This Dasatinib molecular weight indicates a fundamentally different innate response to infection between WT and MMP-9−/− mice which may contribute to an atypical fecal microbiome in MMP-9−/− mice. Recent evidence also indicates that MMPs regulate the intercellular expression of several key mediators of cell-cell binding including claudin-5 and occludin [30]. For instance, in the context

of lung injury, the pore-forming cytotoxin α-hemolysin from Staphylococcus aureus upregulates the zinc-dependent metalloprotease ADAM10, resulting in cleavage of E-cadherin and disruption of intercellular tight junctions [31]. Most MMPs are secreted factors, but many of the proteases localize to cell surfaces where they associate with and regulate a variety of adhesion molecules, such as CD44 and β-integrins [32, 33]. This indicates that MMPs could alter the binding efficiency of intestinal bacteria to VE 821 host colonocytes, thereby altering the pathobiology of an infectious colitis. MMP-7 also affects gut microbe homeostasis through cleavage of reduced cyptdin-4 (r-Crp4), a mouse Paneth cell-derived Ulixertinib α-defensin. In an in vitro model, cleavage of the peptide resulted in increased survival of Salmonella enterica serovar Typhimurium, E. coli ML35, Staphylococcus aureus, Bifidobacterium

bifidum, Bifidobacterium longum, Lactobacillus casei Bacteroides thetaiotaomicron, and Bacteroides vulgatus relative to undigested r-Crp4 [34]. Therefore, the OSBPL9 presence of MMPs in the colonic mucosa can mediate physiological parameters that impact on both gut homeostasis and host-microbe interactions. Disruption of these interactions

leads to an altered microbial ecology and disease [35]. Segmented filamentous bacteria (SFB) “”Arthromitus immunis” [36]; provides mucosal protection against C. rodentium infection, as well as mediates the production of the proinflammatory cytokines IL-17 and IL-22 [23]. In the present study, qPCR analysis of the fecal microbiome revealed a larger population of SFB and higher mRNA levels of IL-17 in MMP-9−/− mice compared to WT controls, even under baseline conditions. “A. immunis” inhibits colonization of rabbit enteropathogenic Escherichia coli O103 and protects against subsequent disease development [37]. In this study, electropherograms showed that C. rodentium became a dominant component of the detectable microbiota in WT, but not MMP-9−/− mice. As noted by others [37], this study shows that the presence of SFB may provide protection against C. rodentium colonization, although our results demonstrate that commensal SFB does not offer full protection against C. rodentium-induced colitis in C57BL/6 J mice. This observation emphasizes that a shift in the bacterial population does not have an all-or-none effect; rather, it produces a graded series of responses. In previous studies, infection of C57BL/6 J mice with C. rodentium reduced fecal microbial diversity and evenness due to the dominance of C.

Our cell aggregation assay also showed that hypoxia inhibited hepatoma cell aggregation in our study (data not shown). To explore whether Tg737 is involved in invasion and migration induced by hypoxia, we examined the different expression

levels of Tg737 under normoxic and hypoxic conditions. The data confirmed that hypoxia induced the downregulation of Tg737 expression in HCC cell lines. In addition, hypoxia induced changes in adhesion, and the migration and invasion capacities of HCC cells were abrogated by restoring Tg737 expression levels. Taken together, these results suggest that hypoxia may increase the invasion and migration of HCC cells in a Tg737-dependent manner. The hypoxia-induced invasion and migration mediated by Tg737 is poorly understood. A hallmark of the invasion and migration of solid tumors is that this process requires cell-cell/matrix molecules that influence the adhesion, JPH203 purchase migration, and invasion of cancer cells [30]. Polycystin-1 is a large, plasma membrane receptor encoded by the PKD1 gene, which is mutated in autosomal-dominant polycystic kidney disease (ADPKD). Polycystin-1 is involved in several biological functions including proliferation, morphogenesis, and anti-apoptotic processes [31, 32]. Moreover, polycystin-1 appears to be associated with the focal adhesion

