epidermidis ATCC 12228, considered as biofilm negative, and some

epidermidis ATCC 12228, considered as biofilm negative, and some clinical staphylococcal isolates without ica genes (also aap−) can form biofilms on some polytetrafluroethylene PTC124 vascular grafts after several days of incubation under static conditions. The majority of the ica-positive nasopharyngeal S. epidermidis isolates were also able to produce slime, which was monitored using the CRA test. This is in agreement with the data presented by other authors (Arciola et al., 2002; Stevens et al., 2008; El-Mahallawy et al., 2009); the presence of the ica operon was strongly associated with a slime-positive phenotype. However, ica-negative and slime-positive isolates in the CRA test were

also described in the present paper. Arciola et al. (2006) found a rather good concordance between the occurrence of ica genes, monitored using PCR-based analysis, and the CRA test. According to these authors, the MtP method appeared to be less appropriate for an accurate identification of staphylococcal capability of biofilm formation. In our study, there was a relation between the ability of biofilm formation by the MtP method and slime production in the CRA test among the ica-positive staphylococcal isolates. In contrast, most of the ica-negative strains

were positive by the CRA selleckchem test and possessed a biofilm-negative phenotype determined using the MtP method, especially for isolates harboring the aap gene. The literature data available regarding the CRA test yielded contrasting conclusions. Bozkurt et al. (2009) indicate that the CRA test should not be used for a biofilm formation ability assay in vitro of S. epidermidis because of misleading results. The specificity of this test is limited to the determination of staphylococcal ability to secrete slime rather than for the detection of bacterial adhesion and rapid growth in the form of a biofilm on the material’s surface. On the other hand, some authors (Arciola et al., 2006; Jain & Agarwal, 2009) recommended the CRA test as a reliable method to determine biofilm production. In our opinion, CRA and MtP tests are reliable methods to determine the ability of

slime/biofilm formation only in ica-positive S. epidermidis strains. Although previous studies (Vandecasteele et al., 2003; Cafiso et al., Urease 2004) have suggested that there is no strict association between the presence of the icaABCD operon and in vitro biofilm formation in invasive, colonizing and contaminant S. epidermidis, among the colonizing strains tested in our study, most of the biofilm producers (monitored using the MtP method) were the ica positive. In conclusion, S. epidermidis isolates possess the potential ability to form biofilms by ica-dependent and/or ica-independent mechanisms. In our opinion, further studies are needed to determine reliable, short-time criteria for the assessment in vitro of biofilm formation in staphylococci.

jgidoegov/) (Position: scaffold_80:317485–317760) and the entir

jgi.doe.gov/) (Position: scaffold_80:317485–317760) and the entire A3aPro sequence from P. sojae was submitted to GenBank

(accession no. JX118829). Thus, based on the A3aPro sequencing information, we have identified a novel transposon-like DNA element A3aPro in many Phytophthora genomes that could provide a potential target for plant disease diagnosis. In this study, we developed a LAMP assay for P. sojae based on a special identifiable target A3aPro and demonstrated that it was specific and efficient. Phytophthora sojae isolates were obtained from diseased soybean stems collected from various provinces Selleckchem AZD6738 in China from 2002 to 2011. All tested P. sojae isolates were isolated using a leaf disk-baiting method from buy FG-4592 diseased soybean plots (Jinhuo & Anderson, 1998). Using the same method, additional P. sojae isolates were baited from soybean residues and soil carried by soybeans imported from the USA, Brazil, Argentina and Canada. Thirteen known races (R2, R3, R6, R7, R8, R12, R14, R17, R19, R20, R28, R31, and P7071) of P. sojae were provided by B. Tyler and J. Peng. The P. sojae isolates, as well as isolates of Phytophthora spp., Pythium spp., Fusarium spp., and various other pathogens used in this study, are maintained in a collection in the Department of Plant Pathology, Nanjing Agricultural University, China, and are listed in Table

