Blood lymphocytes were washed once in cold PBS, and following centrifugation (680 g, 18°C, 10 min) the pellet was resuspended in 2 ml red blood cell lysis buffer [0·15 m NH4Cl, 0·01 m KHCO3 and 10 µm ethylenediamine tetraacetic acid (EDTA) Na2·2H2O] and incubated for 2 min at room temperature. The volume was then adjusted to 30 ml using

sterile PBS and centrifuged. Following two subsequent washes, the cell pellet was resuspended in IMDM (Sigma) supplemented with 10% fetal bovine serum (FBS; Gibco, Mulgrave, Australia) and anti-mycotic solution (10 mg/l; Sigma). PBMCs/CRL-9850 cells were plated in six-well tissue culture plates (Corning, Sigma) at 5 × 106 cells/well and incubated at 5% CO2, 37°C for 24 h prior to stimulation with bacteria, as described by Amrouche et al. [21]. Briefly, 106 freshly prepared viable (live or GIT) or equivalent (∼106 CFU/ml) heat-killed bacteria were added per 106 cells https://www.selleckchem.com/products/Staurosporine.html and co-cultured for 72 h at 5% CO2, 37°C. At 6, 12, Roxadustat solubility dmso 24, 48 and 72 h, 500 µl samples of the culture medium were collected and analysed for cytokine secretion by

ELISA (Becton Dickinson, San Jose, CA, USA), in accordance with the manufacturer’s instructions. Data are expressed as the mean cytokine response minus background (pg/ml) of each treatment from triplicate wells, plus or minus the standard error of the mean. Treg/Th17 populations were characterized following PBMC/bacteria co-culture. Briefly,

106 PBMC were co-cultured with either live or killed bacteria, lipopolysaccharides (LPS; Sigma) or media alone, in a 24-well plate at 37°C in 5% CO2 for 96 h, then cells were washed twice using FACS buffer (PBS + 2% FCS) and centrifuged at 500 g for 10 min. PBMC were resuspended at 106 cells/ml, and surface marker staining was performed using fluorescein isothiocynate (FITC)-labelled anti-human CD4, allophycocyanin-labelled anti-human CD25/CD3 (Becton-Dickinson), peridinin chlorophyll protein (PerCP)-labelled anti-human CD3 (Biolegend, San Diego, CA, USA) and PerCP cyanine (Cy)5·5-labelled anti-human CCR6 (CD196). Intracellular staining was performed using phycoerythrin (PE)-labelled anti-human FoxP3/RORγt (BD Sclareol Pharmingen and R&D Systems, Minneapolis, MN, USA, respectively), according to the manufacturer’s instructions. Samples were read using a BD FACSCalibur, data acquired using CellQuest program (Becton Dickinson Biosciences), and analysis performed using Gatelogic version 3·07 software (Inivai, Victoria, Australia). Absolute numbers of Treg cells and Th17 cells were calculated as a percentage of the total lymphocyte number. All co-cultures were carried out in triplicate. Results obtained were analysed as a split plot in time design with three main factors: strains (six levels) and treatments (three levels) as the main plot and time (five levels) as a subplot.

For example, Th17-cell priming requirements have elicited disputes, primarily due to inconsistencies between mouse and human cytokine requirements and in particular due to the controversial role of TGF-β in Th17-cell differentiation [65]. Although Th-cell polarization is a multilayered process that is dependent on signal strength and

the engagement of different co-stimulatory molecules following antigen processing, and the establishment of a complex immunological synapse, the focus of interest has been on cytokine requirements. Most of the approaches to dissect Th17 priming conditions have therefore used polyclonal stimulation of naïve Apoptosis inhibitor T cells with anti-CD3 and anti-CD28 antibodies in the presence of well-defined cytokine combinations in vitro. However, human Th17-cell polarization following antigen-specific stimulation with microbes has recently revealed that priming requirements differ, depending on microbial antigen selleck compound specificity even within the same class of Th cells [12]. Microbial ligands that generate Th17-cell responses through TLR and CLR signaling have primarily, although not exclusively, been defined for C. albicans [66, 67]. Fungal components have been shown to bind to

Dectin1, Dectin2, and Mincle expressed on APCs, which leads to the recruitment of the tyrosine kinase Syk, activation of the adaptor CARD9, and finally to secretion of IL-23, IL-1, IL-6 [66, 67], which are involved in the generation of human Th17 cells. Interestingly, the generation of C. albicans-specific human Th17 cells has been shown to be highly dependent on IL-1β, while S. aureus-specific Th17 cells can be primed in its absence [12]. This not only indicates different pathways for the generation of human Th17 cells but also a strong link between microbial antigen specificities of Th cells with their respective priming requirements.