proteins talin, vinculin, FAK and paxillin [33]. Zhang et al. [9] also found that polycystin-1 influences the adhesion, migration, and invasion of cancer cells. As stated above, polycystin-1 is thought to be a cell adhesion molecule, see more possibly a member of the immunoglobulin superfamily of cell adhesion molecules. Furthermore, preliminary yeast 2-hybrid screens with Tg737 have identified several potential protein partners, including www.selleckchem.com/products/prt062607-p505-15-hcl.html polycystin 1, catenin, P120 catenin, Snx1, and HNF4α [34]. Due to the importance of polycystin 1 in the adhesion, invasion

and migration of cancer cells and as a potential protein partner of Tg737, we hypothesized that Tg737-mediated hypoxia-induced increases in invasion and migration 17-DMAG (Alvespimycin) HCl require polycystin 1. As shown in our results, the expression of both Tg737 and polycystin 1 decreased after exposure of HCC cells to hypoxia. Moreover, the expression of polycystin 1 was restored under hypoxia by transfection of pcDNA3.1-Tg737. These data suggest that the effects of Tg737 on HCC cell migration and invasion under hypoxia may be at least partially mediated by the polycystin 1 pathway. A large amount of evidence suggests that some cytokines and chemokines secreted by cancer cells are important modulators of migration and invasion. Among these, IL-8 and TGF-β1 have important roles in the invasion and metastasis of many types of tumors [35, 36]. Furthermore, IL-8 and TGF-β1 signaling were recently investigated during the progression of ADPKD in PKD1 mutant models [37, 38].

In many plant beneficial rhizobacteria, QS mechanisms induce the synthesis of antimicrobial secondary metabolites and extracellular lytic enzymes with inhibitory effects towards other bacteria, fungi, protozoa, and nematodes [12]. The quorum quenching strategy using the lactonase AiiA was exploited to simultaneously quench the two AHL systems discovered in the endophytic strain G3 of S. plymuthica and

Torin 2 price investigate their role in controlling biocontrol-related phenotypes. The phenotypic analysis revealed that the strain G3/pME6863 expressing aiiA had https://www.selleckchem.com/products/isrib-trans-isomer.html reduced antifungal activity, chitinolytic and proteolytic activities, but increased of IAA biosynthesis, and had no impact on siderophore production compared with the strain carrying the vector TPX-0005 control G3/pME6000 and the wild type G3, indicating that QS control multiple biocontrol-related phenotypes in this strain. These results are in agreement with previous observations in the rhizospheric S. plymuthica HRO-C48 expressing AHL lactonases [14]. Depletion of AHLs with this lactonase resulted in altered adhesion and biofilm formation in vitro.

This was different from the closely related S. plymuthica strains HRO-C48 and RVH1, where biofilm formation for both strains is AHL-independent. In addition, in contrast to HRO-C48, swimming motility was not controlled by AHL-mediated QS [14, 33]. Attachment is required for biofilm formation and these are key processes in the interaction between bacteria and plant tissues which have been shown to rely on quorum sensing [44]. For example, in the biocontrol bacterium Pseudomonas chlororaphis strain 30-84, QS systems and their control over phenazine production play a role in the successful formation of surface-attached

populations required for biofilm formation. Transcriptome analysis revealed that phenazines as signals, up-regulated many of the genes related to cell adhesion and biofilm development, such old as fimbrial and lipopolysaccharides (LPS) genes [45]. The SwrIR quorum sensing system in S. marcescens MG1 plays a key role in biofilm development, from attachment to swarming motility, biofilm maturation and detachment, although QS regulation of adhesion in MG1 is surface dependent [37]. In S. marcescens strain 12, biofilm formation seems to rely on smaI, although this was measured using an attachment assay to a plastic microtitre plate [38], where SmaI is mainly responsible for C4-HSL synthesis. Pantoea stewartii causing Stewart’s vascular wilt and leaf blight in sweet corn and maize utilizes the EsaI/EsaR QS system to control virulence and effective colonization. EsaI shares 80% similarity to SplI of G3 and is a typical AHL synthase that also catalyzes preferentially the synthesis of 3-oxo-C6-HSL.

