scholarly journals Campylobacter jejuni Lipooligosaccharides Modulate Dendritic Cell-Mediated T Cell Polarization in a Sialic Acid Linkage-Dependent Manner

2011 ◽  
Vol 79 (7) ◽  
pp. 2681-2689 ◽  
Author(s):  
Marieke Bax ◽  
Mark L. Kuijf ◽  
Astrid P. Heikema ◽  
Wouter van Rijs ◽  
Sven C. M. Bruijns ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Campylobacter Jejuni ◽  
Cell Polarization ◽  
Neurological Deficits ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Content Type ◽  
Th Cell ◽  
Th Differentiation ◽  
Functional Consequences

ABSTRACTCarbohydrate mimicry betweenCampylobacter jejunilipooligosaccharides (LOS) and host neural gangliosides plays a crucial role in the pathogenesis of Guillain-Barré syndrome (GBS).Campylobacter jejuniLOS may mimic various gangliosides, which affects the immunogenicity and the type of neurological deficits in GBS patients. Previous studies have shown the interaction of LOS with sialic acid-specific siglec receptors, although the functional consequences remain unknown. Cells that express high levels of siglecs include dendritic cells (DCs), which are crucial for initiation and differentiation of immune responses. We confirm that α2,3-sialylated GD1a/GM1a mimic and α2,8-sialylated GD1c mimic LOS structures interact with recombinant Sn and siglec-7, respectively. Although the linkage of the terminal sialic acid of LOS did not regulate expression of DC maturation markers, it displayed clear opposite expression levels of interleukin-12 (IL-12) and OX40L, molecules involved in DC-mediated Th cell differentiation. Accordingly, targeting DC-expressed siglec-7 with α2,8-linked sialylated LOS resulted in Th1 responses, whereas Th2 responses were induced by targeting with LOS containing α2,3-linked sialic acid. Thus, our data demonstrate for the first time that depending on the sialylated composition ofCampylobacter jejuniLOS, specific Th differentiation programs are initiated, possibly through targeting of distinct DC-expressed siglecs.

scholarly journals The Host Antimicrobial Protein Calgranulin C Participates in the Control ofCampylobacter jejuniGrowth via Zinc Sequestration

2018 ◽  
Vol 86 (6) ◽  
Author(s):  
Janette M. Shank ◽  
Brittni R. Kelley ◽  
Joseph W. Jackson ◽  
Jessica L. Tweedie ◽  
Dana Franklin ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Poultry Meat ◽  
Antimicrobial Protein ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Full Resolution ◽  
Factor Alpha

ABSTRACTCampylobacter jejuniis a leading cause of bacterially derived gastroenteritis worldwide.Campylobacteris most commonly acquired through the consumption of undercooked poultry meat or through drinking contaminated water. Following ingestion,Campylobacteradheres to the intestinal epithelium and mucus layer, causing toxin-mediated inflammation and inhibition of fluid reabsorption. Currently, the human response to infection is relatively unknown, and animal hosts that model these responses are rare. As such, we examined patient fecal samples for the accumulation of the neutrophil protein calgranulin C during infection withCampylobacter jejuni. In response to infection, calgranulin C was significantly increased in the feces of humans. To determine whether calgranulin C accumulation occurs in an animal model, we examined disease in ferrets. Ferrets were effectively infected byC. jejuni, with peak fecal loads observed at day 3 postinfection and full resolution by day 12. Serum levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α) significantly increased in response to infection, which resulted in leukocyte trafficking to the colon. As a result, calgranulin C increased in the feces of ferrets at the time whenC. jejuniloads decreased. Further, the addition of purified calgranulin C toC. jejunicultures was found to inhibit growth in a zinc-dependent manner. These results suggest that upon infection withC. jejuni, leukocytes trafficked to the intestine release calgranulin C as a mechanism for inhibitingC. jejunigrowth.

scholarly journals Role of Neuraminidase-Producing Bacteria in Exposing Cryptic Carbohydrate Receptors forStreptococcus gordoniiAdherence

2018 ◽  
Vol 86 (7) ◽  
pp. e00068-18 ◽  
Author(s):  
Alex Wong ◽  
Margaret A. Grau ◽  
Anirudh K. Singh ◽  
Shireen A. Woodiga ◽  
Samantha J. King
Keyword(s):  
Sialic Acid ◽  
Oral Cavity ◽  
Bacterial Species ◽  
Dependent Manner ◽  
Neuraminidase Treatment ◽  
Content Type ◽  
Oral Epithelial Cells ◽  
Oral Environment ◽  
Oral Epithelial

