21±0.33 ng/ml vs. 0.32±0.03 ng/ml, p<0.0001). In contrast, sFRP5 was not significantly altered in septic patients (19.72±3.06 ng/ml vs. 17.48±6.38 ng/ml, p=0.07). On admission to the ICU, wnt5a levels exhibited a significant positive correlation with the leukocyte count (rs=0.3797, p=0.004). Interestingly, in patients recovering

from sepsis, wnt5a levels significantly declined within 5 days (2.17±0.38 ng/ml to 1.03±0.28 ng/ml, p<0.01). In contrast, if sepsis was worsening, wnt5a levels increased in the same time period by trend (2.34±0.59 ng/ml to 3.25±1.02 ng/ml, p>0.05). sFRP5 levels did not significantly change throughout the study period. The wnt5a/sFRP5 system is altered in human sepsis and might therefore be of interest for future studies on molecular pathophysiology of this common human disease. “
“Infection

with hepatitis C virus (HCV) is a major risk factor for chronic hepatitis, PLX4032 learn more cirrhosis and hepatocellular carcinoma. Once robust cell culture systems for production of recombinant infectious HCV became available, evidence on molecular mechanisms underlying assembly and release of the virus particles began to accumulate. Recent studies have demonstrated that lipid droplets and viral nonstructural proteins play key roles in HCV morphogenesis. This review considers the current knowledge about maturation of HCV structural proteins and production of viral infectious particles. Hepatitis C virus, discovered in 1989, is a major causative agent of human liver diseases, infecting approximately 2% of the population (130 million people) worldwide

(1). HCV typically establishes a chronic infection in the liver that can lead to serious hepatic disorders, such as chronic hepatitis, hepatic cirrhosis and hepatocellular carcinoma. It has been shown that HCV, like many other RNA viruses, circulates in infected individuals as a population of diverse but closely Etofibrate related variants which are referred to as quasispecies (2). The quasispecies model of mixed virus populations may confer a significant survival advantage because the simultaneous presence of multiple variant genomes and/or the high rate of generation of new variants allow rapid selection of mutants which are better suited to new environmental conditions (3). No vaccine that can prevent this viral infection exists. At present, the approved therapy is a combination of pegylated interferon-alpha and ribavirin that successfully eradicates HCV in around one half of infected individuals (4). HCV is an enveloped plus-strand RNA virus of the Hepacivirus genus of the Flaviviridae family. The HCV genome is approximately 9.6 kb in length and consists of an open reading frame encoding a polyprotein of ∼3000 amino acids and UTRs located at the 5′ and 3′ termini. The UTRs are highly structured sequences encompassing critical cis-active RNA elements which are essential for genome replication and translation.

11–20 As the ablation of CD25-expressing cells almost uniformly augmented resistance with reduced recoverable in vivo pathogen

burden, Treg cells were appropriately described as ‘a dangerous necessity’ based on their detrimental roles in host defence and essential roles in sustaining immune tolerance.21 However, with the subsequent identification of Foxp3 as the lineage-defining marker for Treg cells, and the up-regulation of CD25 expression on activated T cells that occurs after infection, the conclusions of initial studies Dabrafenib using CD25 expression as a surrogate marker for Treg cells deserve critical buy Olaparib re-evaluation using experimental strategies that identify and manipulate these cells based on Foxp3 expression. This review will summarize the recent literature describing infection outcomes and the immune response to infection using approaches that manipulate Treg cells based on Foxp3 expression, and frame these conclusions in the context of previous studies evaluating the importance of CD25+ CD4+ Treg cells and the epidemiology of human infection. Although an over-simplification, this analysis will be subdivided for pathogens that primarily cause acute versus persistent infection.

For each type of infection, the impacts resulting from the manipulation of Foxp3+ cells in infection outcomes, relevance of Foxp3+ Treg-cell antigen specificity and individual Foxp3+ cell intrinsic molecules in mediating immune suppression are discussed (Table 1). Lastly, how shifts in Treg-cell suppression Guanylate cyclase 2C impact infection outcomes and our more basic understanding for how T cells are activated in vivo are also summarized. Pathogens that cause acute infection stimulate the activation of protective immune components almost immediately

after infection. When the pathogen dose or initial rate of pathogen replication are below a preset threshold (lethal dose), innate immune components keep the infection at bay until pathogen-specific adaptive immune effectors that more efficiently mediate pathogen eradication are expanded and mobilized. On the other hand, with higher inocula, these normally protective responses are overwhelmed and the host succumbs to infection. It is in this latter context that initial studies using Foxp3DTR transgenic mice that co-express the high-affinity human diphtheria toxin (DT) receptor with Foxp3, allowing Foxp3+ Treg cells to be selectively ablated with low-dose DT, first uncovered somewhat paradoxical protective roles for these cells in host defence.