F and Fw colonies are characterized by a typical massive rim, hence rimmed, in contrast to rimless (R, W) colonies. Colonies of the parental R strain and all daughter

clones have a finite growth, their diameter being in rimmed clones about 15 mm, in rimless ones about 20 mm (after 10 days’ growth). Colonies ripen into final color and pattern by about 7th day upon planting, while learn more still growing slowly, to reach their final diameter by day 15 (Figure 1a). Figure 1 Summary of clone phenotypes under various growth conditions. a. Comparison of two basic phenotypes: R (rimless “”wild type”") and F (rimmed) Top: appearance of colonies at given time-points; middle – sketches (contours and cross-sections) of fully developed colonies; bottom – time-course of colony growth (N = 10-16 for each point, +/- SD). b. Dependence of colony patterning (7 days old) on the density of Selleckchem Sirolimus planting (shown below the figures; bar = 1 cm). Note confluent colonies characteristic by their separate centers and common rim (black arrow), undeveloped

(dormant) forms (white arrow), and an undifferentiated macula formed at high plating density (right). As the F morphotype plays a central role in this study, its development deserves a closer scrutiny. No matter how the colony was planted, in days 1-3 it grows as a central navel: a compact body on the agar plate only slowly propagating sideways. This phase is followed in days 3-5 by spreading of FK506 concentration the flat

interstitial circle. Microscopic observations revealed a margin of extracellular material containing small swarms of bacteria at the colony periphery at this stage (M. Schmoranz, AM and FC, unpublished observations), a phenomenon well established in Serratia sp. (e.g. [8, 13]). In days 5-7 this lateral propagation comes to end and the peripheral rim is formed; the central navel grows red in this phase. In following days, the rim also turns red and the growth proceeds towards a Clomifene halt. The flat interstitial ring remains colorless (Figure 1). Fully developed F colonies can be obtained only if bacteria are planted in densities 1-20 per 9-cm dish. At the density of tens per dish, the colonies grow much smaller; below a critical distance, they tend to fuse into a confluent colony with many centers bounded by a common rim (Figure 1b; see also Figure 2a). At densities of hundreds per dish, colonies remain very small and undifferentiated. Yet higher density of planting leads to a compact, undifferentiated body – a macula (Figure 1b). The scenario is similar for all four clones used in this study, except that rimless colonies (R, W) never fuse (Figure 2a). The development and behavior of standard colonies (as described above) were essentially independent on the way of planting (i.e.

4d). The partial protective selleck compound effect was characterized by a significant decrease in apoptotic cells compared to TRD alone (fig. 4e+f). Co-incubation with BSO did not result in any significant effect on cell viability, apoptosis and necrosis compared to TRD alone (fig. 6d-f) (table 2). Compared to all other cell lines, HT1080 cells were characterized by a unique and occasionally completely contrary response to radical scavenging by NAC (fig. 4g-i). NAC co-incubation did not result in cell rescue but led to further significant reduction of viable cells compared to TRD alone (fig. 4g). This deleterious effect of NAC was mirrored by significantly enhanced

apoptosis and necrosis compared to TRD alone (fig. 4h+i). Co-incubation with BSO did not result in any significant effect on cell viability, apoptosis and necrosis compared to TRD alone CFTRinh-172 solubility dmso (fig. 5g-i). The results for 6 hours co-incubation with NAC and BSO are provided in additional file 2 and 3, respectively and summarized in table 2. The reversibility of TRD