S1. Phytophthora isolates were cultured in tomato juice medium (Zheng, 1995) (L−1, 200 mL tomato juice, 0.1 g CaCO3 and 15 g agar mixed with sterile distilled water, and autoclaved at 120 °C for 20 min). Mycelia of each Phytophthora and Pythium isolate were obtained by growing the isolates in tomato juice broth at 18–25 °C (temperature-dependent isolates) for at least 3 days. Mycelia of the other fungi were grown in potato dextrose broth (Erwin et al., 1996). The mycelia

were harvested by filtration and frozen at −20 °C. Mycelia DNA was isolated using the DNAsecure Plant Kit (TIANGEN) according to the manufacturer’s protocol. DNA concentrations were determined spectrophotometrically or by quantitation on 1% agarose gels stained with ethidium bromide in comparison with commercially obtained standards and stored at −20 °C. A set of four species-specific second LAMP primers was designed based on the P. sojae identifiable target A3aPro. Briefly, using the A3aPro sequence of P. sojae as a bait to do a blastn search did not showed any similarity with other sequenced strains of Phytophthora infestans, Phytophthora ramorum and Hylaperonospora parasitica. Then we obtained similar-A3aPro sequences in the genome databases for P. infestans, P. ramorum and H. parasitica. Phytophthora infestans DNA sequence was available from the Broad Institute (http://www.broad.mit.edu/) (Position: supercontig_1.1849:1900–2350); P. ramorum DNA sequence was available from the JGI (http://www.jgi.doe.gov/) (Position: scaffold_1220:1–342); H. parasitica genome sequence was available from http://vmd.vbi.vt.

, 2009; Vance et al, 2009) FUS/TLS mutations were also found in

, 2009; Vance et al., 2009). FUS/TLS mutations were also found in other populations in Europe, Japan and the US and it is estimated that FUS/TLS mutations cause familial

ALS in 4–5% of cases (Belzil et al., 2009; Blair et al., 2010; Chio et al., 2009b; Damme et al., 2009; Drepper et al., 2010; Ticozzi et al., 2009b; Corrado et al., 2010; Groen et al., 2010; Suzuki et al., 2010). In addition, one de novo truncation mutation was reported (Dejesus-Hernandez et al., 2010). The FUS/TLS gene is located on chromosome 16. Also known as hnRNPP2, it belongs to the FET family of RNA-binding proteins and it is an hnRNP. The protein consists of an N-terminal region rich in glutamine, glycine, serine and tyrosine residues (QGSY region) Ibrutinib immediately followed by a glycine-rich domain. It contains an RNA-recognition motif (RRM) and multiple arginine, glycine, glycine (RGG) repeats implicated in RNA binding,

a zinc finger and a C-terminal region that is highly conserved (Lagier-Tourenne & Cleveland, 2009). FUS/TLS is involved in pre-mRNA splicing as well as in the export of fully processed mRNA to the cytoplasm and thus shuttles between the nucleus and the cytoplasm (Zinszner et al., 1997). It may also play an important role in transport of mRNA (Yoshimura et al., 2006). In addition, it is important in gene regulation and it was recently shown that Selleck Olaparib ID-8 FUS/TLS can serve as a transcriptional regulatory sensor of DNA damage signals leading to gene-specific repression of gene transcription (Wang et al., 2008). FUS/TLS is ubiquitously expressed and