ABSTRACTStreptococcus gordoniiis an early colonizer of the oral cavity. Although a variety ofS. gordoniiadherence mechanisms have been described, current dogma is that the major receptor forS. gordoniiis sialic acid. However, as many bacterial species in the oral cavity produce neuraminidase that can cleave terminal sialic acid, it is unclear whetherS. gordoniirelies on sialic acid for adherence to oral surfaces or if this species has developed alternative binding strategies. Previous studies have examined adherence to immobilized glycoconjugates and identified binding to additional glycans, but no prior studies have defined the contribution of these different glycan structures in adherence to oral epithelial cells. We determined that the majority ofS. gordoniistrains tested did not rely on sialic acid for efficient adherence. In fact, adherence of some strains was significantly increased following neuraminidase treatment. Further investigation of representative strains that do not rely on sialic acid for adherence revealed binding not only to sialic acid via the serine-rich repeat protein GspB but also to β-1,4-linked galactose. Adherence to this carbohydrate occurs via an unknown adhesin distinct from those utilized byStreptococcus oralisandStreptococcus pneumoniae. Demonstrating the potential biological relevance of binding to this cryptic receptor, we established thatS. oralisincreasesS. gordoniiadherence in a neuraminidase-dependent manner. These data suggest thatS. gordoniihas evolved to simultaneously utilize both terminal and cryptic receptors in response to the production of neuraminidase by other species in the oral environment.

scholarly journals Active Packaging of Immobilized Zinc Oxide Nanoparticles Controls Campylobacter jejuni in Raw Chicken Meat

2020 ◽  
Vol 86 (22) ◽  
Author(s):  
Mohammed J. Hakeem ◽  
Jinsong Feng ◽  
Azadeh Nilghaz ◽  
Luyao Ma ◽  
Hwai Chuin Seah ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Shelf Life ◽  
Campylobacter Jejuni ◽  
Zinc Oxide Nanoparticles ◽  
Chicken Meat ◽  
Oxide Nanoparticles ◽  
Dependent Manner ◽  
Zno Nps ◽  
Content Type ◽  
Active Food Packaging

ABSTRACT Zinc oxide nanoparticles (ZnO NPs) are regarded as a safe and stable antimicrobial that can inactivate bacteria by several potential working mechanisms. We aimed to incorporate ZnO NPs into packaging material to control Campylobacter in raw chicken meat. ZnO NPs were first incorporated into three-dimensional (3D) paper tubes to identify the lethal concentration against Campylobacter jejuni, which was selected as the working concentration to develop 2D functionalized absorbing pads by an ultrasound-assisted dipping technique. The functionalized pad was placed underneath raw chicken meat to inactivate C. jejuni and the predominant chicken microbiota at 4°C within 8 days of storage. Immobilized ZnO NPs at 0.856 mg/cm2 reduced C. jejuni from ∼4 log CFU/25 g raw chicken meat to an undetectable level after 3 days of storage. Analysis by inductively coupled plasma-optical emission spectroscopy showed that the Zn level increased from 0.02 to 0.17 mg/cm2 in treated raw chicken meat. Scanning electron microscopy validated the absence of nanoparticle migration onto raw chicken meat after treatment. Inactivation of C. jejuni was associated with the increase of lactic acid produced by Lactobacillus in raw chicken meat in a pH-dependent manner. Less than 5% of Zn2+ was released from ZnO NPs at neutral pH, while up to 88% was released when the pH was <3.5 within 2 days. Whole-transcriptome sequencing (RNA-Seq) analysis demonstrated a broad effect of ZnO NPs on genes involved in various cellular developmental processes as annotated by gene ontology. Taken together, the results indicate that functionalized absorbing pads inactivated C. jejuni in raw chicken meat by immobilized ZnO NPs along with the controllable released Zn2+. IMPORTANCE Prevalence of Campylobacter in raw poultry remains a major food microbiological safety challenge. Novel mitigation strategies are required to ensure the safety and quality of poultry products. Active food packaging can control pathogens without directly adding antimicrobials into the food matrix and extend the food’s shelf life. The functionalized absorbing pad with ZnO NPs developed in this study was able to inactivate C. jejuni in raw chicken meat and keep the meat free from C. jejuni contamination during shelf life without any observed migration of nanoparticles. The controllable conversion of immobilized ZnO NPs to free Zn2+ makes this approach safe and eco-friendly and paves the way for developing a novel intervention strategy for other high-risk foods. Our study applied nanotechnology to exploit an effective approach for Campylobacter control in raw chicken meat products.