Neurotoxic lesions or pharmacological inactivation of hippocampal areas CA3 or CA1 have been reported to produce different effects PD0325901 on the encoding and retrieval of contextual memories [47, 48]. The CA3 region, with its extensive recurrent collateral system, is thought to be a crucial site for hippocampal function. This region supports processes involved in spatial pattern association, spatial pattern completion, novelty detection, and short-term memory. The CA1 region supports processes associated with temporal pattern completion and intermediate-term

memory. Furthermore, CA3, in conjunction with CA1, supports temporal pattern separation [49]. In a water maze test, recent and remote memory are similarly impaired after hippocampal damage [50]. In the LBH589 present study, the distribution of methylene blue dyes in stereotactic injection is time dependent. Stereotactic injection of dye with infusion time of 30 min resulted in distribution of dye to the whole hippocampus and some diffusion to the lateral ventricle, suggesting that

LPS injection was not only detrimental to CA3 but also to the CA1 region. LPS injection causes microglia activation with subsequent neuronal death in CA3, which mirrors the impaired performance in the water maze test. In contrast, LPS combined with IL-13 injection triggered microglia death, reduced proinflammatory cytokine secretion [6], and decreased neuron death. This cascade of events improved performance on the water maze test. Due to the diffuse involvement of the whole hippocampus by stereotactic injection, the functional outcome is not solely attributable to CA3 but also to CA1 function. In conclusion, this study reveals that IL-13 induces ER stress, resulting in reduced damage of neuronal cells through calpain activation cleavage

of C/EBP-β and PPAR-γ, which parallel the PLA2-triggered C/EBP-α and COX-2 activation pathway. A proposed mechanism for IL-13-enhanced aggravated microglia death is shown in Figure 7. The current findings demonstrate the mechanisms involved in the regulation of IL-13 in activated microglia and point to new directions for therapeutic research on neuroinflammatory disorders. Many of the methods listed here have been published previously but are Progesterone repeated here for clarity [5]. LPS from Escherichia coli serotype 0111:B4 prepared by phenolic extraction and gel filtration chromatography obtained from Sigma-Aldrich. IL-13 was purchased from PeproTech. Calpain inhibitors were purchased from BIOMOL. Recombinant calpain was obtained from Merck Biosciences. Antibodies used in the present study were listed in Table 1. Lipofectin transfection reagent was purchased from Invitrogen. Specific siRNA and scrambled siRNA control were synthesized by Santa Cruz Biotechnology, Inc. or Dharmacon (Boulder, CO, USA). Other chemicals were of the best grade available from commercial sources.

BamHI-BamHI fragments hybridized INCB024360 with the probe D were ligated into the same site of pUC19, and the resulting plasmids transformed in E. coli H1717. Positive clones were selected by colony blot hybridization with the same probe, and one of the recombinant plasmids, termed pVMB1, was extracted (Fig. 2). The nucleotide sequence of the 5121-bp fragment from pVMB1 was determined by primer

walking. Two entire ORF located divergently were identified; these were named mhuAB (V. mimicus heme utilization). The two other partial genes (orf1 and orf4) were not relevant to iron acquisition or iron-regulated gene expression. As shown in Figure 3a, each of the mhuA and mhuB genes possesses the predicted RBS and promoter elements (−35 and −10). Potential Fur boxes sharing 15/19 and 12/19 base matches with the E. coli consensus Fur box (24) are located in the upstream regions of mhuA and mhuB, respectively, overlapping with the −35 elements. Although the normal initiation codon (AUG) was missing at the predicted start position of mhuB transcript, an alternative initiation codon, UUG (25), was found in seven bases downstream of the RBS. V. mimicus has been reported to produce 77-kDa (IutA) and 80-kDa IROMP, whose N-terminal amino acid sequences have been determined to be EEQTLFDEMV and EQQSQFNEVV,