under normal conditions it is mainly localized in the nucleus (Hackl & Luhrmann, 1996). In cultured hippocampal pyramidal neurons, FUS/TLS was localized not only in the nucleus but also in the dendrites (Fujii et al., 2005). This punctuate dendritic localization was dependent on an intact microtubule and actin network, and activation of mGluR5 metabotropic glutamate receptors stimulated FUS/TLS accumulation at the spines of excitatory synapses (Fujii et al., 2005). FUS/TLS-knockout mice die immediately after birth (Hicks et al., 2000) or are rarely alive at weaning (Kuroda et al., 2000). In an outbred strain, FUS/TLS-knockout mice survived but showed male sterility and reduced fertility of females (Kuroda et al., 2000). It was reported that heterozygous FUS/TLS mice were indistinguishable from wildtype littermates (Kuroda et al., 2000). Neurons deficient in FUS/TLS showed abnormal spine morphology and lower spine density (Fujii et al., 2005). It is estimated that FUS/TLS mutations account for ∼5% of familial ALS and thus again for < 1% of total ALS (Lagier-Tourenne & Cleveland, 2009). FUS/TLS-linked ALS is a dominant disease, except in the original Cape Verdian family in which the FUS/TLS mutation is recessive (Kwiatkowski et al., 2009).

They were instructed to ignore the auditory stimulation and watch

They were instructed to ignore the auditory stimulation and watch a Dabrafenib silenced, subtitled movie of their choice on a computer screen in front of them (distance = 120 cm). Figure 1 schematically pictures the experimental design. Stimulus-onset asynchrony (SOA) was set to 150  ms. The onset of first deviant tones was always unpredictable, and violated in the pitch dimension the first-order formal regularity established by standard

tone repetition. We assume that also the repeated deviant tone violated the first-order regularity established by standard tones. In both cases, a first-order prediction error response is elicited. Two ‘repetition probability’ conditions were created: in a ‘high-repetition probability’ condition, deviant tones were always repeated; in a ‘low-repetition probability’ condition, deviant tones were either repeated or followed by a standard tone with equal probability. Two ‘temporal regularity’ conditions were created, producing ‘isochronous’ and ‘anisochronous-onset’ sequences. Large jitter values may induce significant differences in single-trial peak latencies, leading to an artifactual reduction of event-related deflection amplitudes (low-pass effect of averaging procedure; see Spencer, 2005). We thus kept anisochrony to a perceptible minimum, limiting the SOA jitter to ± 20% (in randomized steps of 5 ms, range 120–180 ms, uniform distribution). The same number of deviant pairs was used

in both deviant repetition probability conditions. In the high-repetition probability Osimertinib datasheet condition, there were 1200 standard and 240 deviant stimuli, accounting for 120 deviant pairs. Standard tones had a probability of 83.33%, and deviant tones 16.67% (each deviant considered as a single event). They were administered in one block of about 3.6 min. In the learn more low-repetition probability condition, global oddball values were adapted to 87% standard and 13% deviant tones: 2400 standard, 360 deviant stimuli, accounting for 120 deviant pairs and 120 single deviant tones (one block, about 6.9 min). This way, we could control for refractoriness-dependent

differences on the elicitation of first deviant N1 amplitudes, as the length of standard sequences (mean n = 10) before first deviant onset was the same across higher-order formal regularity conditions: high-repetition probability, 1200 standards/120 first deviants; low-repetition probability, 2400 standards/240 first deviants, pooled from both paired and single events. Block order presentation was randomized within subjects. An additional condition with repetition probability set to 75% was also included. Its effects are reported in the Supporting Information, section A, as they were uninformative to the aims of distinguishing between high and low deviant repetition probabilities. Electroencephalogram (EEG) was continuously recorded using an ActiveTwo amplifier system (BioSemi, Amsterdam, the Netherlands; http://www.biosemi.

These findings also support the existing free-radical theory of a

These findings also support the existing free-radical theory of aging, which states that organisms become older and become senescent because cells acquire free radical-induced damage over time (Harman, 1981; Ames et al., 1993; Beckman & Ames, 1998). As the process of PCD has been found to be evolutionarily conserved (Ameisen, 2002), revealing its mechanism in a bacterial system such as Xcg could be of great help