This has important consequences for the functionality of Th17 cells, since C. albicans-specific, and thus IL-1β-dependent Th17 cells have been shown to co-express IL-17 and IFN-γ but not IL-10, while S. aureus-specific Th17 cells have been shown to be IFN-γ negative but IL-10 positive [12]. IL-1β therefore acts as a molecular switch factor for the generation of pro- versus anti-inflammatory Idoxuridine Th17-cell properties [3, 68]. A model disease to exemplify the two-sided interactions of environment and Th cells is chronic mucocutaneous candidiasis, a rare disease characterized by chronic and persistent infection of skin and mucosa with Candida species [69]. Numerous mutations affecting the differentiation and function of Th17 cells have been described for chronic mucocutaneous candidiasis. Namely, humans with loss-of-function mutations in CARD9 and STAT3 or gain-of-function mutations in STAT1 have reduced Th17 cells [70-72]. In other families, IL-17 or its receptor is mutated, or autoantibodies against IL-17 are secreted [73, 74].

Accordingly, patients have been classified depending on their number of naive, memory and switched-memory

B cells [8, 9]. Furthermore, a low percentage of memory B cells in CVID patients has been associated with a worse clinical presentation and poor response to Selleck AZD1152 HQPA vaccines [10-12]. Loss of memory B cells also occurs from the onset of acute HIV infection. Recently, low frequencies of CD27+ memory B cells and decreased production of antibodies have been described in successfully treated HIV patients in spite of drug-suppressed viraemia. Surface expression levels of TNF-related apoptosis-inducing ligand (TRAIL) on memory B cells correlated negatively with their peripheral blood frequency [13]. The generation of memory B cells and plasma cells is essential to establish efficient humoral immune responses. Co-operation of B cell receptor (BCR)-activated B cells with helper T cells is relevant and occurs through contact between T cell membrane molecules (CD40L, ICOS, etc.) and their corresponding B cell ligands [14]. The importance of several of these components of the immune system has been exemplified by naturally occurring immunodeficiencies [15]. Furthermore, secretion of cytokines by T cells also instruct the differentiation of B cells, selleck kinase inhibitor including interleukin (IL)-21 as one of the more potent cytokines

for human B cell proliferation and differentiation [16-20]. Following antigenic stimulation, Toll-like receptor (TLR) can provide an additional signal for the differentiation of B cells and even substitute T cell-derived signals [21, 22]. Apart from their effect on proliferation and differentiation, several of these stimuli also influence B cell survival. BCR activation has been shown to induce B cell apoptosis in the absence of survival signals such as that provided through CD40. Mainly produced by activated CD4+ follicular T cells [19, 23, 24], IL-21 is a type I cytokine that belongs to a family that uses the

common cytokine receptor γ-chain as a component of their receptors [25, 26]. The stimulatory or inhibitory effect of IL-21 L-gulonolactone oxidase depends on the maturation and activation status of the B cell, the co-stimulatory accompanying signal and the presence of other cytokines. In humans, IL-21 is a potent inductor of plasma cell differentiation if combined with anti-CD40 [16], induces class-switch recombination and secretion of immunoglobulin (Ig)G and IgA in pre-switched IgM memory B cells [19, 27] and is able to induce plasma cell differentiation and immunoglobulin production even by naive B cells [16]. However, IL-21 triggers B cell death when BCR is ligated [16, 28]. A balance between apoptosis-inducing and survival signals must exist to preserve B cell homeostasis.

[109] Pre-eclampsia is a pregnancy-related syndrome that Neratinib mouse affects multiple systems and clinically presents as hypertension, proteinuria, edema, and in its more sever forms evidence

of fetal compromise, neurologic abnormality, liver and hematologic dysfunction.[110] The complexity of the syndrome defies the development of a panel of genetic screens or biomarkers.[111] While the basic cause of the disease is as yet unknown, multiple hypotheses exist. These include failure of placentation[112] and thus reduced utero-placental perfusion, intolerance to volume expansion generated by pregnancy,[113] infection,[114] and inflammation.[115] It is hotly debated as to whether failed placentation is caused or a by-product of broken maternal immune tolerance.[116, 117] Many agree that a common final pathway to the manifestation of the disease is endothelial cell damage occurring in a variety of vascular beds.[118] While the Selleckchem beta-catenin inhibitor disease is thought of as being unique in human, many recognize the potential positive role of the integration of research in human and animal models in understanding the underlying mechanisms.[119, 120] The hallmarks of pre-eclampsia most sought

