, 2001b, 2007, 2008). Mutation in the lytM gene was subsequently transduced into the S. aureus lyt− strain (Mani et al., 1993; Ramadurai & Jayaswal, 1997) to potentially create an autolysin-free lyt−:lytM double mutant. For genetic complementation of the lytM mutant, an approximately 2.2-kb DNA fragment was PCR amplified using primers P5 and P6 and S. aureus SH1000 genomic DNA as template. This amplicon represents a fragment starting 890 nt upstream and ending 364 nt downstream of the lytM gene that was cloned into the BamHI and HindIII find more sites

of shuttle plasmid pCU1 (Augustin et al., 1992) and subsequently transferred to a lytM mutant of S. aureus SH1000. Mid-exponential-phase cultures (OD600 nm=0.6) were diluted 50-fold in a nephelo culture flask (Wheaton) containing 50 mL fresh TSB with a flask-to-medium volume ratio of 6 : 1 and growth was followed by measurement of OD600 nm spectrophotometrically. In another experiment, cultures pregrown to an OD600 nm=0.5 were added with oxacillin at a final concentration of 15 μg mL−1 and subsequent growth was measured

spectrophotometrically. Primers P7 and P8 were used to amplify a 1223-bp DNA fragment using genomic DNA from S. aureus SH1000 as a template. This amplicon represents the upstream and 23 nt of the 5′-end of the lytM gene. The amplicon was cloned in the correct orientation upstream of a promoterless lacZ gene of vector pAZ106 (Chan et al., 1998) and was introduced into the chromosome of S. aureus INCB024360 manufacturer RN4220 by electroporation with selection on erythromycin. Phage 80α lysate of the resulting transformant was used to transduce the lytM promoter:lacZ fusion into strain S. aureus SH1000 and its derivative agr mutant (Shenkman et al., 2001). A single copy insertion of the fusion in the chromosome was confirmed by Southern blot analysis. The activity of β-galactosidase in the reporter strain was assayed using

O-nitrophenyl-β-d-galactopyranoside as the substrate as described previously (Singh et al., 2001a, b). The lytM ORF was PCR amplified using the primer pairs P9 and P10 and S. aureus Staurosporine cell line SH1000 genomic DNA as the template. The amplified lytM gene was cloned in frame at the BamHI and HindIII sites of the overexpression vector pRSETa (Invitrogen) to produce pRSETa–lytM, which was then transferred into E. coli BLR(DE3)pLysS (Novagen). The resulting transformants were grown in LB containing ampicillin (50 μg mL−1), chloramphenicol (30 μg mL−1) and tetracycline (12 μg mL−1) to an OD600 nm of 0.4 and induced for the synthesis of His-tagged LytM by the addition of 2.5 mM of isopropyl-β-thiogalactopyranoside (IPTG) for 2.5 h. The induced culture was harvested and resuspended in 50 mM Tris-HCl buffer (pH 7.5), sonicated and centrifuged. The supernatant fluid was applied to a nickel-charged agarose affinity column and eluted with 400 mM imidazole using the Xpress Purification system (Invitrogen).

Strains, plasmids and primers used in this study are shown in Supporting Information, Roscovitine nmr Table S1. All V. cholerae reporter strains and mutants were derived from C7258 (El Tor biotype, 1991 isolate from Perú). The E. coli strains TOP10 (Invitrogen) and SM10λpir (De Lorenzo et al., 1993) were used for cloning and plasmid propagation. For routine cultivation, strains were grown in Luria–Bertani (LB) medium (pH 7.4) supplemented with

ampicillin (Amp, 100 μg mL−1), polymixin B (PolB, 100 U mL−1) or 5-bromo-4-chloro-3-indolyl-d-galactopyronoside (X-Gal, 20-μg mL−1) as required. For the phosphate limitation studies, V. cholerae strains were grown in an EZ-rich defined medium (Teknova Inc.) consisting of MOPS minimal medium (pH 7.2) supplemented with d-glucose (0.2%), ACGU solution, supplement EZ (Teknova Inc.) and different concentrations of inorganic phosphates (high phosphate, 1.32 mM K2HPO4; low phosphate, 0.132 mM K2HPO4). To construct AG 14699 a V. cholerae quorum-sensing reporter strain, we initially amplified 737- and 821-bp DNA fragments flanking the V. cholerae C7258 lacZ promoter using the primer