scholarly journals 5-Lipoxygenase Negatively Regulates Th1 Response during Brucella abortus Infection in Mice

2015 ◽  
Vol 83 (3) ◽  
pp. 1210-1216 ◽  
Author(s):  
Júlia Silveira Fahel ◽  
Mariana Bueno de Souza ◽  
Marco Túlio Ribeiro Gomes ◽  
Patricia P. Corsetti ◽  
Natalia B. Carvalho ◽  
...  
Keyword(s):  
Brucella Abortus ◽  
Critical Role ◽  
Lipid Mediators ◽  
Negative Regulator ◽  
Host Responses ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Wild Type ◽  
Content Type ◽  
Deficient Mice

Brucella abortusis a Gram-negative bacterium that infects humans and cattle, causing a chronic inflammatory disease known as brucellosis. A Th1-mediated immune response plays a critical role in host control of this pathogen. Recent findings indicate contrasting roles for lipid mediators in host responses against infections. 5-Lipoxygenase (5-LO) is an enzyme required for the production of the lipid mediators leukotrienes and lipoxins. To determine the involvement of 5-LO in host responses toB. abortusinfection, we intraperitoneally infected wild-type and 5-LO-deficient mice and evaluated the progression of infection and concomitant expression of immune mediators. Here, we demonstrate thatB. abortusinduced the upregulation of 5-LO mRNA in wild-type mice. Moreover, this pathogen upregulated the production of the lipid mediators leukotriene B4and lipoxin A4in a 5-LO-dependent manner. 5-LO-deficient mice displayed lower bacterial burdens in the spleen and liver and less severe liver pathology, demonstrating an enhanced resistance to infection. Host resistance paralleled an increased expression of the proinflammatory mediators interleukin-12 (IL-12), gamma interferon (IFN-γ), and inducible nitric oxide synthase (iNOS) during the course of infection. Moreover, we demonstrated that 5-LO downregulated the expression of IL-12 in macrophages duringB. abortusinfection. Our results suggest that 5-LO has a major involvement inB. abortusinfection, by functioning as a negative regulator of the protective Th1 immune responses against this pathogen.

scholarly journals Type II Toxoplasma gondii Induction of CD40 on Infected Macrophages Enhances Interleukin-12 Responses

2014 ◽  
Vol 82 (10) ◽  
pp. 4047-4055 ◽  
Author(s):  
Pedro Morgado ◽  
Dattanand M. Sudarshana ◽  
Lanny Gov ◽  
Katherine S. Harker ◽  
Tonika Lam ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Transcript Level ◽  
Forward Genetics ◽  
Interleukin 12 ◽  
Type I ◽  
Dependent Manner ◽  
Type Ii ◽  
Content Type ◽  
Type Iii ◽  
Infected Cells

ABSTRACTToxoplasma gondiiis an obligate intracellular parasite that can cause severe neurological disease in infected humans. CD40 is a receptor on macrophages that plays a critical role in controllingT. gondiiinfection. We examined the regulation of CD40 on the surface ofT. gondii-infected bone marrow-derived macrophages (BMdMs).T. gondiiinduced CD40 expression both at the transcript level and on the cell surface, and interestingly, the effect was parasite strain specific: CD40 levels were dramatically increased in type IIT. gondii-infected BMdMs compared to type I- or type III-infected cells. Type II induction of CD40 was specific to cells harboring intracellular parasites and detectable as early as 6 h postinfection (hpi) at the transcript level. CD40 protein expression peaked at 18 hpi. Using forward genetics with progeny from a type II × type III cross, we found that CD40 induction mapped to a region of chromosome X that included the gene encoding the dense granule protein 15 (GRA15). Using type I parasites stably expressing the type II allele ofGRA15(GRA15II), we found that type I GRA15IIparasites induced the expression of CD40 on infected cells in an NF-κB-dependent manner. In addition, stable expression of hemagglutinin-tagged GRA15IIin THP-1 cells resulted in CD40 upregulation in the absence of infection. Since CD40 signaling contributes to interleukin-12 (IL-12) production, we examined IL-12 from infected macrophages and found that CD40L engagement of CD40 amplified the IL-12 response in type II-infected cells. These data indicate that GRA15IIinduction of CD40 promotes parasite immunity through the production of IL-12.

