, 2004b). Unexpectedly, data on fibronectin-binding adhesins and invasins of S. lugdunensis are scarce. Binding to fibronectin has previously been

investigated in a small collection of strains, but all of eleven isolates showed only weak binding to fibronectin compared with that of strain Cowan I of S. aureus (Paulsson et al., 1993). S. lugdunensis has been described as being part of several niches of the human skin flora (Bieber & Kahlmeter, 2010). The clinical presentation of S. lugdunensis-caused infections is similar to infections caused by S. aureus. Staphylococcus lugdunensis can cause potentially fatal endocarditis, osteomyelitis, and skin and soft tissue infections (Vandenesch et al., 1993; Pareja et al., 1998; Patel et al., 2000; Hellbacher et al., 2006; Frank et al., 2008). Staphylococcus lugdunensis is thought to be rarely FAK inhibitor isolated; nevertheless, the low prevalence of S. lugdunensis in skin infection has recently been questioned (Bocher et al., 2009). We therefore sought to analyze the invasion of epithelial and endothelial cells (human urinary bladder carcinoma cell line 5637 and the endothelial cell line EA.hy 926) using a previously described fluorescence-activated cell-sorting (FACS)-based invasion assay. We correlated these results

with the binding of clinical isolates of S. lugdunensis to fibronectin. The bacteria used were S. aureus Cowan I, Staphylococcus carnosus TM 300 and eight clinical isolates of S. lugdunensis: Stlu 12, Stlu 30, Stlu 33, Stlu 35, Stlu 36, Stlu 39, Stlu 50, and Stlu 108 and the isogenic knockout mutant CHIR-99021 in vivo Stlu 108Δfbl::ermB (Table 1).

All S. lugdunensis isolates used in this study were confirmed by two reference methods: S. lugdunensis specific tanA and fbl PCRs and by MALDI-TOF MS, as described previously (Noguchi et al., 2009; Szabados et al., 2010; Szabados et al., 2011). Human urinary bladder carcinoma cell line 5637 (DSMZ, Braunschweig, Germany) and endothelial cell line EA.hy 926 (DMSZ) were used throughout this study. Bacteria were grown until the mid-logarithmic phase, as described previously (Szabados et al., 2008). The mutagenesis construct for the homologous recombination cloned into pBT2, and named pMB2503, has previously been described (Marlinghaus Phosphoglycerate kinase et al., 2011). The homologous recombination of the fbl gene in strain Stlu 108 was also performed as previously described (Marlinghaus et al., 2011). The Δ fbl knockout mutant was confirmed by sequencing (data not shown). Human urinary bladder carcinoma cell line 5637 was cultured in RPMI 1640 with phenol red (PAA, Pasching, Austria). The endothelial cell line EA.hy 926 was cultured in HAT medium (Invitrogen) with addition of HAT medium supplement (hypoxanthine, aminopterin, and thymidine). Both media were also supplemented with 10% heat-inactivated fetal calf serum (PAA) and 1 g L−1 pyruvate (Invitrogen) and 1.5 g L−1 glucose (Invitrogen).

However, no protein accumulation occurred in the PMS controls.

After 10 days of incubation the Z-VAD-FMK in vitro culture entered the stationary phase. During this period the concentration of chrysene in the medium decreased from 400 to 140 mg L−1, i.e. 60% of the chrysene was degraded during the 12 days of incubation. TLC of the ethyl acetate extract of the supernatants from the washed-cell incubations with chrysene showed the presence of polar metabolites. Metabolic intermediates were tentatively identified by comparing their Rf values with those of the respective standard reference compounds. Chrysene moved along with the solvent front. 1-Hydrox-2-naphthoic acid (Rf 0.43) and salicylic acid (Rf 0.15) were identified as the probable intermediates. A spot with Rf value of 0.86 did not match with any standards tested. The extracts were then analysed by HPLC and the individual spots on TLC were further characterized by LC-ESI-MS. Retention times from HPLC analysis (Fig. 2) and LC-ESI-MS