in deciphering the evolutionary linkage of this process. We thank Bhaskar Sanyal and Ashish Shrivastva for their help in performing ESR spectroscopy and HPLC analysis, respectively. “
“The chrysene-degrading bacterium Pseudoxanthomonas selleck products sp. PNK-04 was isolated from a coal sample. Three novel metabolites, hydroxyphenanthroic acid, 1-hydroxy-2-naphthoic acid and salicylic acid, were identified by TLC, HPLC and MS. Key enzyme activities, namely 1-hydroxy-2-naphthoate hydroxylase, 1,2-dihydroxynaphthalene dioxygenase, salicylaldehyde dehydrogenase and catechol-1,2-dioxygenase, were noted in the cell-free extract. These results suggest

that chrysene is catabolized via hydroxyphenanthroic acid, 1-hydroxy-2-naphthoic EPZ5676 order acid, salicylic acid and catechol. The terminal aromatic metabolite, catechol, is then catabolized by catechol-1,2-dioxygenase to cis,cis-muconic acid, ultimately forming TCA cycle intermediates. Based on these studies, the proposed catabolic pathway for chrysene degradation by strain PNK-04 is chrysene hydroxyphenanthroic acid 1-hydroxy-2-naphthoic acid 1,2-dihydroxynaphthalene salicylic acid catechol cis,cis-muconic acid. Polycyclic aromatic hydrocarbons (PAHs) are compounds of environmental and health concern. Some PAHs and their biotransformation products have been shown to be toxic, mutagenic and carcinogenic to higher organisms and resistant to microbial degradation (Cerniglia, 1992; Kanaly & Harayama, 2000). Low-molecular-weight PAHs, composed of two or three aromatic rings, can be biodegraded under favourable Fossariinae conditions; PAHs with four rings

or more are recalcitrant to biodegradation and may persist for long periods in the environment. Chrysene is a high-molecular-weight PAH consisting of four fused benzene rings. Among PAHs, it is classified as a priority pollutant by the US Environmental Protection Agency (Smith et al., 1989). The major goal of bioremediation is to transform organic pollutants into simple innocuous metabolites or mineralize them into carbon dioxide and water (Alexander, 1999). Microorganisms play an important role in the degradation of aromatic hydrocarbons in both terrestrial and aquatic systems. The use of microorganisms for bioremediation requires knowledge of the metabolic pathway of aromatic compounds in the organisms. However, successful bioremediation has been limited by the failure to remove high-molecular-weight PAHs (Wilson & Jones, 1993) such as chrysene. There are very few reports on the utilization of chrysene as a sole carbon source (Demane’che et al.

The API 20E and 20NE were performed in triplicate,

with V

The API 20E and 20NE were performed in triplicate,

with V. harveyi LMG 4044T and V. campbellii LMG 11216T included as references. Salt tolerance was determined in PY broth [0.3% w/v neutralized peptone (Oxoid) and 0.1% w/v yeast extract (BD)] supplemented with NaCl concentrations between 0% and 10% (w/v) for 72 h at 28 °C with shaking. Growth responses to temperatures between 4 and 45 °C were tested in PY broth with 2% w/v NaCl for 72 h with shaking. Antibiotic sensitivity was determined using the disk susceptibility assay as described by the Clinical and Laboratory Standards Institute (2008a, b) for ampicillin and gentamicin (10 μg), chloramphenicol, kanamycin and oxytetracycline (30 μg), erythromycin

(15 μg), sulphisoxazole (300 μg), trimethoprim-sulphamethoxazole 1/19 (1.25/23.75 μg) Selleckchem Galunisertib and vibriostatic agent O129 (Oxoid) (10 and 150 μg). For fatty acid analyses, cells were grown for 24 h at 28 °C on tryptone soy agar medium supplemented with 1.5% NaCl (w/v). Fatty acid composition was determined using the Sherlock Microbial Identification System (MIDI), according to the manufacturer’s instructions (Microbial Identification Inc.). Genomic DNA was extracted using the Wizard Genomic DNA Purification Kit (Promega) Nivolumab research buy from overnight cultures grown in MB at 28 °C with shaking, according to the manufacturer’s instructions. The 16S rRNA genes were amplified as described by Lane (1991) and sequenced using the