scholarly journals Helicobacter pylori VacA Suppresses Lactobacillus acidophilus-Induced Interferon Beta Signaling in Macrophages via Alterations in the Endocytic Pathway

mBio ◽  
2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Gudrun Weiss ◽  
Sam Forster ◽  
Aaron Irving ◽  
Michelle Tate ◽  
Richard L. Ferrero ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factor ◽  
Lactobacillus Acidophilus ◽  
Interferon Beta ◽  
Eradication Therapy ◽  
Endocytic Pathway ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Content Type ◽  
H Pylori

ABSTRACT Helicobacter pylori causes chronic gastritis and avoids elimination by the immune system of the infected host. The commensal bacterium Lactobacillus acidophilus has been suggested to exert beneficial effects as a supplement during H. pylori eradication therapy. In the present study, we applied whole-genome microarray analysis to compare the immune responses induced in murine bone marrow-derived macrophages (BMDMs) stimulated with L. acidophilus, H. pylori, or both bacteria in combination. While L. acidophilus induced a Th1-polarizing response characterized by high expression of interferon beta (IFN-β) and interleukin 12 (IL-12), H. pylori strongly induced the innate cytokines IL-1β and IL-1α. In BMDMs prestimulated with L. acidophilus, H. pylori blocked the expression of L. acidophilus-induced IFN-β and IL-12 and suppressed the expression of key regulators of the Rho, Rac, and Cdc42 GTPases. The inhibition of L. acidophilus-induced IFN-β was independent of H. pylori viability and the virulence factor CagPAI; however, a vacuolating cytotoxin (vacA) mutant was unable to block IFN-β. Confocal microscopy demonstrated that the addition of H. pylori to L. acidophilus-stimulated BMDMs redirects intracellular processing, leading to an accumulation of L. acidophilus in the endosomal and lysosomal compartments. Thus, our findings indicate that H. pylori inhibits the development of a strong Th1-polarizing response in BMDMs stimulated with L. acidophilus by blocking the production of IFN-β in a VacA-dependent manner. We suggest that this abrogation is caused by a redirection of the endocytotic pathway in the processing of L. acidophilus. IMPORTANCE Approximately half of the world’s population is infected with Helicobacter pylori. The factors that allow this pathogen to persist in the stomach and cause chronic infections have not yet been fully elucidated. In particular, how H. pylori avoids killing by macrophages, one of the main types of immune cell underlying the epithelium, remains elusive. Here we have shown that the H. pylori virulence factor VacA plays a key role by blocking the activation of innate cytokines induced by the probiotic Lactobacillus acidophilus in macrophages and suppresses the expression of key regulators required for the organization and dynamics of the intracellular cytoskeleton. Our results identify potential targets for the treatment of H. pylori infection and vaccination, since specific inhibition of the toxin VacA possibly allows the activation of an efficient immune response and thereby eradication of H. pylori in the host.

scholarly journals The Campylobacter jejuni Ferric Uptake Regulator Promotes Acid Survival and Cross-Protection against Oxidative Stress

2016 ◽  
Vol 84 (5) ◽  
pp. 1287-1300 ◽  
Author(s):  
Momen Askoura ◽  
Sabina Sarvan ◽  
Jean-François Couture ◽  
Alain Stintzi
Keyword(s):  
Oxidative Stress ◽  
Campylobacter Jejuni ◽  
Galleria Mellonella ◽  
Acid Stress ◽  
Cross Protection ◽  
Infection Model ◽  
Dependent Manner ◽  
Ferric Uptake Regulator ◽  
Content Type ◽  
Acidic Conditions

Campylobacter jejuniis a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanisms by whichC. jejunisurvives stomach acidity remain undefined. In the present study, we demonstrated that theC. jejuniferric uptake regulator (Fur) plays an important role inC. jejuniacid survival and acid-induced cross-protection against oxidative stress. AC. jejuniΔfurmutant was more sensitive to acid than the wild-type strain. Profiling of the acid stimulon of theC. jejuniΔfurmutant allowed us to uncover Fur-regulated genes under acidic conditions. In particular, Fur was found to upregulate genes involved in flagellar and cell envelope biogenesis upon acid stress, and mutants with deletions of these genes were found to be defective in surviving acid stress. Interestingly, prior acid exposure ofC. jejunicross-protected against oxidative stress in a catalase (KatA)- and Fur-dependent manner. Western blotting and reverse transcription-quantitative PCR revealed increased expression of KatA upon acid stress. Electrophoretic mobility shift assays (EMSAs) demonstrated that the binding affinity between Fur and thekatApromoter is reducedin vitrounder conditions of low pH, rationalizing the higher levels of expression ofkatAunder acidic conditions. Strikingly, the Δfurmutant exhibited reduced virulence in both human epithelial cells and theGalleria mellonellainfection model. Altogether, this is the first study showing that, in addition to its role in iron metabolism, Fur is an important regulator ofC. jejuniacid responses and this function cross-protects against oxidative stress. Moreover, our results clearly demonstrate Fur's important role inC. jejunipathogenesis.