respectively (9, 10). An amino acid sequence compatible with the latter Pexidartinib cell line was found in the N-terminal portion of the deduced amino acid sequence of MhuA. To gain better separation of the IROMP, SDS-PAGE was carried out under the conditions shown in Figure 3b. As a result, the IROMP were separated into five protein bands, and the N-terminal amino acid sequences of the smallest band and a second large-molecular weight band corresponded with those of 77-kDa IutA (Fig. 3b, lane 1, open arrowhead) and 80-kDa MhuA (Fig. 3b, lane 1, solid arrowhead), respectively. The functions of the three other IROMP are at present unknown.

The protein product of mhuA shared homology with the heme/hemoglobin receptors of Vibrio species (11, 12, 26), ranging from 33% to 62% identity and from 52% to 80% similarity (Table 2). Selected proteins were aligned with MhuA (Fig. Inositol monophosphatase 1 4). A probable TonB box (28NEVVVTA34) present in MhuA, which is thought to interact physically with TonB protein, was similar in amino acid sequence to those in the heme/hemoglobin receptors of other Vibrio species (1, 27). Furthermore, MhuA possesses FRTP and NPNL amino acid boxes characteristic of the bacterial heme/hemoglobin receptors (28). However, the conserved histidine residue between FRTP and NPNL boxes (corresponding to His-461 in the Yersinia enterocolitica HemR, a receptor for heme/heme-containing proteins) (28) was not found in MhuA.

They include the assimilation of cholesterol, cholesterol binding to the SRT1720 cell line bacterial cell wall, microbial transformation of cholesterol to coprostanol, and enzymatic deconjugation of bile salts (7, 8, 11, 12). Gilliland et al. (7) found that certain Lactobacillus acidophilus strains could assimilate the cholesterol in the growth medium, thus making it unavailable for absorption from the intestines into the blood. Another plausible mechanism of cholesterol removal is the binding of cholesterol to bacterial cells. Nakajima et al. (8) focused on the cholesterol-lowering activity of milk fermented with an EPS-producing lactic acid bacterium. The authors reported that EPS has a

potential to interfere with the absorption of cholesterol, or

of bile acids, from the intestines by binding and removing them from the body in a manner similar to selleck screening library the process that was reported for plant-based polysaccharides or dietary fiber. Artificial cell microencapsulation (immobilization) is a technique used to encapsulate biologically active materials in specialized ultra-thin semi-permeable polymer membranes (13). Jones et al. (6) examined the potential of artificial cell-microencapsulated genetically engineered Lactobacillus plantarum 80 (pCBH1) cells for bile acid deconjugation to lower cholesterol. Researchers found that microencapsulated cells deconjugated tested bile salts successfully. However, to the best of our knowledge, the literature contains no report evaluating cholesterol removal by immobilized cells using other possible Oxalosuccinic acid mechanisms. The aims of the present study were to evaluate: (i) the relationship between EPS production and cholesterol removal rates; (ii) cholesterol removal by dead and resting cells; (iii) the effect of cholesterol on EPS production; and (iv) the immobilization

effect on cholesterol removal by five strains of Lactobacillus delbrueckii subsp. bulgaricus, isolated from home-made yoghurt and selected according to their exopolysaccharide production capacity. Lactobacillus delbrueckii subsp. bulgaricus strains used in this study were obtained from the stock collection of Biotechnology Laboratory at Gazi University, Faculty of Science and Arts, Department of Biology (Ankara, Turkey). L. delbrueckii subsp. bulgaricus ATCC 11842 was from the American Type Culture Collection (Rockville, MD, USA) and the other strains were isolated from traditional home-made yoghurt. Their identity and EPS production capacity were confirmed as previously described (14). The cultures were maintained by subculturing 1% inocula into MRS broth (Lactobacillus medium according to de Man Rogosa & Sharpe; Merck, Darmstadt, Germany) and incubating them for 18 hr at 42°C. All of the Lactobacillus strains had been stored at −20°C in MRS broth with 10/100 ml glycerol, and subcultured twice until they were used in the experiments.