27f and 1492r oligonucleotides as sequencing primers. For the MLSA, the five protein-coding loci rpoA (RNA polymerase α-subunit), pyrH (uridylate kinase), topA (topoisomerase I), ftsZ (cell division protein FtsZ) and mreB (rod shaping protein MreB) were used. Genes were amplified by PCR and sequenced as described for rpoA and pyrH genes (Thompson et al., 2005), and topA, ftsZ and mreB genes (Sawabe et al., 2007). In addition, sequencing of 16S rRNA and rpoA genes was carried out for V. rotiferianus strain CAIM 994. Sequences of other protein-coding loci for this strain were retrieved from public databases (GenBank and http://www.taxvibrio.lncc.br/). Bcl-w Sequences generated in this study have been deposited in GenBank under the accession numbers GU018180–GU018182 and GU111249–GU111259 (Supporting Information, Table S3). Sequences were initially aligned with those of their closest relatives available in GenBank using the blastn program (Altschul et al., 1990). Subsequently, sequences of our two strains, close relatives and type strains of related vibrios were aligned by arb (Ludwig et al. 2004) or clustal_x (Thompson et al., 1997) for 16S rRNA and protein-coding genes, respectively. For arb alignments, manual corrections were performed, where necessary, based on 16S rRNA gene secondary structure.

31–33 Most assays target parasite DNA sequences common to all hum

31–33 Most assays target parasite DNA sequences common to all human schistosome species. Assays using species-specific probes are less sensitive.34 A real-time PCR assay to detect schistosome DNA in plasma was found to be 100% sensitive in parasite proven established infection, and showed superior diagnostic sensitivity compared with serology in AS.16 In Wichmann’s series of eight patients with AS, schistosome DNA could be demonstrated in 10 mL

plasma from all, at an average of 40 days after exposure, and at an average of 14 days after symptom onset, while schistosome EIA antibody detection was still negative in three of eight patients. This was also the case in the present cluster, E7080 but then the time lapse between first exposure and diagnosis was considerably longer (mean 78 d). This suggests that schistosome DNA detection in serum appears to be superior to egg detection and serum antibody assays as a qualitative marker of early symptomatic infection, and that

a Nutlin-3a cost 2 mL serum sample may contain enough schistosome DNA to be amplified, at least when infected with S mansoni. Actually the number of copies per genome of the 121-bp tandem repeat sequence target gene may vary considerably between human schistosome species.17 To be clinically useful in a post-travel setting, where only limited amounts of blood are routinely taken, its sensitivity should also be assessed in acute urinary schistosomiasis (Schistosoma hematobium) using an equally small serum sample. Furthermore, the minimum time lapse after infection needed to detect parasite DNA by this method has not yet been determined. The amount of schistosome DNA copies in serum did not diminish significantly, despite a very clear drop in the mean eosinophil count and the halting of egg excretion 5 weeks after initial praziquantel treatment. This is in line with results of animal studies, and probably results from the continued release of cell-free DNA from degrading schistosomes, from persisting schistosomes still immature at the time when the initial praziquantel

treatment was given.16,25 Clearance of this circulating cell-free DNA is Tangeritin apparently a very slow process. In Wichmann’s series of patients with AS, schistosome DNA was still detectable in most patients even up to 15 months after treatment. Only by then the plasma DNA concentration had substantially declined. Schistosome DNA detection in serum obviously fails as an early quantitative marker of therapeutic success, in contrast with PCR assays on fecal samples.31 It is tempting to assume that the number of cycles required to attain parasite DNA detection in a blood sample by a real-time PCR assay is a reliable marker of parasite burden. However, there is insufficient evidence supporting that thesis, and there is considerable interpersonal variation even when exposure is similar. This study was not designed to address this issue.