characteristics of the metabolites are given in Table 1. HPLC retention times of identified metabolites were identical to those of respective standard reference compounds. LC-ESI-MS of metabolite C1 gave a molecular ion (M+) at m/z 138 and PLX3397 price subsequently at 121 (M+– 17, probably due to loss of OH), 110, 93 (M+– 45, loss of COOH), 80, 77 and 63 (Table 1, C1). The fragmentation pattern is identical to that of standard salicylic acid. The mass spectrum of metabolite C2 showed a base peak at 187 (M+– 1), and subsequent ion fragments at m/z 170 (M+– 17, loss of OH), 154, 143 (M+– 45, loss of COOH), 126 (M+– 17 – 45, losses of OH and COOH), 115 and 79 (Table 1, C2). The fragmentation pattern of this metabolite matched well with that of standard 1-hydroxy-2-naphthoic acid. The LC-MS spectrum of metabolite C3 showed an ion fragment at m/z 239 (M+– 1), a base peak m/z 222 (M++1−OH), and subsequent fragments at 204, 193 (M+– COOH) and 176 (phenanthrene ion). This fragmentation pattern is characteristic of hydroxyphenanthroic

acid (Baboshin et al., 2008). The mass spectra of standards and metabolites are Thalidomide provided as Supporting Information, Figs S1–S3. The enzyme extract prepared from cells grown on different carbon sources showed high activity of 1,2-dihydroxynaphthalene dioxygenase, moderate activity of 1-hydroxy-2-naphthoate hydroxylase and catechol-1,2-dioxygenase, and low activity of salicylaldehyde dehydrogenase; catechol-2,3-dioxygenase and gentisate-1,2-dioxygenase activity was not detected (Table 2). As expected, the crude extract prepared from glucose-grown cells did not show any activity of the above enzymes, thus suggesting the inducible nature of the enzymes involved in the degradation of chrysene. To elucidate the chrysene degradation pathway operating in PNK-04, the expected intermediates of the pathway were supplied as sole source of carbon.

, 1997), which may be necessary for survival.

Because these sterols are synthesized de novo by the organism despite its ability to scavenge available sterols, these VX-809 cost sterols have been called ‘metabolic sterols’ (Haughan & Goad, 1991; Kaneshiro et al., 1994a), and because these sterols appear to be unique to Pneumocystis, they may not only provide excellent drug targets against the organism (Haughan & Goad, 1991), but they may have potential as possible markers for the detection of PCP (Kaneshiro et al., 1999). Cholesterol accounts for up to 81% of the total sterols isolated from Pneumocystis obtained from rat lungs, and it has been postulated that most, if not all, the cholesterol is scavenged from the host (Giner et al., 2002; Worsham et al., 2003). Conversely, one report speculates that P. carinii may synthesize cholesterol through a de novo pathway (Zhou et al., 2002), but to date, there is no evidence to suggest that the organism contains all of the genes necessary to synthesize either cholesterol or ergosterol. Despite the lack of detectable ergosterol in Pneumocystis membranes, genes involved in sterol synthesis have been identified within

its genome, and many of these genes have been click here proven functional based on targeted inhibition of these enzymes and the subsequent reduction in the viability of P. carinii (Kaneshiro et al., 2000). Figure 4 outlines the putative sterol biosynthetic pathway of P. carinii based on our current knowledge, and Table 1 lists of P. carinii sterol enzymes and identifies the reaction products that have been detected in the membranes of the fungus. These