induced cell death by caspase inhibition is divergent mTOR inhibitor and cell line specific Overall, there was no effect on cell viability, apoptosis or necrosis of z-VAD alone in any of the five cell lines. HT29 was the only cell line with a complete protection of TRD induced cell death by z-VAD co-incubation and thus a complete reversibility of TRD induced cell death (fig. 8a). The relatively mild reduction of viable cells by TRD to 69.6% ± 0.3% was significantly abrogated by z-VAD co-incubation and not different from untreated controls (fig. 8a). The protective effect was associated with a significant decrease of apoptotic cells (fig. 8b) without any detectable effect on necrosis (fig. 8c). Figure 8 Effects of caspase-inhibition on Taurolidine

induced cell death in HT29, Chang Liver and HT1080 cells. HT29 (a-c), Chang Liver (d-f) and HT1080 cells (g-i) were incubated with either z-VAD.fmk (1 μM), Taurolidine (TRD) (250 Molecular motor μM) or the combination of both agents (TRD 250 μM + zVAD.fmk 1 μM) and with Povidon 5% (control) for 24 h. The percentages of viable (a, d, g), apoptotic (b, e, h) and necrotic cells (c, f, i) were determined by FACS-analysis for Annexin V-FITC and Propidiumiodide. Values are means ± SEM of 5 (HT29), 6 (Chang Liver) and 4 (HT1080) independent experiments with consecutive passages. Asterisk symbols on brackets indicate differences between treatment groups. *** p ≤ 0.001, ** p ≤ 0.01, * p ≤ 0.05 (one-way ANOVA). In Chang Liver and HT1080 cells, the TRD induced cell death was only partially reversible by z-VAD dependent caspase inhibition. The rescue effect of z-VAD co-incubation did not lead to the same cell viability like untreated controls. In Chang Liver cells, the protective effect of z-VAD co-incubation compared to TRD alone was relatively small (45.7% ± 1.8% vs. 37.4% ± 2.6%) although it reached statistical significance (fig. 8d).

tropicalis and C. parapsilosis

EPZ5676 research buy at different stages of their biofilm development. However, it should be emphasized that all of the foregoing studies were done in mixed culture media and our results are derived from a biofilm model. In addition, as our study was bidirectional, we noted that some of the Candida species also suppressed P. aeruginosa during adhesion, initial colonization and maturation in dual species environment. Particularly, C. albicans at 90 min, C. dubliniensis at 24 h,C. albicans, C. krusei, and C. glabrata at both 24 and 48 h and C. tropicalis at 48 h. Therefore, our results further authenticate the mutual inhibition and aggregation of certain Candida spp. and P. aeruginosa. Further works with multiple strains of Candida from different species are requested to confirm the species specificity of these findings. Ultrastructural views of both monospecies and dual species biofilms confirmed the results obtained from quantitative assays. Basically, all monospecies BI 2536 clinical trial biofilms of both Candida and P. aeruginosa demonstrated a well organized biofilm structure where

yeasts were uniformly distributed with minimal amounts of extracellular substance, dead cells and cellular debris. The mature monospecies biofilms showed a characteristically thick layered structure. In contrast, dual species biofilms consisted of less dense Candida and P. aeruginosa growth, larger numbers of clumped cells, dead cells and cellular debris demonstrating the mutual inhibitory effect of these two pathogens in a dual species environment. Conclusions In conclusion, this study, principally focused on the interactions of Candida spp. and P. aeruginosa during different stages of biofilm development, indicates the latter pathogens have Selleckchem TSA HDAC significant mutual growth

inhibitory Cyclin-dependent kinase 3 effect at various stages of biofilm development in a dual species environment. It is also evident that there are species specific variations of this modulatory effect. Further work is necessary to clarify the molecular basis of these bacterial-fungal interactions, and to understand the pathobiology of mixed bacterial-fungal infections. Methods Experimental design The study comprised a series of experiments to evaluate the combined effect of each of the aforementioned six Candida spp. and P. aeruginosa on their biofilm formation, quantitatively with CFU assay and qualitatively with CLSM and SEM, at three different time intervals, 90 min, 24 h and 48 h. Microorganisms The following Reference laboratory strains of both Candida and P. aeruginosa were used, Candida albicans ATCC 90028, Candida glabrata ATCC 90030, Candida tropicalis ATCC 13803, Candida parapsilosis ATCC 22019, Candida krusei ATCC 6258, Candida dubliniensis MYA 646 and Pseudomonas aeruginosa ATCC 27853. The identity of each organism was confirmed with the commercially available API 32 C (for Candida strains) and API 20 E (for P. aeruginosa) identification systems (Biomérieux, Mercy I’Etoile, France).