The duration of travel and the lag time between return and presen

The duration of travel and the lag time between return and presentation to our unit were significantly more prolonged in cases than in controls (22 days vs 6 days, p = 0.001 and 40 vs 14 days, p < 0.001 respectively). Of the 54 patients with malaria, 35 (64.8%) were receiving chemoprophylaxis that was considered to be inadequate (regarding observance during travel, duration of chemoprophylaxis after return and choice of medication) in 74.3%

of cases. Multivariate regression analysis showed correlations between malaria and travel www.selleckchem.com/products/pexidartinib-plx3397.html to Africa, abdominal pain, vomiting, myalgia, inadequate prophylaxis, and platelets <150.103/µL (Table 6). Sensitivity, specificity, PPV, and NPV of variables appear in Table 7. We evaluated the predictive factors of imported malaria in returning buy SB431542 travelers seen as outpatients and prospectively included on the existence of fever. We showed that the following variables are independent predictive factors of malaria: travel in Africa, abdominal pain, vomiting, myalgia, inadequate chemoprophylaxis, and platelets <150.103/µL. In endemic areas, predictors of malaria have been assessed in populations at risk such as children or hospitalized adults.18,19 Nonetheless, these results cannot apply to non-immune populations such as travelers in whom the prescription of a presumptive antimalarial treatment, in response to the results of blood Etoposide datasheet smears (if they are not routinely

available) is a cause of concern. Three studies previously evaluated factors associated with imported malaria in non-immune travelers returning from the tropics, but the criteria of inclusion was the prescription of a blood smear.13,16,17 In a cohort of 336 Swiss travelers (97

cases and 239 controls),16 variables included in the final model of logistic regression were inadequate chemoprophylaxis, sudden onset, lack of abdominal pain, temperature >39°C, alteration of general status, splenomegaly, hemoglobin <12 g/dL, white cells count <10.103/µL, platelets <150.103/µL and eosinophilia <5%. In another study, performed in 783 French patients admitted in the emergency department of a Parisian hospital,13 factors associated with malaria were travel in sub-Saharan Africa, temperature >38°5C, chills, platelets <130,000/µL, bilirubin >18 µmol/L. In a more recent Danish study, some laboratory variables predictive of malaria were compared in 66 febrile returning travelers with negative blood smears and 40 travelers with malaria (P falciparum : n = 28; P vivax/P ovale: n = 12).17 Platelet and leukocyte counts and coagulation factors II–VII and X were significantly lower in the malaria group. Similarly C-reactive protein, lactate dehydrogenase, and bilirubin levels were significantly higher in this group, particularly in P falciparum group. Although the inclusion criteria was the presence of fever, our study has some limits.

A number of these studies used strains of Lactobacillus plantarum

A number of these studies used strains of Lactobacillus plantarum. For example, L. plantarum CGMCC 1258 was able to lessen

the negative impact of enteroinvasive Escherichia coli ATCC 43893 serotype O124:NM on TEER (Qin et al., 2009), L. plantarum 299v mitigated the TNF-α-induced decrease in TEER (Ko et al., 2007) and L. plantarum MF1298 attenuated the decrease in TEER induced by Listeria monocytogenes 6896 (Klingberg et al., 2005). The aim of this research was to identify lactobacilli isolates, with an emphasis on L. plantarum, that enhance TEER and therefore have the potential to be used as probiotics targeted at improving PLX-4720 intestinal barrier function. Eight commercially used probiotics were compared to determine which had the greatest positive effect on TEER across intestinal epithelial cell layers, and then the best probiotic was used as a benchmark to evaluate several isolates,

including four L. plantarum strains and 15 human oral isolates. The oral cavity was chosen as a source of potential probiotics because evidence suggests that lactobacilli PLX3397 found in human faeces, and therefore present in the intestines, originate from the oral cavity (Dal Bello & Hertel, 2006; Maukonen et al., 2008). The isolate with the greatest positive effect on TEER was further investigated to evaluate its suitability Masitinib (AB1010) for use as a probiotic, including its ability to tolerate gastrointestinal conditions, to