pairs LacZ955/LacZ218 and LacZ63/LacZ758 and the Advantage 2 PCR kit (BD Biosciences Clontech). A 500-bp KpnI and HindIII fragment containing rrnB transcription terminator (rrnBT1T2) (Brosius et al., 1981) and the Vibrio harveyi luxC promoter was extracted from plasmid pLuxLacZ described previously (Silva et al., 2008). The 737-bp fragment located upstream of the lacZ promoter, the rrnB-luxC promoter DNA and the 821-bp Sulfite dehydrogenase fragment lying downstream of the lacZ promoter were sequentially cloned into pUC19 and the entire cassette was transferred to the suicide vector pCVD442 (Donnenberg & Kaper, 1991) to obtain pCVDLuxlacZ. The above suicide vector was transferred from SM10λpir to C7258 by conjugation and the exconjugants were selected on LB agar containing Amp and PolB. The segregant SZS007

in which the lacZ promoter region was replaced by the rrnBT1T2-luxC promoter fragment was obtained by sucrose selection as described previously (Silva et al., 2008) and confirmed by PCR and DNA sequencing. To construct a phoB deletion mutant, we amplified 758- and 760-bp chromosomal DNA fragments located upstream and downstream of phoB, respectively, using the primer pairs PhoB23/PhoB762 and phoB793/phoB1535. The fragments were sequentially cloned into pUC19, confirmed by DNA sequencing and the chromosomal fragment containing the phoB deletion was transferred to pCVD442 (Donnenberg & Kaper, 1991). Similarly, 857- and 828-bp chromosomal DNA fragments flanking luxO were amplified using the primer pairs LuxO133/LuxO972 and LuxO1462/LuxO2272, the chromosomal deletion was constructed in pUC19, confirmed by DNA sequencing and transferred to pCVD442 (Donnenberg & Kaper, 1991).

6 Pandemic (H1N1) 2009 was of some concern to more than half of Queensland travelers. Nonetheless, the majority of Queenslanders would not have postponed their own travel, even if they exhibited symptoms consistent with Pandemic (H1N1) 2009. QSS-2009 was conducted by the Population Research Laboratory (PRL), Institute for Health and Social Science Research, at CQ University Australia.

The authors are particularly grateful for the assistance of the project manager, Ms. Christine Hanley. Peter Aitken is partially supported by the Queensland Emergency Medicine Research Foundation’s Noel Stevenson Fellowship. The authors state they have no conflicts of interest to declare. “
“Background. Data on the burden of illness in travelers departing from both developing and developed countries within the Asia-Pacific region is scarce. We conducted a survey to assess symptoms of infection among travelers within the region. Methods. Selleck Bioactive Compound Library A self-administered questionnaire

was distributed to travelers departing Sydney airport, Australia, for destinations in Asia and departing Bangkok Airport, Thailand, for Australian destinations during the respective winter months of 2007. A two-stage cluster sampling technique was developed selleck screening library to ensure representativeness and a weighting was applied to the Sydney sample. Travelers were assessed for symptoms of infection (fever, sore throat, diarrhea, rash, and myalgia), travel activities, and social contact in the 2 weeks prior to departure. Results. A total of 843 surveys was included in the final sample (Sydney 729, response rate 56%; Bangkok 114, response rate 60%). Overall, 45.6% of respondents were Australian residents and 26.7% were residents of countries in Asia. At least one symptom of infection was reported by 23.8% of respondents and

5.4% reported two or more symptoms of infection in the 2 weeks prior to departure. The proportion reporting symptoms was higher in those departing Bangkok compared to Sydney. Significant risk factors for the reporting of symptoms differed between residents and visitors departing each study site. Activities resulting in high rates of social contact prior to travel, particularly contact with PJ34 HCl febrile persons, were found to be independent predictors of reported symptoms. Conclusions. Self-reported symptoms of infection were common in our sample of travelers. Infectious diseases in travelers can result in spread across international borders and may be associated with the frequency of social contacts and reported illness among travelers. International travelers are at an increased risk of infectious diseases.1 The most frequently reported health problems are traveler’s diarrhea and respiratory tract infections which are generally mild and self-limiting.2,3 However, more severe illnesses in travelers, such as influenza, malaria, dengue, and hepatitis A, are commonly reported.4–7 While previous traveler studies report health problems in between 7.