scholarly journals In VivoMechanisms Involved in Enhanced Protection Utilizing an Fc Receptor-Targeted Mucosal Vaccine Platform in a Bacterial Vaccine and Challenge Model

2014 ◽  
Vol 83 (1) ◽  
pp. 77-89 ◽  
Author(s):  
Constantine Bitsaktsis ◽  
Zulfia Babadjanova ◽  
Edmund J. Gosselin
Keyword(s):  
Immune Responses ◽  
Mucosal Vaccine ◽  
Effector Memory ◽  
Interleukin 12 ◽  
Nasal Passage ◽  
Dependent Manner ◽  
Vaccine Platform ◽  
Universal Vaccine ◽  
Content Type

Targeting antigens (Ag) to Fcγ receptors (FcγR) intranasally (i.n.) enhances immunogenicity and protection against intracellular and extracellular pathogens. Specifically, we have demonstrated that targeting fixed (inactivated)Francisella tularensis(iFT) organisms to FcR in mice i.n., with MAb-iFT immune complexes, enhancesF. tularensis-specific immune responses and protection againstF. tularensischallenge. Furthermore, traditional adjuvant is not required. In addition, we have demonstrated that the increased immunogenicity following the targeting of iFT to FcR is due, in part, to enhanced dendritic cell (DC) maturation, enhanced internalization, and processing and presentation of iFT by DCs, as well as neonatal FcR (FcRn)-enhanced trafficking of iFT from the nasal passage to the nasal mucosa-associated lymphoid tissue (NALT). Using this immunization and challenge model, we expanded on these studies to identify specificin vivoimmune responses impacted and enhanced by FcR targeting of iFT i.n. Specifically, the results of this study demonstrate for the first time that targeting iFT to FcR increases the frequency of activated DCs within the lungs of MAb-iFT-immunized mice subsequent toF. tularensisLVS challenge. In addition, the frequency and number of gamma interferon (IFN-γ)-secreting effector memory (EM) CD4+T cells elicited byF. tularensisinfection (postimmunization) is increased in an interleukin 12 (IL-12)-dependent manner. In summary, these studies build significantly upon previously published work utilizing this vaccine platform. We have identified a number of additional mechanisms by which this novel, adjuvant-independent, FcR-targeted mucosal vaccine approach enhances immunity and protection against infection, while further validating its potential as a universal vaccine platform against mucosal pathogens.

scholarly journals Suppression of Staphylococcus aureus Superantigen-Independent Interferon Gamma Response by a Probiotic Polysaccharide

2020 ◽  
Vol 88 (4) ◽  
Author(s):  
Wonbeom Paik ◽  
Francis Alonzo ◽  
Katherine L. Knight
Keyword(s):  
Staphylococcus Aureus ◽  
Bloodstream Infection ◽  
Interferon Gamma ◽  
T Cell Activation ◽  
Cell Activation ◽  
Nk Cell ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Content Type ◽  
Ifn Γ

ABSTRACT Staphylococcus aureus is a Gram-positive opportunistic pathogen that causes a variety of diseases. Bloodstream infection is the most severe, with mortality rates reaching 20 to 50%. Exopolysaccharide (EPS) from the probiotic Bacillus subtilis reduces bacterial burden and inflammation during S. aureus bloodstream infection in mice. Protection is due, in part, to hybrid macrophages that restrict S. aureus growth through reactive oxygen species and to limiting superantigen-induced T cell activation and interferon gamma (IFN-γ) production during infection. A decrease in IFN-γ production was observed within 24 h after infection, and here, we investigated how EPS abrogates its production. We discovered that S. aureus uses a rapid, superantigen-independent mechanism to induce host IFN-γ and that this is mediated by interleukin-12 (IL-12) activation of NK cells. Furthermore, we found that EPS limits IFN-γ production by modulating host immunity in a Toll-like receptor 4 (TLR4)-dependent manner, a signaling pathway that is required for EPS-mediated protection from S. aureus infection in vivo. We conclude that EPS protects hosts from acute bloodstream S. aureus infection not only by inducing macrophages that restrict S. aureus growth and inhibit superantigen-activated T cells but also by limiting NK cell production of IFN-γ after S. aureus infection in a TLR4-dependent manner.

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.

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