In an excellent review of measures of oxidative stress, Halliwell and colleagues

discuss more broadly the different measures of oxidative stress, including reasons leading to poor correspondence between markers, like the rapid metabolism of isoprostanes compared with the slower metabolism of oxidized proteins.51 Two major goals for controlling development of CKD are early detection and slowing progression to end-stage renal disease. Using oxidative stress biomarkers in a panel of biomarkers of processes known to impact on CKD development may allow early click here detection. Slowing its development is more problematic. Traditionally, inhibition of the renin-angiotensin-aldosterone system has been used to slow the progression of CKD,54 with established therapies relying on pharmacologic blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. However, decline of GFR and elevated serum creatinine have continued in treated patients,55,56 and the need for novel treatments and interventions continues. Although the prophylactic use of anti-oxidant therapies in the treatment and amelioration of CKD is still in dispute, oxidant dysregulation occurs with age and age is one of the greatest risk factors for CKD. Some modifiable pathways and anti-oxidant treatments are summarized in Figure 2. There are many anti-oxidants that might be mentioned here,

but we have selected some that have some demonstrated benefits in CKD. Vitamin E comprises a family of eight different lipid-soluble tocopherols and GS-1101 molecular weight tocotrienols that scavenge free radicals by incorporating into the plasma membrane of cells, thus halting lipid peroxidation chain reactions.57 Vitamin E foodstuffs primarily consist of α-tocotrienol, which has a higher anti-oxidant efficacy; however, α-tocopherol has higher bioavailability in vivo than the other

seven compounds and so the focus has been on its usage. The basis of vitamin E supplementation is to enhance α-tocopherol levels in cell plasma membranes to prevent lipid peroxidation and resultant oxidative stress. Vitamin E is often delivered with vitamin Benzatropine C in an attempt to boost the anti-oxidant efficacy, as vitamin C has been shown to assist in recycling vitamin E. One drawback of α-tocopherol is that it takes several days of pretreatment to exhibit anti-oxidant effects.58 Trolox (±-6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid), is an analogue of α-tocopherol that has shown far better free radical scavenging properties owing to its water solubility. The majority of in vivo studies using Trolox have reported beneficial effects in acute cases of renal injury such as ischaemia reperfusion, due to rapid solubility and increased potency.59 A combination supplement containing both α-tocopherol and Trolox may offer greater efficacy due to the fast-acting activities of Trolox combined with the sustained scavenging actions of α-tocopherol.

1). Excessive Treg activity is observed in persistent

infections such as murine models of Leishmaniasis, malaria and tuberculosis [39–41] and in human diseases such as upper GI persistence of Helicobacter pylori, human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infections [42–45], suggesting the possibility of a link between pathogen persistence and Treg-mediated suppression. Subversion of Treg function for the generation of appropriate immune responses to effect efficient pathogen clearance may therefore be an advantage or, indeed, a necessity. Indeed, accumulating evidence supports the selleck chemicals llc assertion that interactions between Tregs and an infective/inflammatory environment leads to the subversion of their suppressive function. The salient experiments demonstrate a direct effect of Toll-like receptor (TLR) ligation on Tregs to block their suppression [46,47] and modulation of dendritic cell (DC) activity by lipopolysaccharide (LPS) to induce restricted Treg activity [48] in a manner that is

independent of direct ligation of the TLR on Tregs[49,50]. Indeed, appropriately activated DC can break the ‘anergic’ state of Tregs and promote proliferation in this usually hypoproliferative population [51]. Our own (unpublished) observations and those of others suggest that proinflammatory cytokines, selleck inhibitor in particular IL-1β, IL-6 and tumour necrosis factor (TNF)-α, released by DC following interaction with pathogens, can subvert the suppressive effects of Tregs. Both IL-1β and IL-6 can block Treg-mediated suppression of effector cell proliferation [48,52], although IL-6 may require the presence of IL-1 to overcome regulation [49]. There are some data from humans to suggest that TNF-α

can inhibit Treg function [53] with some supporting, but circumstantial, evidence showing a numerical increase in forkhead box P3 (FoxP3)+ CYTH4 T cells and restoration of defective regulatory function in patients with rheumatoid arthritis treated with anti-TNF-α therapy [54]. The inevitable question is whether subverted Tregs remain ‘dormant’ Tregs or undergo a stable change of phenotype to an alternative lineage. IL-17 is a proinflammatory cytokine with non-redundant functions in the clearance of extracellular pathogens (see also [55] for further detail). This is seen readily in both IL-17R-deficient mice, which demonstrate great susceptibility to lethal bacterial infections [56,57], and in IL-17-deficient humans as part of the hyper-immunoglobulin E (IgE) syndrome (HIES), where recurrent infections are a feature [58,59]. The significant proinflammatory features of IL-17 have been reviewed previously, as has the compelling evidence for the role of IL-17 in inflammatory/autoimmune conditions of mice and the considerable body of evidence suggesting an important role for IL-17 in the aetiopathogenesis of inflammatory and autoimmune diseases in humans [60,61].