after in animal models are hypertension, renal dysfunction (proteinuria), and further, conditions such as poor trophoblast invasion and endothelial damage. Current models address some of these issues. There have been rare reports of spontaneous pre-eclampsia in related non-human primates.[121] These species have also been used to develop models of pregnancy-related hypertension and proteinuria based on injection during mid-gestation of inflammatory mediators, such as tumor necrosis factor[122] or antibodies to interleukin 10.[123] There are strains of mice that spontaneously develop hypertension, proteinuria, smaller litters, and fetal demise, and these have been used to model pre-eclampsia.[124, Dapagliflozin 125] There are also models of spontaneous pregnancy-associated hypertension with fetal compromise

in rats.[126] There also exist genetically manipulated mouse and rat models. In one interesting genetic model of hypertension in pregnancy, female mice transgenic for human angiotensinogen are mated to males transgenic for human rennin.[127] The resulting pregnancy is marked by distortion of placental anatomy, elevation of circulation vascular endothelial growth factor (VEGF) receptor in mid-gestation (12–13 of 19–20 days), hypertension, fetal intrauterine growth retardation, and systemic maternal disorders including proteinuria and convulsion. In the rat version of this model,[128] the hypertensive disease experienced by the pregnant rat is thought related to secretion of rennin from the placenta into the maternal circulation.

To assess VIP production in endometrial CD4 lymphocytes, cells recovered from endometrium after mechanical disruption were cultured with GolgiStop™ for 4 h in a flat-bottomed plate. In both situations, after washing in PBS, cells were fixed and permeabilized with the Fix/Perm kit (at the manufacturer’s recommended concentrations; Becton Dickinson). After washing, permeabilized cells were incubated for 30 min with rabbit anti-VIP antibody (Peninsula-Bachem Inc.), then washed and incubated with fluorescein isothiocyanate (FITC)-conjugated anti-rabbit antibody (Santa Cruz Biotechnology). Cells were then washed with PBS–2% FCS to allow membrane closure

and finally surface-stained with phycoerythrin cyanin5 (PECy5)-conjugated anti-CD4 antibody (Becton Dickinson). Ten thousand events were acquired in a FACS Aria II cytometer® and results were analysed using WinMDI software®. Negative control samples were incubated in parallel selleck products with an irrelevant, isotype-matched antibody. Results for positive cells are expressed as a percentage of the respective population MLN0128 research buy and the quadrant was set using irrelevant isotype-specific antibody.

The percentage of CD25+FoxP3+ or VIP+ cells was obtained inside the electronically gated CD4+ cell population using WinMDI software®. Determination of VIP, VPAC1 and VPAC2 expression levels was performed in PBMCs from RSA and fertile women after co-culture with trophoblast cells for 24 h by RT–PCR and real-time RT–PCR. Briefly, maternal PBMC total RNA was isolated with TRIzol reagent (Life Technologies, Grand Island, NY, USA), followed by reverse transcription according to the manufacturer’s instructions (Promega). For amplification Farnesyltransferase of the resulting

cDNA, 1 or 2 μl of the RT mixture were used. The sample volume was increased to 25 μl with 0·2 mM deoxynucleotide triphosphates (dNTPs), 0·25 uM specific primers, 3 mM MgCl2, 2 U Taq DNA polymerase and 1:30 000 dilution of Sybr Green. Real-time PCR reactions were performed in a DNA Engine Opticon (MJ Research, Inc., Waltham, MA, USA) after a predenaturation step at 95°C for 5 min; we used a denaturation step at 95°C for 30 s, an annealing step at 58°C for 30 s and elongation step at 72°C for 30 s for a total of 40 cycles. An additional extension step at 72°C for 10 min was carried out. PCR products were quantified in Opticon Software® and normalized to endogenous glyceraldehyde 3-phosphate dehydrogenase (GAPDH). The primers and thermal profiles were selected with the software Primer-3, as described previously [20]. PCR products were electrophoresed through a 2% ethidium bromide-stained agarose gel, visualized by transillumination and photographed. As a positive control for VIP and VPAC receptors we used human neuronal cell line SH-SY5Y, cultured as described previously [27].