However, the diagnosable proportion increased to 80.0 % (at heart rate 60–64 beats/min), 85.7 % (at heart rate

55–59 beats/min), and 100.0 % (at heart rate ≤54 beats/min), showing a positive correlation between the diagnosable proportion for the reconstruction images at optimal conditions and heart rate at CCTA by 16-slice MDCT. Fig. 5 Relationship between diagnosable proportion and heart rate. There was a positive correlation between the diagnosable proportion and heart CP 690550 rate. a images at mid-diastole, b images at optimal conditions 3.6 Safety and Tolerability No subject died and no adverse reaction that required termination of study drug administration occurred during the study period. 4 Discussion In the present study, injection of the study drug was found to be effective to rapidly lower the heart rate soon after

administration. The study drug, with a half-life of only 4 min, did not have a prolonged β-blocking effect after CCTA and lowered the heart rate only during CCTA (Fig. 3); therefore, hemodynamics do not need to be monitored for a long period after CCTA. In fact, in clinical practice using oral agents, patients must attend the hospital to take a β-blocking agent 1–2 h before initiation of CCTA and to monitor their heart rate to determine whether it meets the conditions for CCTA. This means it takes several hours before CP673451 in vitro starting CCTA. In the case of this study drug, in contrast, administration is possible immediately before CCTA, allowing early completion of imaging. The results from the present PF-02341066 in vitro study confirmed that this drug can be administered to patients just before CCTA, in contrast to oral agents requiring administration 1–2 h before CCTA. Thus, this drug appears to increase the efficiency of CCTA. On the other hand, while bradyarrhythmia and hypotension induced by the β1-blocking

effect and bronchoconstriction and peripheral circulatory disorder induced by the β2-blocking effect are known adverse reactions Amisulpride of β-blockers, the primary adverse reactions to the study drug are likely to be bradyarrhythmia and hypotension because of the high selectivity of this drug for β1-receptors (β1/β2: 251/1) [23, 24]. In the present study, no subject developed bradyarrhythmia and hypotension. Furthermore, this drug was shown to lower the heart rate only during CCTA (for approximately 30 min) and not to have a prolonged effect after the completion of CCTA, confirming its safety. Meijboom et al. [25] and Marano et al. [26] confirmed the high diagnostic performance of CCTA in multivendor, multicenter clinical studies using other CT models. In the present study using 16-slice CTs from Siemens, Toshiba, and GE, which are widely used in Japan, CCTA was performed only in subjects with a pre-CT heart rate as high as 70–90 beats/min, confirming the efficacy and safety of injection of the short-acting β1-receptor blocker landiolol hydrochloride.

Site directed mutagenesis of impC Our results suggest that impC does not have a critical role in inositol production and hence our inability to obtain an impC mutant may indicate that impC has a Lorlatinib order different or secondary function that prevents isolation of a mutant. For example, the enzyme might form part of an enzyme complex, and play a vital structural role in maintaining the integrity of that complex. Deletion of the gene would

then have both enzymatic and structural effects. An analogous situation was found with the E. coli SuhB protein; where phenotypes in suhB mutants were not related to IMPase activity, as a point mutation in the active Vismodegib in vivo site did not produce the suppressing phenotype [40]. We therefore used the same approach to try to separate enzymatic activity from a structural role. A D93N change in E. coli SuhB and an equivalent D90N change in the human IMPase suppress activity [40, 46] (Figure 1B). Site-directed mutagenesis was used to introduce a corresponding mutation (D86N) in the M.