Equivalent OD600 nm for each extract was used for serial twofold see more dilutions. Two microliters of each dilution was applied to a nitrocellulose membrane (Hybond; Amersham). OMP immunodetection was performed with the following monoclonal antibodies (MAbs) (ref.): anti-lipopolysaccharide (A76/12G12/F12) anti-Omp16 MAb (A68/08C03/G03) at 1/100 anti-Omp25 MAb (A68/4B10/F5) at 1/100, anti-Omp31 MAb (A59/10F9/G10) at 1/10 and anti-Omp36 Mab (A68/25G5/A5) at 1/100. Horseradish peroxidase-conjugated goat antimouse antibodies (Amersham) were used at 1/5000 along with the ECL system (Amersham)

to develop blots for chemoluminescence before visualization on film. Dot blots using MAbs specific for Omp16 (PAL lipoprotein) were used as internal loading controls. Brucella melitensis were grown for 20 h in 2YT medium at 37 °C.

Bacteria pellets were fixed overnight in a solution containing 2.5% glutaraldehyde and 0.1 M phosphate Lorlatinib buffer (pH 7.4). After fixation, cells were washed, postfixed with 1% osmium tetroxide for 1 h, washed again and subjected to serial dehydration with ethanol. Samples were embedded in resin, thin-sectioned and stained with uranyl acetate and Reynold’s lead citrate. Finally, the samples were examined using a TEM (Technai 10; Philips) at the Unité Interfacultaire de Microscopie Electronique (University of Namur, Belgium). The surface attachment assay was performed using the crystal violet method, as described previously (O’Toole Tolmetin et al., 1999): 200 μL cultures were grown overnight in a 96-well polystyrene plate in 2YT medium. Plates were incubated at 37 °C for 20 h with agitation. Biofilm formation was assayed by the ability of cells to adhere to the polystyrene wells. The liquid medium was removed and the attached cells were washed with sterile PBS (pH 7.4). The attached bacteria were visualized by staining with 0.05% solution of crystal violet

(GRAM’S solution; Merck) for 2 min at room temperature, followed by rinsing with water and air drying. Quantification of surface-attached bacteria was achieved by dissolving crystal violet in 200 μL of 100% ethanol. The ethanol was transferred and the volume was brought to 1 mL with dH2O and the absorbance was determined at 596 nm in a spectrophotometer (Genesys). The infections of HeLa cells were performed as described previously (Delrue et al., 2001). A ΔvjbR mutant was used as a negative control for replication defects during the cellular infection. Each infection was perfomed in triplicate. The adherence of Brucella strains to monolayers of HeLa cells was performed on glass cover slips according to the protocol described in Castaňeda-Roldán et al. (2004). Plates were centrifuged for 10 min at 200 g at room temperature in a Jouan centrifuge and placed in a 5% CO2 atmosphere at 37 °C. After 1, 6, 24, 30 and 48 h of infection, wells were washed three times with PBS and incubated for 20 min with 4% paraformaldehyde to fix cells and bacteria.

This is also supported by the observation that the immune cell infiltration is blocked after repeated treatment with FK506. Moreover, the symptom development correlates well with the increased production of humoral factors implicated in the pathogenesis of inflammatory skin diseases from keratinocytes. These results suggest a mechanism underlying the dermatitis development in K5-PLCε-TG mice as depicted in Fig. 10; hyperactivation of the PLCε-mediated signaling in keratinocytes upregulates the production of humoral factors possessing the function of recruitment and/or activation of immune cells such as Th cells, and the

resulting immune cells produce proinflammatory factors leading to the symptom selleck screening library development. FK506 Among the factors highly produced by PLCε-overexpressing

keratinocytes, IL-23 seems to play a crucial role in the development of the skin symptoms in K5-PLCε-TG mice because the symptoms were suppressed by its blockade (Fig. 8). This is supported by the observation that the symptom development in K5-PLCε-TG mice correlates well with the infiltration of IL-22-producing CD4+ T cells, which are likely to be Th17 cells activated by IL-23 26, 31. Also, chemokines, such as CCL20 and CXCL10 (Fig. 7), are likely to be involved in the symptom development in K5-PLCε-TG mice through inducing Th-cell infiltration. Most of the Th cells accumulated in the symptomatic K5-PLCε-TG mouse skin are