SCID mice reconstituted with XBP1−/− B cells fail to produce antibodies against polyoma virus and succumb at higher rate than control recipients. Enforced expression of XBP-1 in BCL1-3B3 cells, a B cell line, drive these cells towards plasma cell differentiation, and intense signals for XBP-1 transcripts were found in plasma cells from the sinovium from two patients with rheumatoid arthritis. These data demonstrate an essential and sufficient role for XBP-1 in directing plasma cell differentiation [85]. Consistent with this idea, activation of the UPR pathway was observed

during differentiation of antibody secreting B cells [87]. PARP inhibitor The CH12 murine B cell lymphoma was used as a model for plasma cell differentiation as they become IgM secreting cells in response to LPS. Treatment of CH12 cells with LPS elevated XBP-1 transcripts and induced the production of chaperones BiP and GRP94 before the translation of Ig chains occurred. Still, the highest levels of transcripts and chaperones were observed when intracellular Ig chains were also elevated. The increase in Igμ, Igκ, BiP, and GRP94 transcripts and proteins correlated with the induction of XBP-1 expression and ATF6 cleavage, MEK inhibitor but not CHOP induction. On the other hand, the treatment of those cells with tunicamycin robustly induced UPR targets and CHOP. These data suggest that other signals rather than unfolded/misfolded

Ig chains activate, at least in part, the UPR pathway [87]. In accordance with these data, the induction of XBP-1 mRNA in murine B lymphocytes was strongly increased in the presence of IL-4 in a protein synthesis-independent manner [53]. In addition, GRP78 and CHOP transcripts were up regulated after IL-4 treatment, suggesting

that UPR target genes are regulated by IL-4. Nevertheless, the splicing of XBP-1 mRNA by IRE1α depended on Ig synthesis. In addition, XBP-1 seemed to be required for Ig secretion by plasma cells: forced expression of XBP-1s enhanced IgM secretion in activated BCL1 cells (mature B cell lineage), and XBP-1s expression GBA3 restored IgM and IgG2b production in XBP1-deficient B cells. These findings support the requisite of UPR activation for plasma cell function [53]. In contrast with these findings [87], another study [88] employed I.29 μ+ lymphoma cell line treated with LPS as a model for plasma cell differentiation. XBP-1 was found in high amounts only when increased IgM synthesis was detected in day 3 and 4 post-stimulation. These differences could be explained by the different readout between the studies: one measured XBP-1 transcripts [87], while the other looked for the protein [88]. Microarray gene expression analysis was used to identify genes related to the secretory pathway (ER protein folding, protein glycosylation, vesicle trafficking) and cell differentiation whose expression relied on XBP-1.

To prevent chronic inflammation, the liver must modulate innate and adaptive immune responses to these diverse antigens [1, 3]. Conversely, the liver is an important organ in host defence against parasitic and microbial infections [4]. Thus, immune responses can be initiated in the liver to eliminate microbial infection [5-7]. Further understanding of the mechanisms RGFP966 that determine the balance between immunity to pathogens and tolerance to diverse dietary and other antigens will provide new insights into the design of therapeutic strategies to regulate immunity in liver infection,

autoimmunity and transplantation. Hepatic B cells comprise approximately 5% of intrahepatic lymphocytes [8-10]. Limited studies have addressed the function

of hepatic B cells in vitro [11] and in the regulation of experimental autoimmune biliary disease [12-14]. It has been shown that LPS-treated hepatic B cells enhance the production of interferon (IFN)-γ by liver natural killer (NK)1·1+ cells [11] and promote liver inflammation in the non-obese diabetic (NOD).c3c4 mouse model of autoimmune cholangitis Enzalutamide concentration [13], suggesting that hepatic B cells can regulate hepatic immune responses positively. In contrast, the Toll-like receptor (TLR) ligands LPS (TLR-4) and cytosine–phosphate–guanosine (CpG) (TLR-9) can stimulate interleukin (IL)-10-producing regulatory B cells (Breg) (B10) and regulate immune responses negatively [15-17]. Given that LPS is delivered continuously by the liver via the portal blood, we hypothesize that the ability of

hepatic B cells to regulate immune responses positively might be due to a lack of LPS-activated Breg in the liver. In this study we demonstrate that, unlike splenic B cells, hepatic B cells lack B10 cells and comprise significantly smaller proportions of B1a and marginal zone (MZ)-like B cells [16]. In addition, when compared with liver conventional myeloid (m)DCs from B cell-deficient mice, those from B cell-competent wild-type mice were more immunostimulatory, as evidenced by higher levels of maturation marker expression Cobimetinib supplier in response to in-vivo LPS stimulation, and by a greater production of proinflammatory cytokines following ex-vivo LPS stimulation. Male C57BL/6 (B6; H2b) and B6·129S2-Ighmtm1Cgn/J (μMT) mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). B6·129P2-IL-10tm1Cgn mice (IL-10 reporter) were kindly provided by Dr David Rothstein (University of Pittsburgh). They were housed under specific pathogen-free conditions at the University of Pittsburgh School of Medicine, with unlimited access to food and water.