putative P. carinii sterol enzyme genes were identified based on sequence similarity to other known fungal sterol enzymes; however, functional analyses are necessary to determine their function. To date, only three of these genes, ERG7 (lanosterol synthase), ERG11 (lanosterol 14α demethylase) and ERG6 (sterol C-24 methyl transferase), have been the subject of research investigations. The activity of lanosterol synthase or Erg7 results in the conversion of the last acyclic sterol precursor into lanosterol, the first cyclic sterol intermediate of the sterol pathway. In Saccharomyces cerevisiae, loss of lanosterol synthase function results in a nonviable phenotype; similarly, inhibition of the P. carinii enzyme has been shown to reduce the viability of P. carinii in vitro (Kaneshiro et al., 2000). Saccharomyces cerevisiae Erg7 localizes to lipid particles, and when expressed in an S. cerevisiae ERG7 null mutant, homologs of Erg7 from the plant pathogen Arabidopsis thaliana and the parasite T. cruzi localized to lipid particles in an S. cerevisiae ERG7 mutant (Milla et al., 2002a, b). Lipid particles are thought to derive from the endoplasmic reticulum (ER), where neutral lipids accumulate within the lipid bilayer and bud off into the cytoplasm after reaching a certain size (Athenstaedt et al., 1999).

“
“Kynurenic acid (KYNA) is an astrocyte-derived non-competitive antagonist of the α7 nicotinic acetylcholine receptor (α7nAChR) and inhibits the NMDA receptor (NMDAR) competitively. The main aim of the present study was to examine the possible effects of KYNA (30 – 1000 nm), applied locally by reverse dialysis for 2 h, on extracellular GABA levels in the rat striatum. KYNA

concentration-dependently reduced GABA levels, with 300 nm KYNA causing a maximal reduction to ~60% of baseline concentrations. The effect of KYNA (100 nm) was prevented by co-application of galantamine (5 μm), an agonist at a site of the α7nAChR that is very similar to that targeted by KYNA. Infusion of 7-chlorokynurenic acid (100 nm), an NMDAR antagonist acting selectively at the glycineB site of GSK2118436 research buy the receptor, affected neither basal GABA levels nor the KYNA-induced reduction in GABA. Inhibition of endogenous KYNA formation Trametinib by reverse dialysis of (S)-4-(ethylsulfonyl)benzoylalanine (ESBA; 1 mm) increased extracellular GABA levels, reaching a peak of 156% of baseline levels after 1 h. Co-infusion of 100 nm KYNA abolished the effect of ESBA.

Qualitatively and quantitatively similar, bi-directional effects of KYNA on extracellular glutamate were observed in the same microdialysis samples. Taken together, the present findings suggest that fluctuations in endogenous KYNA levels, by modulating α7nAChR function, control extracellular GABA levels in the rat striatum. This effect may be relevant for a number of physiological and pathological processes involving the basal ganglia. “
“The brain corticotropin-releasing factor (CRF) system triggers a variety of neuroendocrine and behavioural responses to stress. Whether maternal behaviour and emotionality in lactation are modulated by CRF has rarely been investigated. In the present study, we measured CRF mRNA expression within the parvocellular part of the paraventricular nucleus in virgin and

lactating Wistar rats PLEKHB2 bred for high (HAB) and low (LAB) anxiety-related behaviour or non-selected for anxiety (NAB). Further, we intracerebroventricularly infused synthetic CRF or the CRF receptor (CRF-R) antagonist D-Phe to manipulate CRF-R1/2 non-specifically in lactating HAB, LAB, and NAB dams, and monitored maternal care, maternal motivation, maternal aggression, and anxiety. The CRF mRNA expression in the parvocellular part of the paraventricular nucleus was higher in HAB vs. LAB rats independent of reproductive status. The lactation-specific decrease of CRF mRNA was confirmed in LAB and NAB dams but was absent in HAB dams. Intracerebroventricular CRF decreased maternal care under basal conditions in the home cage in all breeding lines and reduced attack behaviour in HAB and LAB dams during maternal defence. In contrast, D-Phe rescued maternal care after exposure to maternal defence in the home cage without influencing maternal aggression.

