levels of c-di-GMP during entry into stationary phase due to the downregulation ofyuxHby Spo0A∼P. We also present evidence that YpfA has a mild influence on biofilm formation.In toto, our results demonstrate the existence of a functional c-di-GMP signaling system inB. subtilisthat directly inhibits motility and directly or indirectly influences biofilm formation.

scholarly journals The Transcriptional Regulator BpsR Controls the Growth ofBordetella bronchisepticaby Repressing Genes Involved in Nicotinic Acid Degradation

2018 ◽  
Vol 200 (12) ◽  
pp. e00712-17 ◽  
Author(s):  
Manita Guragain ◽  
Jamie Jennings-Gee ◽  
Natalia Cattelan ◽  
Mary Finger ◽  
Matt S. Conover ◽  
...  
Keyword(s):  
Nicotinic Acid ◽  
Biofilm Formation ◽  
Transcriptional Control ◽  
Bordetella Bronchiseptica ◽  
Negative Regulator ◽  
Growth Defect ◽  
Content Type ◽  
Polysaccharide Production ◽  
Expression Of Genes

ABSTRACTMany of the pathogenic species of the genusBordetellahave an absolute requirement for nicotinic acid (NA) for laboratory growth. These Gram-negative bacteria also harbor a gene cluster homologous to theniccluster ofPseudomonas putidawhich is involved in the aerobic degradation of NA and its transcriptional control. We report here that BpsR, a negative regulator of biofilm formation and Bps polysaccharide production, controls the growth ofBordetella bronchisepticaby repressing the expression ofnicgenes. The severe growth defect of the ΔbpsRstrain in Stainer-Scholte medium was restored by supplementation with NA, which also functioned as an inducer ofnicgenes at low micromolar concentrations that are usually present in animals and humans. Purified BpsR protein bound to thenicpromoter region, and its DNA binding activity was inhibited by 6-hydroxynicotinic acid (6-HNA), the first metabolite of the NA degradative pathway. Reporter assays with the isogenic mutant derivative of the wild-type (WT) strain harboring deletion innicA, which encodes a putative nicotinic acid hydroxylase responsible for conversion of NA to 6-HNA, showed that 6-HNA is the actual inducer of thenicgenes in the bacterial cell. Gene expression profiling further showed that BpsR dually activated and repressed the expression of genes associated with pathogenesis, transcriptional regulation, metabolism, and other cellular processes. We discuss the implications of these findings with respect to the selection of pyridines such as NA and quinolinic acid for optimum bacterial growth depending on the ecological niche.IMPORTANCEBpsR, the previously described regulator of biofilm formation and Bps polysaccharide production, controlsBordetella bronchisepticagrowth by regulating the expression of genes involved in the degradation of nicotinic acid (NA). 6-Hydroxynicotinic acid (6-HNA), the first metabolite of the NA degradation pathway prevented BpsR from binding to DNA and was the actualin vivoinducer. We hypothesize that BpsR enablesBordetellabacteria to efficiently and selectively utilize NA for their survival depending on the environment in which they reside. The results reported herein lay the foundation for future investigations of how BpsR and the alteration of its activity by NA orchestrate the control ofBordetellagrowth, metabolism, biofilm formation, and pathogenesis.

scholarly journals An IgaA/UmoB Family Protein fromSerratia marcescensRegulates Motility, Capsular Polysaccharide Biosynthesis, and Secondary Metabolite Production

2018 ◽  
Vol 84 (6) ◽  
Author(s):  
Nicholas A. Stella ◽  
Kimberly M. Brothers ◽  
Jake D. Callaghan ◽  
Angelina M. Passerini ◽  
Cihad Sigindere ◽  
...  
Keyword(s):  
Secondary Metabolites ◽  
Secondary Metabolite ◽  
Intracellular Signaling ◽  
Biofilm Formation ◽  
Capsular Polysaccharide ◽  
Biologically Active ◽  
Public Health Importance ◽  
Content Type ◽  
Polysaccharide Biosynthesis ◽  
Transcriptional Changes