None of the travelers had symptoms suggesting mountain sickness. This is in agreement with the study of Cooper et al. which suggested that healthy elderly travelers can easily tolerate stays at moderate altitudes.18 Multivariate analysis demonstrated that only travel to East Asia (OR 4.66) and backpacking (OR 1.94) were associated with illness. The fact that backpacking mode of travel and not age or eating and drinking habits was associated with illness might suggest that the environmental

health hazards, both those associated with the destination and those associated with personal exposure, affect the health of the traveler. The environmental factors are probably more complex, extending beyond food and drink hygiene. These might include variables such as efficient sewage systems in the boarding facility, crowding, personal hygiene, TGF-beta inhibitor and parasite infestations. Interestingly, illness in our study was associated with traveling to East Asia, while visiting India was not associated with an increased risk of illness. While 38% of the travelers visiting Thailand reported an illness, only 24% of those visiting India did so. This is in contrast to studies by Rack et al. and Greenwood et al. that found visiting India to be an increased risk.9,19 A possible explanation

for our finding might be that Thailand has become an increasingly Inhibitor Library research buy popular destination in recent years among Israeli travelers of all ages. Its perception as a developing country has been consistently eroded,

a process that has been accompanied by an increasing disregard for the recommended dietary restrictions by Israeli tourists. India, on the other hand, is still perceived as carrying high health risks. Another possible explanation is that our cohort of short-term travelers differs substantially from the cohorts included in the GeoSentinel study. The majority of our cohort of travelers to India were adults who traveled in organized tours for less than a month, and not backpackers traveling for several months, who constitute many of the GeoSentinel study participants. Elderly travelers were significantly more compliant with anti-malarial medications prescribed as chemoprophylaxis than younger travelers (61% vs 34%, respectively). This is in accordance with the rates reported in other surveys Niclosamide of European, North American, and Israeli travelers.2,9,13,20 Many travelers, especially younger ones, fear the potential side effects of anti-malarial drugs, particularly neuropsychiatric problems associated with mefloquine. This was stated as a reason for not taking these medications by 29% of the younger travelers compared to only 7% of elderly travelers who did not take chemoprophylaxis as recommended. Perhaps as a compensatory measure, significantly more of the younger travelers used mosquito repellants (60% vs 47%) for protection.

, 1983). Later, it was shown that overexpression of STH was essential for growth by wild-type Escherichia coli on acetate and for growth by mutant E. coli with phosphoglucose isomerase deleted on glucose. These observations supported the notion that the physiological role of STH is to convert excess NADPH into NADH (Canonaco et al., 2001; Sauer et al., 2004; Zhu et al., 2005; Zhao et al., 2008). The high cost of cofactors has spurred interest in using STH as a means to regenerate them during industrial production

(Boonstra et al., 2000a; van der Donk & Zhao, 2003; Wandrey, 2004). STH BIBF-1120 has been used as a biocatalyst to regenerate cofactors in the syntheses of hydromorphone and poly(3-hydroxybutyrate), a biodegradable polymer (Boonstra et al., 2000a; Kabir & Shimizu, 2003; Sánchez et al., 2006). STH has also been used to regenerate cofactors in an organic Compound Library cell assay solvent-based reverse micelle system (Ichinose et al., 2005) as well as in a cytochrome P450BM3-catalyzed reaction system (Mouri et al., 2009). Furthermore, overexpression of STH in yeast, which does not naturally possess it, improves the production of 2-oxoglutarate and glycerol (Nissen et al., 2001; Hou et al., 2009). The

biochemical properties of STH are less well studied. Published information is limited to molecular mass and a few kinetic constants enzymes from a few species (Voordouw et al., 1979; Boonstra et al., 1999; Ichinose et al., 2005; Mouri et al., 2009). Here, we report the detailed biochemical properties of E. coli STH (EcSTH) as a fused protein. Our work is undertaken not only to provide a foundation for future investigations of the crystallographic structure and the catalytic mechanism but also to impart the basic knowledge needed for cofactor regeneration in metabolic engineering for industrial applications. Escherichia coli MG1655, E. coli DH5α and plasmid pBluescript SK(+) were preserved in our laboratory. NADH, isopropyl-β-d-1-thiogalactopyranoside

(IPTG) and adenine nucleotide were purchased from Sangon (Shanghai, China), and thio-NAD+ from 3B Scientific GNA12 Corporation (Wuhan, China). Protein molecular weight standards and restriction enzymes were obtained from Fermentas (Shanghai, China). PrimerSTAR® HS DNA polymerase was purchased from TaKaRa (Dalian, China). Nitrocellulose membranes (Amersham Biosciences, Germany), His-tagged polyclonal antibodies (Cell Signaling Technology Inc., Beverly, MA), alkaline phosphatase-conjugated anti-rabbit immunoglobulin G (IgG) (Promega, Madison, WI) and Lumi-Phos™ Chemiluminescent Substrate (Pierce, Rockford, IL) were used for Western blots. According to the genomic sequence of E. coli MG1655 (NCBI accession no. NC_000913), a specific primer pair was designed for amplifying the complete sth gene.