196 μg/mL, 6.384 μg/mL, and 41.952 μg·h/mL and were 31, 4 and 16% higher following TDF coadministration. After TDF alone, the steady-state geometric mean TFV Cmin, Cmax and AUC were 0.052 μg/mL, 0.262 μg/mL and 2.590 μg·h/mL, respectively. These values decreased by 12, 25 and 15%, respectively, after FPV coadministration Y-27632 price and by 9, 18 and 7%, respectively, after FPV/RTV coadministration. During FPV/RTV dosing, the geometric

mean ritonavir Cmin, Cmax and AUC were 0.177 μg/mL, 0.858 μg/mL and 5.104 μg·h/mL, respectively (data not shown). During TDF coadministration, these increased slightly in groups C and D [GMR (90% CI) 1.09 (0.80–1.49) for AUC0−24 h, 1.12 (0.81–1.55) for Cmax, and 1.05 (0.79–1.40) for Cmin]. The regimens were generally well tolerated, although possibly drug-related maculopapular rash was observed in 38% (15 of 39) of the subjects: during FPV dosing alone in six subjects (three grade 1, two grade 2 and one

grade 3), during FPV/TDF dosing in four subjects (two grade 1 and two grade 2), during FPV/RTV+TDF dosing in four subjects (all grade 2), and during FPV/RTV dosing in one subject (grade 4). Laboratory parameters remained stable over the study period. Our results show that, when TDF is coadministered with either unboosted FPV or FPV/RTV, a small reduction in GSK1120212 price TFV exposure and increase in APV exposure occur. In previous TDF–FPV/RTV coadministration studies, the effect of adding an FPV regimen to a TDF regimen was not evaluated. However, two studies that evaluated APV pharmacokinetics following the addition of TDF 300 mg qd to an FPV/RTV 700/100 mg bid or 1400/200 mg

qd regimen noted negligible increases in steady-state APV Cmin values (by 4% [15] and 2% [19], respectively). The APV and TFV pharmacokinetic changes observed in our study were unlikely to be clinically important because the steady-state geometric mean TFV Cmin remained within the range reported in HIV-infected patients treated with TDF 300 mg qd without concurrent FPV [22–24], and the geometric find more mean APV Cmin for unboosted FPV (0.351 μg/mL) and FPV/RTV (2.88 μg/mL) during TDF coadministration remained 2.4- and 19.7-fold higher than the documented protein binding-adjusted 50% inhibitory concentration (IC50) for wild-type HIV isolates (0.146 μg/mL), respectively [25]. The pattern of plasma Cmin and AUC changes that we observed during TDF–FPV and TDF–FPV/RTV coadministration was different from the pattern reported when TDF was given with ATV [10,26], ATV/RTV [10,11,27], LPV/RTV [12,13,24,28] or indinavir (IDV) [13] (increase in TFV and decrease in PI), DRV or brecanavir (BCV) (increase in TFV and PI) [14,29], nelfinavir (NFV) (no change in TFV and decrease/no change in NFV and/or active metabolite M8) [30,31], saquinavir (SQV) (increase in TFV and increase/no change in SQV) [22,32], or TPV/RTV (no change/increase in TFV and decrease in TPV) [33]. Interactions between TDF and PIs can potentially occur at the kidney and/or the gut level.

[4] Enterotoxigenic E. coli (ETEC and EAEC) cause approximately Selleck PR 171 half of TD in Latin America, Africa, South Asia, and the Middle East.[5, 6] It was first shown by Kean[7] that antibiotics can prevent a large proportion of TD. In the 1970s and 1980s, doxycycline and fluoroquinolones were successfully used to prevent TD.[8, 9] A National Institutes of Health (NIH) Consensus Development Conference in 1985, however, discouraged using prophylactic antibiotic treatment because of concern about absorbable antibiotics contributing to the development

of resistance strains.[10] Rifaximin is a non-systemic, gut-selective antibiotic that has activity against enteric bacterial pathogens causing TD in multiple areas of the world.[11, 12] The small study size of previous studies has yielded inconsistent findings. The purpose of this meta-analysis was to integrate all available data to provide a clearer understanding of rifaximin’s efficacy. A systematic search of the literature in PubMed (up to November 2011), the Cochrane Central Register of Controlled Trials (Cochrane Library Issue 4,