tuberculosis impC gene using the integrating plasmid pFM96 previously used for complementation. This plasmid (pFM123) was introduced into the SCO strain FAME7, and the resultant strain (FAME11) was streaked onto sucrose/inositol plates. DCO colonies were analysed, Selleckchem GSK872 and, in contrast to the situation with pFM96, all were shown to be wild-type (n = 52). The fact that the functional impC gene could not be replaced

by this mutated gene, even in the presence of inositol (p < 0.01), shows that the mutation did inactivate enzymatic activity, and (assuming that the structure was not affected) that it is this enzymatic activity that is essential, rather than an additional structural role. Enzyme activities In order to gain a greater understanding of the function of these IMPases, we expressed impC as a recombinant protein. However, despite using different plasmid constructs and strategies, we were unable to obtain a soluble protein (not shown). As an alternative to directly assaying enzyme activity, we assayed IMPase activity in cell extracts of the mutant strains to obtain information about their relative contributions to inositol synthesis. We compared enzyme activities in whole cell ADAMTS5 extracts from the wild-type and mutant strains (Tables 3 and 4). Of the seven substrates tested, phosphate release as a result of adding the enzyme source was significantly higher than controls for fructose bisphosphate (FBP), the inositol phosphates, 5′ AMP and p-nitrophenyl-phosphate. Deletion of the impA, suhB, or cysQ genes made no significant difference to IMPase activity. The cysQ mutants had significantly less FBPase than the parent strain, (P < 0.05; t-test). However, the fructose FBPase activity in the H37Rv control for the cysQ mutants (Table 4) is significantly less than in H37Rv control used for impA and suhB mutants (P < 0.

Moreover, the CD spectrum of NA-CATH:ATRA1-ATRA1 in SDS was comparable to that of NA-CATH in TFE, suggesting that the alterations made in the sequence of NA-CATH:ATRA1-ATRA1 significantly increased its propensity for forming CAL-101 cell line helical structure. When the peptide sequences are projected on a helical wheel (Figure 4B), the contribution of the substitutions at positions 18 and 25 to a potential hydrophobic face of the NA-CATH:ATRA1-ATRA1 peptide are observed at the top of the helical wheel diagram.

On net, the Ala->Phe and Pro->Leu substitutions at positions 18 and 25, respectively, increase the hydrophobicity at those positions, which may improve the interactions between the peptides and the hydrophobic tails in surfactant micelles (and lipid membranes), find more further stabilizing helical structure in NA-CATH:ATRA1-ATRA1 when interacting with anionic surfactants or lipids. Similarly, if the

ATRA2 and ATRA1 peptides are projected individually in helical wheel format, the contribution of these two positions can be seen to the potential hydrophobic peptide face of each peptide (Figure 4C). ATRA-1 may present a more helical face that is also significantly more uniform than that of ATRA-2, with the side chain of phenylalanine LY411575 ic50 at the 3rd position of ATRA-1 exhibiting significantly greater hydrophobic character than the alanine residue at the same position in ATRA-2. Discussion In this study, we tested the in vitro susceptibility of Staphylococcus aureus to an elapid snake-derived cathelicidin, NA-CATH, as well as related novel, synthetic peptides and compared the performance of these peptides to that of the human cathelicidin LL-37. We demonstrated that LL-37 has similar potency in vitro against S. aureus to NA-CATH, as opposed to our earlier findings for E. coli and other Sitaxentan gram-negative bacteria where we determined NA-CATH to be more potent than LL-37 [25, 26]. The EC50 values were

converted from μg/ml to μM to reflect the number of molecules of peptide and to accommodate the different molecular weights of the peptides. Therefore, on a molar basis, LL-37 was slightly (2.4-fold) more effective against S. aureus than the NA-CATH, but the difference was not statistically significant. The EC50 for the D-enantiomer, D-LL-37, was found to be ~10 fold higher than for LL-37, suggesting that it is less effective as an antimicrobial peptide under these conditions for S. aureus. Three 11-residue peptides based on the ATRA motifs of the NA-CATH sequence (ATRA-1, ATRA-2, and ATRA-1A) were compared. The three ATRA peptides all had a nominal charge of +8 at pH 7, and their sequences differed only by the residues at the 3rd (F/A) and 10th position (L/P). On a molar basis, ATRA-1 is significantly more potent against S. aureus than ATRA-2, by ~10-fold.