Whole-cell patch-clamp

recordings showed that the input resistance and membrane capacitance of the EGFP-positive Purkinje cells from mice that underwent IUE at E11.5 selleck compound were similar to those of wild-type Purkinje cells (Table 1). In addition, there were no significant differences in either the PF– or CF–EPSC kinetics (Table 1). The PF– and CF–EPSCs in the EGFP-positive Purkinje cells showed the typical paired-pulse facilitation and paired-pulse depression, respectively, that were observed in wild-type Purkinje cells (Fig. 2B and Table 1). By the end of the third postnatal week in mice, most wild-type Purkinje cells lose their redundant CFs and become innervated by a single CF. EGFP-positive Purkinje cells electroporated at E11.5 were similarly innervated by a single CF, as shown by their single threshold for excitation (Fig. 2C). Furthermore, the input–output

relationships of the PF–EPSC were not significantly different between the electroporated EGFP-positive and wild-type Selleck EPZ015666 Purkinje cells (Fig. 2D), indicating that the PF inputs to Purkinje cells were also intact. Finally, the conjunctive stimulation of PFs and the depolarization of Purkinje cells induced LTD similarly in both wild-type and electroporated Purkinje cells (Fig. 2E; 67 ± 5% at t = 25–30 min, n = 7 from four wild-type mice; 69 ± 6% at t = 25–30 min, n = 7 from four electroporated Purkinje cells; Mann–Whitney U-test, P = 0.947). Together, these results indicate that IUE

did not alter the basic membrane properties, EPSC parameters, or short-term or long-term synaptic plasticity of the transfected Purkinje cells. To examine whether cell-type-specific and inducible promoters were compatible with the IUE method for Purkinje cells, we employed an inducible Cre/loxP system (Matsuda & Cepko, 2007). The Purkinje-specific L7 promoter (Oberdick et al., 1990; Smeyne et al., 1991; Tomomura et al., 2001) was used to express the conditionally active form of Cre recombinase ERT2CreERT2, in which the ligand-binding domain of the estrogen receptor tuclazepam was mutated; the Cre recombinase is activated in response to 4OHT (Matsuda & Cepko, 2007). By coexpressing pCALNL-DsRed2, which contains the CAG promoter and a stop signal flanked by loxP sequences, the reporter gene DsRed2 was designed to be expressed in a 4OHT/Cre- and L7-dependent manner (Fig. 3A). To unconditionally label all the electroporated cells, pCAG-EGFP was co-electroporated with the pL7-ERT2CreERT2 and pCALNL-DsRed2. After IUE at E11.5, the mice received an intraperitoneal injection of 4OHT or vehicle at P6 and were fixed at P14 (Fig. 3A). As expected, only mice that received 4OHT displayed DsRed2 signals in the cerebellum (Fig. 3B). Confocal microscopy further confirmed that the DsRed2 signals were observed only in a subset of EGFP-positive Purkinje cells (Fig. 3C).

Proportion of patients with a CD4 count <500 cells/μL receiving TDF/FTC or TDF/3TC as part of a fully suppressive combination ART regimen Proportion of patients avoiding 3TC or FTC as the sole active drug against HBV in ART Tenofovir is a nucleotide reverse transcriptase inhibitor with activity against CAL 101 both HIV and HBV [50–51]. There is RCT and observational evidence that tenofovir should be included within ART for HBV coinfection: i) HBV as a cause of end-stage liver disease in coinfected patients has reduced significantly since

the large scale use of tenofovir [30,52–53]; ii) TDF is effective in suppressing HBV replication and reducing DNA viral load in monoinfected and coinfected persons, whether they are HBeAg positive or negative, and independent of the presence of 3TC resistant virus [54–55], and is also active against