ABSTRACTSecondary metabolites are an important source of pharmaceuticals and key modulators of microbe-microbe interactions. The bacteriumSerratia marcescensis part of theEnterobacteriaceaefamily of eubacteria and produces a number of biologically active secondary metabolites. In this study, we screened for novel regulators of secondary metabolites synthesized by a clinical isolate ofS. marcescensand found mutations in a gene for an uncharacterized UmoB/IgaA family member here namedgumB. Mutation ofgumBconferred a severe loss of the secondary metabolites prodigiosin and serratamolide. ThegumBmutation conferred pleiotropic phenotypes, including altered biofilm formation, highly increased capsular polysaccharide production, and loss of swimming and swarming motility. These phenotypes corresponded to transcriptional changes infimA,wecA, andflhD. Unlike other UmoB/IgaA family members,gumBwas found to be not essential for growth inS. marcescens, yetigaAfromSalmonella enterica,yrfFfromEscherichia coli, and an uncharacterized predicted ortholog fromKlebsiella pneumoniaecomplemented thegumBmutant secondary metabolite defects, suggesting highly conserved function. These data support the idea that UmoB/IgaA family proteins are functionally conserved and extend the known regulatory influence of UmoB/IgaA family proteins to the control of competition-associated secondary metabolites and biofilm formation.IMPORTANCEIgaA/UmoB family proteins are found in members of theEnterobacteriaceaefamily of bacteria, which are of environmental and public health importance. IgaA/UmoB family proteins are thought to be inner membrane proteins that report extracellular stresses to intracellular signaling pathways that respond to environmental challenge. This study introduces a new member of the IgaA/UmoB family and demonstrates a high degree of functional similarity between IgaA/UmoB family proteins. Moreover, this study extends the phenomena controlled by IgaA/UmoB family proteins to include the biosynthesis of antimicrobial secondary metabolites.

scholarly journals Species Widely Distributed in Halophilic Archaea Exhibit Opsin-Mediated Inhibition of Bacterioruberin Biosynthesis

2018 ◽  
Vol 201 (2) ◽  
Author(s):  
Ronald F. Peck ◽  
Serena M. Graham ◽  
Abby M. Gregory
Keyword(s):  
Regulatory Mechanism ◽  
Halophilic Archaea ◽  
Halobacterium Salinarum ◽  
Efficient Production ◽  
Carotenoid Pigment ◽  
Prosthetic Group ◽  
Content Type ◽  
Genes Encoding ◽  
The Common ◽  
Insight Into

ABSTRACT Halophilic Archaea are a distinctive pink color due to a carotenoid pigment called bacterioruberin. To sense or utilize light, many halophilic Archaea also produce rhodopsins, complexes of opsin proteins with a retinal prosthetic group. Both bacterioruberin and retinal are synthesized from isoprenoid precursors, with lycopene as the last shared intermediate. We previously described a regulatory mechanism by which Halobacterium salinarum bacterioopsin and Haloarcula vallismortis cruxopsin inhibit bacterioruberin synthesis catalyzed by lycopene elongase. In this work, we found that opsins in all three major Halobacteria clades inhibit bacterioruberin synthesis, suggesting that this regulatory mechanism existed in the common Halobacteria ancestor. Halophilic Archaea, which are generally heterotrophic and aerobic, likely evolved from an autotrophic, anaerobic methanogenic ancestor by acquiring many genes from Bacteria via lateral gene transfer. These bacterial “imports” include genes encoding opsins and lycopene elongases. To determine if opsins from Bacteria inhibit bacterioruberin synthesis, we tested bacterial opsins and found that an opsin from Curtobacterium, in the Actinobacteria phylum, inhibits bacterioruberin synthesis catalyzed by its own lycopene elongase, as well as that catalyzed by several archaeal enzymes. We also determined that the lycopene elongase from Halococcus salifodinae, a species from a family of Halobacteria lacking opsin homologs, retained the capacity to be inhibited by opsins. Together, our results indicate that opsin-mediated inhibition of bacterioruberin biosynthesis is a widely distributed mechanism found in both Archaea and Bacteria, possibly predating the divergence of the two domains. Further analysis may provide insight into the acquisition and evolution of the genes and their host species. IMPORTANCE All organisms use a variety of mechanisms to allocate limited resources to match their needs in their current environment. Here, we explore how halophilic microbes use a novel mechanism to allow efficient production of rhodopsin, a complex of an opsin protein and a retinal prosthetic group. We previously demonstrated that Halobacterium salinarum bacterioopsin directs available resources toward retinal by inhibiting synthesis of bacterioruberin, a molecule that shares precursors with retinal. In this work, we show that this mechanism can be carried out by proteins from halophilic Archaea that are not closely related to H. salinarum and those in at least one species of Bacteria. Therefore, opsin-mediated inhibition of bacterioruberin synthesis may be a highly conserved, ancient regulatory mechanism.

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.

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