This is not what we observed. In contrast, the absence of the proximal promoter did not decrease circulating sST2 concentrations, either in naïve or allergen-challenged mice. Although the cellular source of sST2 in the blood is still not known, these findings suggest fibroblasts are not a major source under the conditions tested. It remains possible, however, that fibroblasts and/or the proximal promoter and enhancer are important for sST2 induction in

other physiological settings; this is something future studies with these mice may help reveal. In the course of these experiments we also found that fibroblasts use the proximal promoter to express ST2L and are functionally responsive to IL-33, as demonstrated by the AZD3965 ic50 gene induction of the neutrophil-attracting CXCL1 and other chemokines. Examination of these mice in models of fibrosis could therefore be informative due to the central role of fibroblasts and recent evidence implicating IL-33 in fibrotic disease [21]. Finally, we hypothesize that there are other nonimmune cell types that require the proximal promoter for ST2L expression and that these mice may thus be useful for examining tissue-specific IL-33 responses in vivo. A targeting vector was

constructed to delete a region in the ST2 locus beginning 4490 bp upstream of the +1 initiation site (ACGTGGGT) in exon 1b and ending at the 3′ end of exon 1b (83 bp downstream from the +1 site), as illustrated in Fig. 1A. The Inhibitor Library targeting construct was electroporated into 129×C57Bl/6 F1 hybrid ES cells and clones were then transfected with a CRE recombinase-expressing plasmid to delete the Neo cassette prior to injecting for germline transmission in C57Bl/6 mice using standard conditions. For splenocytes, spleens were minced

and single cell suspensions were collected through a nylon mesh. RBCs were lysed and cells were cultured for 3 h in RPMI with 10% FBS prior to RNA isolation. For mast cells, bone marrow cells were cultured in Iscove’s Modified Dulbecco’s Medium supplemented with 10% FBS, IL-3 (5 ng/mL, Amgen), and SCF (100 ng/mL, Silibinin Amgen) at approximately 2–5 × 105 cells/mL. Every 3–4 days nonadherent cells were transferred to new flasks. Flow cytometry was performed after 5 weeks using antibodies to ST2 (MD Bioproducts, clone DJ8) and c-kit (CD117, BD Pharmingen, clone 2B8). BMMCs were cultured overnight at 105 cells/well with or without IL-33 (Amgen) and IL-6 was measured in the supernatant by ELISA (R&D Systems). For fibroblasts, deboned tails from 12-week-old euthanized mice were minced in HBSS followed by digestion in a 1:1 solution of collagenase (Type XI-S Sigma in HBSS; 2000 U/mL) at 37°C for 30 min, and then 0.05% trypsin at 37°C for 20 min, followed by quenching (DMEM + 15% heat-inactivated calf serum). Cells were cultured in 10 cm plates for 5–7 days.

Most iKIRs recognize HLA class I ligands and function as important receptors in the maintenance

of NK-cell self-tolerance. In contrast, neither the ligands nor the function of most aKIRs have been established [4]. We haverecently shown in patients undergoing solid organ transplantation a protective effect of B haplotype genes regarding posttransplant CMV infection and reactivation [5, 6]. Similar studies have shown congruent results for donor activating KIR genotype in recipients of hematopoietic stem cell transplantation [7, 8]. These data suggest that NK cells might recognize CMV-infected cells via activating KIR receptors. Primary CMV infection most frequently occurs subclinically, and no studies have so far studied Kinase Inhibitor Library research buy NK cells during primary CMV infection. However, recent evidence suggests that murine NK cells may display immunological memory comparable to that of B and T lymphocytes [9, 10]. In mice infected with murine CMV, the repertoire of Ly49 (the murine homologue of KIR) on NK cells stays permanently altered [11]. The potential for CMV to modulate NK-cell surface receptors is underlined by the fact that in humans, latent CMV infection has been shown to induce permanent up-regulation of the activating NK-cell receptor natural