some ADV-resistant HBV strains; iii) regression of extensive fibrosis has been demonstrated with use of TDF in coinfection [30]; and iv) a systematic review of RCTs of available HBV antiviral agents in HBV monoinfection demonstrated that TDF had the best results as regards HBV DNA decline, normalisation of ALT and HBeAg seroconversion [56]. Additionally, the majority of patients reach and maintain an undetectable HBV viral load on TDF-based ART, which is correlated with a lower baseline HBV VL and longer duration of treatment. Also: i) high rates of HBeAg seroconversion and HBsAg loss can be achieved; ii) TDF-based ART is effective irrespective of baseline CD4+ Alectinib chemical structure cell counts; and iii) switching to TDF-3TC or TDF alone in HBV/HIV-infected patients with HBV resistant to 3TC is effective in achieving suppression of HBV replication. Combining TDF with either FTC or 3TC provides benefits, with improved HBV DNA level responses. Previous RCT or cohort analyses

have not reported the superior efficacy of dual therapy over TDF monotherapy in long-term HBV suppression in coinfection [19,57–58], although this has recently been reported [59] and additionally has been demonstrated in monoinfection for patients in the immune tolerant phase [60]. In a mouse model, TDF/FTC combination therapy DOK2 provides more effective HBV suppression than therapy with either drug alone [61]. In a small study on antiviral-naïve coinfected individuals, combining FTC with tenofovir has been shown to be more effective than FTC alone [62] and in decompensated HBV monoinfection and minimal prior treatment, TDF/FTC was more likely to result in viral suppression than TDF monotherapy [63]. Dual therapy may theoretically protect against the development of resistance and reactivation. Although TDF phenotypic resistance has not been documented in coinfected patients with up to 5 years of follow-up, a mutation (A194T) has been identified in individuals treated under suboptimal viral control which in vitro imparts partial TDF resistance [58].

CMC is widely used as an index of functional connectivity between the primary motor cortex and limb muscles, and Granger causality is used across many fields of science to detect the direction of coherence. To calculate CMC and Granger causality, we used electroencephalography

(EEG) to measure activity over the cortical region that governs leg muscles, and surface electromyography (EMG) over the right and left tibialis anterior muscles, Selleck Everolimus in 15 healthy term and preterm neonates, during spontaneous movements without any external stimulation. We found that 17 leg muscles (10 right, seven left) in 12 neonates showed significant CMC, whose magnitude significantly correlated with postnatal age only in the beta frequency band. Further analysis revealed Granger causal drive from EEG to EMG in 14 leg muscles. Our findings suggest that the primary motor cortex drives muscle activity when neonates move their limbs. Moreover, the positive correlation between CMC magnitude and postnatal age suggests that corticomuscular communication begins to develop during the neonatal Sorafenib order stage. This process may facilitate

sensory-motor integration and activity-dependent development. “
“Muscle β-catenin has been shown to play a role in the formation of the neuromuscular junction (NMJ). Our previous studies showed that muscle-specific conditional knockout of β-catenin (HSA-β-cat−/−) results in early postnatal death in mice. To understand the underlying mechanisms, we investigated the electrophysiological

properties of muscle cells from HSA-β-cat−/− and control mice, and found Orotic acid that, in the absence of muscle β-catenin, the resting membrane potential (RMP) depolarised in muscle cells from the diaphragm, gastrocnemius and extensor digitorum longus muscles. Furthermore, in a primary line of mouse myoblasts (C2C12 cells) transfected with small-interfering RNAs targeting β-catenin, the RMP was depolarised as well. Finally, the expression levels of the α2 subunit of sodium/potassium adenosine triphosphatase were reduced by β-catenin knockdown in vitro or deletion in vivo. These results suggest a possible mechanism underlying the depolarised RMP in the absence of muscle β-catenin, and provide additional evidence supporting a role for β-catenin in the development of NMJs. “
“CCAAT enhancer-binding protein β is a transcription factor that is involved in many brain processes, although its role in neuronal survival/death remains unclear. By using primary cultures of rat cerebellar granule neurons, we have shown here that CCAAT enhancer-binding protein β is present as all of its isoforms: the transcriptional activators liver activator proteins 1 and 2, and the transcriptional inhibitor liver inhibitory protein. We have also shown that liver activator protein 1 undergoes post-translational modifications, such as phosphorylation and sumoylation.