October 2011), Embase (up to November 2011), and the Science Citation Index (up to November 2011) was conducted to identify relevant randomized controlled trials (RCTs) for our meta-analysis. In addition, references from the trials were further searched manually to Z-VAD-FMK price identify potentially relevant studies. The following selection criteria were applied: (1) study design: randomized, controlled trial; (2) study population: healthy, adult civilian travelers or military members aged ≥18 years; (3) intervention: prophylactic administration of rifaximin; (4) comparison intervention: placebo; (5) outcome measures: the primary efficacy end point was occurrence of diarrhea during 14 days of treatment with rifaximin or placebo. TD was defined as passage of at least three unformed stools within a 24-hour period plus one or more of the following signs or symptoms

of enteric infection: PD184352 (CI-1040) abdominal pain or cramps, nausea, vomiting, fever (≥37.8°C), fecal urgency, passage of gross blood or mucus in stool, tenesmus, or moderate to severe increase in intestinal gas.[13] Secondary end points included: incidence of the required antibiotic treatment, occurrence of mild diarrhea (MD; defined as a passage of one to two unformed stools during a 24-hour period plus at least one of the described abdominal symptoms for TD), incidence of TD occurring in the 7-day follow-up period, incidence of TD associated with isolation of diarrheagenic E. coli (ie, ETEC, EAEC), TD associated with unidentified pathogens, and any adverse events. Two review authors independently extracted details of randomization methods, blinding of treatments, and outcome assessments. Standardized, detailed forms for extraction of data from the selected trials (Table 1) were developed.

In the last step of the biosynthesis reactions, the aminotransferase encoded by the rfbE gene synthesizes GDP-α-perosamine from GDP-4-keto-6-deoxymannnose (Albermann & Piepersberg, 2001). The

rfbE (per) mutant of EHEC O157:H7 shows decreased viability in mouse and bovine intestine (Sheng et al., 2008). WecA protein polymerizes nucleotide-activated monosaccharides on the surface of the inner membrane of bacteria (Bengoechea et al., 2002), and WaaL protein ligates the polysaccharide to core-lipid A (Hug & Feldman, 2011). The waaL deletion mutant of uropathogenic E. coli has reduced viability in the mouse urinary tract (Billips et al., 2008). Based on these reports, the virulence properties of EHEC O157:H7 are thought to involve the LPS O-antigen, but whether GSK2118436 order the LPS O-antigen is required for animal killing by EHEC has not yet been determined. To understand the molecular mechanisms of animal killing by pathogenic bacteria, bacterial virulence must be evaluated in animal

models. A recent study revealed that oral administration of EHEC O157:H7 kills germ-free mice (Eaton et al., 2008; Fukuda et al., 2011). The use of MS-275 concentration germ-free mice for a genetic survey of EHEC virulence genes, however, would require very large numbers of animals and is thus associated with serious ethical and financial issues. Although insects lack an acquired immune system, they have innate immune systems that are Metformin clinical trial highly conserved with mammals (Okada & Natori, 1983; Lehrer & Ganz, 2002). Antimicrobial peptides have a central role in the humoral innate immune system and are conserved among many living organisms, including insects and mammals (Okada & Natori, 1983; Meister et al., 1997; Natori et al., 1999; Natori, 2010). Similar to mammals, insects have a cytokine-like peptide that activates the expression of antimicrobial peptides (Meister et al., 1997; Tauszig et al., 2000; Ishii et al., 2010). Therefore, insects can be effectively used to investigate the molecular interactions between pathogenic bacteria and innate immune

systems. Silkworms, larvae of the lepidopteran species Bombyx mori, are rarely killed by laboratory strains of E. coli, whereas they are killed by human pathogenic bacteria such as Staphylococcus aureus, V. cholerae, and Pseudomonas aeruginosa (Kaito et al., 2002). We identified S. aureus virulence genes using a silkworm infection model (Kaito et al., 2005, 2006; Matsumoto et al., 2007, 2010; Nagata et al., 2008; Ikuo et al., 2010; Miyazaki et al., 2011). Silkworms have several advantages as an infection model. They have a larger body than nematodes and fruit flies and can therefore be injected with quantitative amounts of bacterial solution for assessment of the bacterial virulence; that is, the 50% lethal dose (LD50) can be determined (Kaito & Sekimizu, 2007; Miyazaki et al., 2011).