IL-22-producing Th cells (Fig. 6), which is different from the case of the hapten-induced contact hypersensitivity model where essentially no IL-22-producing cells were detected 18. Another difference between these two cases is that Th-cell infiltration in K5-PLCε-TG mice depends on the PLCε genotype whereas that in the contact hypersensitivity model is PLCε-independent 18. These may be accounted for by the difference in the cellular context that influences Th-cell infiltration. In addition to Th cells, Gr-1+ neutrophils may contribute as IL-17 producers (Fig. 6) to the symptom development in K5-PLCε-TG mice. DC may play a role through antigen presentation, Methamphetamine cytokine production upon TLR engagement, etc. 1, 3. DC infiltration at P6, which precedes T-cell infiltration and the symptom development, can be ascribed to elevated expression of CCL20, a chemokine with chemotactic activity for DC precursors 11. The elevated expression of Camp in the whole skin of K5-PLCε-TG mice is intriguing because it was reported that its human ortholog LL-37 could activate pDC upon binding with self-DNA and TLR9 12. Further characterization of T cells and DC accumulated in the symptomatic skin of K5-PLCε-TG mice will provide insights into the mechanism of the skin phenotype development.

, 2002; Lamari et al., 2004), or an extracellular ‘lipid S’ of S. epidermidis (Elliott et al., 2000). In most cases, the chemical structure of the antigens has not been determined. To date, none of these antigens have

led to the development Protease Inhibitor Library cell assay of a commercialized diagnostic test. We have chosen to test, as an antigen for a serodiagnostic, the PNAG, a characteristic and well-characterized component of staphylococcal biofilms (Sadovskaya et al., 2007). As a first step of our study, we investigated cases of chronic infections caused by the strains known as PNAG producers. This problem could be addressed thanks to a TC-GP animal model, mimicking an implant-related infection (Chokr et al., 2007), and a collection of staphylococcal strains with a well-characterized biofilm composition (Sadovskaya et al., 2005, 2006). We developed a sensible ELISA essay, which included coating the Microlon 600 plates with the preparations of purified PNAG, incubation with the animal or human sera, and detection of the bound anti-PNAG antibodies with the appropriate HRP- or AP-conjugated secondary antibodies (Sadovskaya et al., 2007). We have shown that in the chosen animal model, the levels of anti-PNAG antibodies were significantly

higher in guinea-pigs infected with S. epidermidis RP62A compared with healthy animals selleck kinase inhibitor (P>0.01). When the evolution of an antibody response to PNAG in individual guinea-pigs was studied, we observed an increase of the level of antibodies following the implant-related

infection. The results were more ambiguous with human sera. Screening of patients’ sera and the sera of healthy individuals reveals a relatively high level of anti-PNAG immunoglobulin Gs (IgGs) in the sera of healthy controls. The level of these IgGs in patients’ sera was very variable and overall higher, but the difference was insignificant (P>0.05). If this result is rather disappointing, it is nevertheless interesting to try to understand the reason for this phenomenon. Despite the fact that the presence of the ica operon is considered as a marker discriminating between clinical device-associated strains and skin flora (Galdbart et al., 2000; Kozitskaya et al., 2005), Erlotinib cost a significant percentage of commensal CoNS strains in healthy individuals is ica-positive and potentially capable of producing PNAG. The presence of anti-PNAG IgGs in the sera of healthy individuals could thus be explained by their natural exposure to PNAG-producing CoNS and Gram-negative bacteria, the possible presence of these antigens in common vaccine preparations, as well as previous infections and nasal carriage of S. aureus. Biofilm is considered as a main virulence factor of CoNS, a major cause of medical implant-associated infections. Targeting the bacterial biofilm state and particularly the EPS matrix might be a key for the development of therapeutic tools against these infections. We have particularly focused on the biofilm of S.