In 2008, the New Zealand Ministry of Health supported and propagated guidelines for HIV testing in medical settings [22]. This included recommendations that all persons with a history of unprotected sexual exposure that could result in HIV transmission, specifically MSM and those seeking assessment for sexually transmitted infections, should be offered testing. It is important

that this guideline is promoted, and the impact assessed, including collecting information on HIV testing according to sexual behaviour. Moreover, the possibility of HIV infection should be considered in a wide range of clinical situations. Testing needs to be encouraged particularly among Pacific and Māori MSM, who need Proteasomal inhibitors to be made aware of the value of HIV testing and of accessible venues where this can be undertaken. Our findings also show that testing for HIV must be considered for people of all ages if they are currently, or have been in the past, at risk. In the area of sexual health the emphasis tends Crenolanib in vivo to be on young people, but age should not be a major arbiter of HIV testing. The AIDS Epidemiology Group is funded by the New Zealand Ministry of Health. The authors acknowledge the long-term commitment

from clinicians who provide information on people diagnosed with HIV infection in New Zealand. “
“The aim of the study was to assess the incidence and costs of adverse events (AEs) among patients with HIV infection treated with nonnucleoside reverse transcriptase inhibitors (NNRTIs) from the health care system perspective. US medical and pharmacy claims during 2004−2009 were examined to select adult new NNRTI users with HIV infection. The incidence of selected AEs and time to occurrence were assessed

during the first year. Episodes of care for each AE were identified using claims associated with AE management. For each AE, a propensity score model was used to match patients with an AE to those without (1:4) based on the propensity of having an AE. Mean total health care costs, AE-associated costs and incremental costs per episode, and annual total health care costs per patient were calculated. Of the 2548 NNRTI-treated patients, 29.3% experienced AEs. The incidence ranged from 0.4 episodes/1000 Protein kinase N1 person-years for suicide/self-injury to 14.9 episodes/1000 person-years for dizziness, 49.8 episodes/1000 person-years for depression and 150.3 episodes/1000 person-years for lipid disorder. The mean AE-associated cost (duration) per episode ranged from $586 (88 days) for lipid disorder to $975 (33 days) for rash, $2760 (73 days) for sleep-related symptoms and $4434 (41 days) for nausea/vomiting. The mean incremental cost per episode ranged from $1580 for rash to $2032 for lipid disorder, $8307 for sleep-related symptoms and $12 833 for nausea/vomiting.

The effect of DHA was also evaluated on two others B. cenocepacia clinical isolates and compared with one representative member AG 14699 of all the 17 Bcc species. To test whether DHA could have a therapeutic potential, we assessed its efficacy using a Galleria mellonella caterpillar model of B. cenocepacia infection. We observed that the treatment of infected larvae with a single dose of DHA (50 mM) caused an increase in the survival rate as well as a reduced

bacterial load. Moreover, DHA administration markedly increases the expression profile of the gene encoding the antimicrobial peptide gallerimycin. Our results demonstrate that DHA has in vitro and in vivo antibacterial activity against Bcc microorganisms. These findings provide evidence that DHA may be a useful nutraceutical for the treatment of CF patients with lung infections caused by antibiotic multiresistant Bcc microorganisms. Bacteria belonging to the Burkholderia cepacia complex (Bcc), a group of 17 closely related species, have emerged as highly problematic opportunistic human pathogens in immunocompromised individuals and in patients suffering from cystic fibrosis (CF) (Mahenthiralingam et al., 2005). Bcc strains posses a wide array of virulence factors that are critical for colonization and disease. The virulence

of the Bcc members is variable, and Burkholderia cenocepacia and ABT-737 chemical structure Burkholderia multivorans are the most common species isolated from the respiratory tract of patients with CF (Drevinek & Mahenthiralingam, Resveratrol 2010). They can spread between patients with CF and are exceptionally resistant to many antimicrobial agents (Mahenthiralingam et al., 2005). In a subset of patients with CF, lung infections with these pathogens lead to declining lung function, with necrotizing pneumonia and a rapidly fatal septicemia termed ‘cepacia syndrome’ (Mahenthiralingam et al., 2005). In an era of increased antibiotics resistance and difficulties in

controlling Burkholderia infections in patients with CF, it is imperative to find new nontoxic antibacterial agents effective against this emerging pathogen. Therefore, in this work, we decided to explore the use of long-chain unsaturated fatty acids (LCUFAs) as anti-Burkholderia agents. The microbicidal activity of selected LCUFAs and their derivatives has been reported on various enveloped viruses (Hilmarsson et al., 2007), parasites (Carballeira, 2008) and pathogenic bacteria such as Pseudomonas aeruginosa, Helicobacter pylori, Staphylococcus aureus and Neisseria gonorrhoeae (Desbois & Smith, 2010). These lipids are found in natural products, human skin and body fluids including respiratory secretions, where they play a role in natural host defense against pathogens (Thormar & Hilmarsson, 2007). They exhibit their antibacterial activities through several mechanisms of action, all of which primarily involve the perturbation of the bacterial cell membrane (Desbois & Smith, 2010).