adhere to intestinal epithelial cells and affect adherence and TEER of enteropathogenic E. coli (EPEC) O127:H6 (E2348/69), a known enteric pathogen (Baldini et al., 1983), during coculture. The source of the bacterial strains used in this study is described in Table 1. Eight commercially used probiotics were chosen on the basis that there were published data showing their efficacy in various in vitro and in vivo models (Table 1). Further strains were either L. plantarum obtained from the Deutsche Sammlung von Mikroorganismen (DSM) or human oral lactobacilli isolates. Human oral isolates were obtained from the mouth lining, tongue and teeth of volunteers using sterile tooth picks, which were incubated individually in 10 mL of Man, Rogosa and Sharpe (MRS) broth overnight at 37 °C (5% CO2) to select for lactic acid bacteria. Cultures were diluted in phosphate-buffered saline (PBS, pH 7.2), plated onto Rogosa agar and incubated in 5% CO2 at 37 °C for 48 h to select for lactobacilli. Putative L. plantarum strains with large white colonies similar to those of known L. plantarum strains were subcultured onto fresh Rogosa agar and incubated at 37 °C (5% CO2) for 48 h. Sample colonies were stored as glycerol stocks at −85 °C. Isolates were identified based on their 16S rRNA gene sequences.

A number of these studies used strains of Lactobacillus plantarum

A number of these studies used strains of Lactobacillus plantarum. For example, L. plantarum CGMCC 1258 was able to lessen

the negative impact of enteroinvasive Escherichia coli ATCC 43893 serotype O124:NM on TEER (Qin et al., 2009), L. plantarum 299v mitigated the TNF-α-induced decrease in TEER (Ko et al., 2007) and L. plantarum MF1298 attenuated the decrease in TEER induced by Listeria monocytogenes 6896 (Klingberg et al., 2005). The aim of this research was to identify lactobacilli isolates, with an emphasis on L. plantarum, that enhance TEER and therefore have the potential to be used as probiotics targeted at improving ALK inhibitor intestinal barrier function. Eight commercially used probiotics were compared to determine which had the greatest positive effect on TEER across intestinal epithelial cell layers, and then the best probiotic was used as a benchmark to evaluate several isolates,

including four L. plantarum strains and 15 human oral isolates. The oral cavity was chosen as a source of potential probiotics because evidence suggests that lactobacilli buy MLN0128 found in human faeces, and therefore present in the intestines, originate from the oral cavity (Dal Bello & Hertel, 2006; Maukonen et al., 2008). The isolate with the greatest positive effect on TEER was further investigated to evaluate its suitability Farnesyltransferase for use as a probiotic, including its ability to tolerate gastrointestinal conditions, to

adhere to intestinal epithelial cells and affect adherence and TEER of enteropathogenic E. coli (EPEC) O127:H6 (E2348/69), a known enteric pathogen (Baldini et al., 1983), during coculture. The source of the bacterial strains used in this study is described in Table 1. Eight commercially used probiotics were chosen on the basis that there were published data showing their efficacy in various in vitro and in vivo models (Table 1). Further strains were either L. plantarum obtained from the Deutsche Sammlung von Mikroorganismen (DSM) or human oral lactobacilli isolates. Human oral isolates were obtained from the mouth lining, tongue and teeth of volunteers using sterile tooth picks, which were incubated individually in 10 mL of Man, Rogosa and Sharpe (MRS) broth overnight at 37 °C (5% CO2) to select for lactic acid bacteria. Cultures were diluted in phosphate-buffered saline (PBS, pH 7.2), plated onto Rogosa agar and incubated in 5% CO2 at 37 °C for 48 h to select for lactobacilli. Putative L. plantarum strains with large white colonies similar to those of known L. plantarum strains were subcultured onto fresh Rogosa agar and incubated at 37 °C (5% CO2) for 48 h. Sample colonies were stored as glycerol stocks at −85 °C. Isolates were identified based on their 16S rRNA gene sequences.