PubMedCrossRef

16. Vadyvaloo V, Arous S, Gravesen A, Hechard Y, Chauhan-Haubrock R, Hastings JW, Rautenbach M: Cell-surface alterations in class IIa bacteriocin-resistant Listeria monocytogenes strains. Microbiology 2004,150(9):3025–3033.PubMedCrossRef 17. Vadyvaloo V, Hastings JW, van der Merwe MJ, Rautenbach M: Membranes of class IIa bacteriocin-resistant GS-4997 Listeria monocytogenes cells contain increased levels of desaturated and short-acyl-chain phosphatidylglycerols. Appl Environ Microbiol 2002,68(11):5223–5230.PubMedCrossRef 18. Vadyvaloo V, Snoep JL, Hastings JW, Rautenbach M: Physiological implications of class IIa bacteriocin resistance in Listeria monocytogenes strains. Microbiology 2004,150(2):335–340.PubMedCrossRef 19. Paulsen IT, Banerjei L, Myers GSA, Nelson KE, Seshadri R, Read TD, Fouts DE, Eisen JA, Gill SR, Heidelberg JF, et al.: Role of mobile DNA in the evolution of vancomycin-resistant Enterococcus faecalis . Science 2003,299(5615):2071–2074.PubMedCrossRef A-1210477 20. Sahm DF, Kissinger J, Gilmore MS, Murray PR, Mulder R, Solliday J, Clarke B: In vitro susceptibility studies of vancomycin-resistant Enterococcus faecalis . Antimicrob Agents Chemother 1989,33(9):1588–1591.PubMed 21. Gonzalez CF, Kunka BS: Plasmid-associated bacteriocin production and sucrose fermentation in Pediococcus acidilactic i. Appl Environ Microbiol 1987,53(10):2534–2538.PubMed 22. Holo H, Nilssen O, Nes

IF: Lactococcin A, a new bacteriocin from Lactococcus lactis subsp. cremoris : isolation and characterization of the protein and its gene. J Bacteriol 1991,173(12):3879–3887.PubMed 23. Elliker PR, Anderson AW, Hannesson G: An agar culture medium for lactic acid Streptococci and Lactobacilli. J Dairy Sci 1956,39(11):1611–1612.CrossRef 24. Bond DR, Tsai BM, Russell JB: Physiological characterization of Streptococcus

bovis mutants that can resist 2-deoxyglucose-induced lysis. Microbiology 1999,145(10):2977–2985.PubMed 25. Jönsson M, Saleihan Z, Nes IF, Holo H: Construction and characterization of three lactate dehydrogenase-negative Enterococcus faecalis V583 mutants. Appl Environ Microbiol 2009,75(14):4901–4903.PubMedCrossRef 26. Holo H, Nes IF: High-frequency transformation, by electroporation, of Lactococcus lactis subsp. cremoris next grown with glycine in osmotically stabilized media. Appl Environ Microbiol 1989,55(12):3119–3123.PubMed 27. Marsili RT: Monitoring bacterial metabolites in cultured buttermilk by high performance liquid chromatography and headspace gas chromatography. J Chromogr Sci 1981,19(9):451. 28. Narvhus JA, Thorvaldsen K, Abrahamsen RK: Quantitative determination of volatile compounds produced by Lactococcus ssp. using direct automatic headspace gas chromatography. XXII Int Dairy Congr: 1990; Alvocidib mw Montreal, Canada 1990, 522. 29. Aakra A, Vebø H, Snipen L, Hirt H, Aastveit A, Kapur V, Dunny G, Murray B, Nes IF: Transcriptional response of Enterococcus faecalis V583 to erythromycin.