Table 2 shows the baseline demographic characteristics and clinical outcomes of participants in the cohort. The group prescribed boosted PIs had a higher median age (42 vs. 41 years, respectively; P=0.01), fewer participants with a history of injecting drug use (22 vs. 30%, respectively; P<0.01), more participants diagnosed with AIDS at baseline (21.5 vs. 9.5%, respectively; P<0.01), a

lower median CD4 count (120 vs. 190 cells/μL; P<0.01) and a higher median viral load (5.0 vs. 4.9 log10 HIV-1 RNA copies/mL, respectively; P<0.01). A higher proportion of individuals on boosted PI-based regimens CYC202 supplier had >95% adherence to therapy than in the NNRTI group (68 vs. 57%, respectively; P<0.01); however, there was no significant difference in the proportion of individuals Anti-infection Compound Library price who achieved virological suppression in the two groups after 1 year of

therapy (67 vs. 66%, respectively; P=0.47). Forty-seven per cent of participants had drug resistance tests performed during therapy; 341 (40%) of the boosted PI group and 444 (54%) of the NNRTI group (P<0.01). Among those tested for drug resistance, 35% had at least one drug resistance mutation; 27% of the boosted PI group and 40% of the NNRTI group (P<0.01). Participants in the NNRTI group had a longer time to development of drug resistance (median 5.6 months; IQR 1.9–16.8 months) as compared with those in the boosted PI group (median 4.4 months; IQR 1.1–12.1 months). The list of drugs available in RLSs gave 11 antiretroviral drugs with 30 possible triple ART combinations. Participants who initiated boosted PI-based regimens had a

higher median GSS after treatment on first-line regimens than those in the NNRTI group (11.0 vs. 9.8, respectively; P<0.001). Figure 1 shows the proportions of individuals with different numbers of combinations of ART Lck by participants on NNRTI (Fig. 1a) and those on boosted PI-based first-line ART (Fig. 1b). The proportion of participants with the maximum number of possible active combinations of ART after first-line therapy among patients on boosted PI first-line therapy (70.7%) was almost twice that of participants starting with NNRTI-based ART (44.5%). The graphs also show that, among participants on boosted PIs, the proportion of participants with all possible combinations (70.7%) was almost eight times higher than the proportion of participants with five or fewer combinations (8.9%), while the corresponding ratio for NNRTI-based ART was almost 1:1. The bivariate and multivariate analyses of factors associated with having the maximum number of possible active combinations of antiretroviral drugs, versus fewer combinations, are shown in Table 3. The median time to testing for drug resistance was 47.2 months (IQR 27.86, 64.53 months).

97, Q-tip, M = 52.52, Alectinib F1,17 = 4.39, P = 0.052; nonpainful stimuli: needle, M = 19.41, Q-tip, M = 20.05, F1,17 = 1.27, P = 0.276). To further investigate whether the effects on pain ratings were influenced by habituation to electrical stimuli,

ratings were subjected to three-way anovas comprising the factors electrical stimulation, visual stimulation and time (first and last 50% of trials). This analysis did not reveal significant effects in relation to the factor time, suggesting that habituation effects did not substantially contribute to the present findings. PDR traces for needle and Q-tip clips (pooled across nonpainful and painful trials) are depicted in Fig. 1C. The dilation started at about 0.4 s after clip onset. PDR traces to needle and Q-tip clips already differed before electrical stimulus onset. A running t-test between both PDR traces revealed significant differences between the clips starting from about click here −0.3 s before electrical stimulus onset until

the end of the trial. For the correlation analysis, we selected the time interval based on our previous study (Höfle et al., 2012) from −0.2 s before to 0.6 s after electrical stimulus onset. Data points were averaged within the interval to obtain a single value for further analyses. The correlation analysis conducted on the average effect (needle minus Q-tip) across participants revealed a significant positive relationship between PDR and perceived unpleasantness (r17 = 0.48, P = 0.046). This finding directly replicated the results of our previous study (Höfle et al., 2012), where a positive correlation of r24 = 0.49 was found for this analysis. A cluster-based analysis on mean ERP values computed over all electrodes and a time