killer cell group antigen 2C (NKG2C) [12-14]. Collectively, these data suggest that latent CMV infection might lead to changes in the KIR repertoire of NK cells or might alter the NK-cell response to CMV in vitro. We therefore assessed in a cohort of healthy donors the expression of inhibitory and activating KIR receptors. KIR either repertoire was assessed both in freshly collected NK cells as well as after PLX-4720 cost co-culture with a CMV-infected fibroblast cell line. Fifty-four healthy donors were genotyped for the nonframework genes 2DL1, 2DL2, 2DL3, 2DL5, 3DL1, 2DS1, 2DS2, 2DS3, 2DS4, 2DS5, and 3DS1. KIR gene frequencies were comparable in 23 CMV-seropositive and 31 seronegative

donors and within the range of published prevalences for Caucasian donors (data not shown). The expression of cell surface inhibitory (2DL1/CD158a, 2DL2/3/CD158b, 2DL5/CD158f, 3DL1/CD158e1) and activating (2DS1/CD158h, 2DS4/CD158i, 3DS1/CD158e2) KIRs by flow cytometry was equally comparable between CMV-seronegative and CMV-seropositive patients (Supporting Information Fig. 1A–E, H and J). No antibodies are available against KIR2DS3 and KIR2DS5, and all antibodies that detect KIR2DS2 cross-react with the inhibitory isoform KIR2DL2. We therefore used quantitative PCR to compare the expression of these receptors in purified NK cells from CMV-seropositive and -seronegative donors. Again, no significant differences were detected between CMV-seropositive and CMV-seronegative donors for KIR2DS2, KIR2DS3, or KIR2DS5 (Supporting Information Fig. 1F, G and I). Previous data demonstrated the expansion of NK cells expressing the activating receptor NKG2C in CMV-seropositive donors [13].

While fluconazole is usually

active against Candida albicans, non-Candida albicans species often require more sophisticated approaches. A rapid species diagnosis is therefore desirable and can be provided by fluorescence in situ hybridisation (FISH). However, broad evaluation studies of described probes are largely lacking and the probe panel that has been described is incomplete. As an addition to previously described C. albicans FISH probes, we evaluated published DNA probes for C. glabrata and C. krusei, as well as newly Caspase phosphorylation designed DNA probes for C. krusei, C. lusitaniae, C. parapsilosis, C. tropicalis, Crypotococcus neoformans and a group of intrinsically fluconazole-resistant Candida species for FISH with 22 reference strains, 23 well-characterised laboratory control strains, 169 isolates from clinical samples and 48 blood cultures. Sensitivity and specificity of >99% were demonstrated for all evaluated this website species-specific probes, whereas the probe that binds to a heterogeneous group of intrinsically fluconazole-resistant Candida species correctly identified eight of nine fluconazole-resistant clinical isolates. FISH yielded reliable results using the classical FISH procedure as well as a recently described slide chamber-based method. Given this good sensitivity and specificity, FISH may be applied for rapid identification of yeast in screening analyses, thus

giving the opportunity for more precise targeting of antimycotic therapy. “
“Candida

species are the fourth most common cause of nosocomial bloodstream infections. An increase in the frequency of infections, which have become refractory to standard antifungal therapy, has been observed. Recent studies have shown that the pro-oxidant properties of diphenyl diselenide (PhSe)2, a structurally simple organoselenium compound, can be toxic to yeast. The objective of this work was to study, under non-reactive oxygen species (ROS)-generating conditions, the effect of different organochalcogenide GPX6 compounds [(PhSe)2, (PhTe)2, (MeOPhSe)2, (p-Cl-PhSe)2 and (F3CPhSe)2] on growth and germ tube formation by Candida albicans. A decrease in C. albicans growth in the presence of crescent concentrations of (PhSe)2, (PhTe)2 and (MeOPhSe)2 was observed. The organochalcogenide compound concentration needed to inhibit 50% (IC50) of the Candida growth was 0.5–2 and 2–10 μmol l−1, at a cell density of 105 and 106 cells ml−1, respectively. The compounds (p-Cl-PhSe)2 and (F3CPhSe)2 were able to inhibit the cell growth, although the inhibition was considerably weaker than that by (PhSe)2, (PhTe)2 and (MeOPhSe)2. In Candida suspensions incubated in a medium containing serum as an inducer of germ tube formation, the presence of either (PhSe)2 or (MeOPhSe)2 at 10 μmol l−1 completely inhibited the number of cells which formed germ tubes. These results demonstrate the potential of organochalcogenide compounds to inhibit both C.