interval from −1 to 0 s revealed significant differences between viewing needle pricks and Q-tip touches from about −0.4 to −0.1 s (illustrated by means of a running t-test in Fig. 2A) and at right-central electrodes, i.e. contralateral to the forthcoming electrical stimulation (Fig. 2B). The mean ERP traces for these electrodes showed a slow negative potential Etofibrate within the time interval of interest, which was more pronounced when viewing needle clips compared with Q-tip touches (Fig. 2C). In the following, we will refer to this slow negative potential as stimulus-preceding negativity (SPN; e.g. Brunia & van Boxtel, 2001). Mean ERP amplitudes (−0.4 to −0.1 s) at right-central electrodes were selected for the further correlation analyses. Time–frequency representations (5–30 Hz) of total oscillatory responses at right-central electrodes showed an initial increase in the alpha band peaking at about 0.1–0.2 s after clip onset (Figs 3A and 4). The alpha power increase was maximal at occipital sites (Fig. 3B, first row). Following the increase, a reduction of ABA was found, which was strongest at right-central electrodes (Fig. 3B, last row).

In fungal cells, there is evidence of some functions of ecto-ATPase (Zhong et al., 2000; Junior et al., 2005; Collopy-Junior et al., 2006; Kiffer-Moreira et al., 2010), but little information is available about the activity of ecto-5′-nucleotidase and its product, adenosine. Identification of the physiological role of this enzyme would contribute to understanding the biochemical aspects of host–parasite interactions involving C. parapsilosis. We would like to thank check details Ms Fatima Regina de Vasconcelos Goulart for preparation of fungal cultures and Mr Fabiano Ferreira Esteves and Ms Rosangela Rosa de Arau´jo for excellent technical assistance. This work was supported by grants from the Brazilian

Agencies Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) and Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ). “
“The main α-glucan synthesized by lichens of the genera Ramalina in the symbiotic state is isolichenan. This polysaccharide was not found in the aposymbiotically cultivated symbionts. It is still unknown if this glucan is produced by the mycobiont only in the presence of a photobiont, in a lichen thallus, or if the isolichenan suppression is influenced by the composition of

culture medium used in its aposymbiotic cultive. Consequently, the latter hypothesis is tested in this study. Cultures of the mycobiont Ramalina complanata were obtained from germinated ascospores and cultivated on 4% glucose Lilly and Barnett medium. Freeze-dried selleck products colonies were defatted and their carbohydrates extracted successively with hot water and aqueous 10% KOH, each at 100 °C. The polysaccharides nigeran, laminaran and galactomannan were liberated, along

with a lentinan-type β-glucan and a heteropolysaccharide (Man : Gal : Glc, 21 : 28 : 51). Nevertheless, the α-glucan isolichenan was not found in the extracts. It follows that it was probably a symbiotic product, synthesized Ibrutinib solubility dmso by the mycobiont only in this particular microenvironment, in the presence of the photobiont in the lichen thallus. A discussion about polysaccharides found in the symbiotic thallus as well as in other aposymbiotic cultivated Ramalina mycobionts is also included. The lichen thallus, the symbiotic phenotype of lichen-forming fungi in association with their photobiont (algae and/or cyanobacteria), contains considerable amounts of polysaccharide. Although this symbiotic nature was first revealed in 1867, the development of a lichen thallus is often so integrated that it has been perceived and studied as a single organism until quite recently (Nash, 2008; Lutzoni & Miadlikowska, 2009). Investigations on lichen polysaccharides were carried out using material extracted from the entire thallus (Gorin & Iacomini, 1984, 1985; Gorin et al., 1993; Teixeira et al., 1995; Olafsdottir & Ingólfsdottir, 2001), with no mention of the origin of component polymers (fungal partner or photobiont).