DEGs specifically modulated by MSU in WT and Nlrp3−/− DCs were further analyzed by MetaCore™ software to identify putative biological pathways and cellular processes they might participate in. Three major biological processes were statistically modulated by MSU in both WT and Nlrp3−/−

DCs compared with untreated controls: the DDR, cell cycle, and apoptosis/survival pathways (Fig. 1A). A significant increase in the expression selleck products of several genes involved in double-strand and base-excision DNA repair (Xrcc1, Rad51, Ogg1, Brca1, Polb, and Tyms), cell cycle progression and proliferation (cyclin B and D, Ttk protein kinase, Prim1 and 2, and Rfc3 and 4), and repression of apoptosis (Xiap and Birc3) was observed only in Nlrp3−/− cells (Fig. 1B and Supporting Information Table 1). These data indicate that cells lacking NLRP3-mediated signaling exhibit a differential response to MSU compared with WT cells. Ibrutinib price To confirm the

physiological relevance of the MSU-induced pathways identified by gene expression array, we next assessed the extent to which MSU stimulation causes DNA damage in DCs. DCs generated from bone marrow (BM) of WT and Nlrp3−/− mice were therefore stimulated with MSU for 24 h and DNA fragmentation in individual cells was assessed by comet assay. This assay exploits a single-cell gel electrophoresis to progressively separate fragmented DNA from intact DNA from lysed cells. The resulting comet-like tail formation is then visualized check details and quantitatively analyzed; tail length reflects the degree of DNA fragmentation (Tail DNA%), while the Olive Tail Moment is an index of DNA damage that considers both the migration of DNA as well as the relative amount of DNA in the tail. No tail was observed in untreated DCs (Fig. 2). Bright comets of fragmented DNA were detected in the majority of MSU-treated DCs, with mean% of total

DNA in the tail and olive moment significantly higher than in untreated controls (Fig. 2). Interestingly, DNA breaks were significantly diminished in Nlrp3−/− DCs compared with WT DCs after stimulation with MSU alone or in the presence of LPS, indicating that LPS priming was not required for DNA damage induced by MSU. Moreover, in the absence of Nlrp3, DNA damage in DCs treated with oxidative H2O2 was also significantly reduced (Fig. 2). We then tested H2AX histone phosphorylation on serine 139 (γH2AX), a primary marker of DNA damage required for triggering DDR in eukaryotic cells [9]. We found that H2AX was readily phosphorylated in WT DCs during MSU stimulation and that γH2AX levels were sustained for up to 24 h (Fig. 3A). Similarly to MSU, stimulation of WT DCs with silica robustly induced γH2AX, indicating that the same pathway is induced by other particulates (Supporting Information Fig. 1).

Five subjects experienced durable chimerism, demonstrated immunocompetence and donor-specific tolerance by in vitro proliferative assays, and were successfully weaned off all immunosuppression one

year after transplantation. None of the recipients produced anti-donor antibody or exhibited engraftment syndrome or graft-versus-host disease. These results suggest that manipulation of a mobilized stem cell graft and nonmyeloablative conditioning selleck represents a safe, practical, and reproducible means of inducing durable chimerism and donor-specific tolerance in solid organ transplant recipients according to the authors. However, in a set-up of dialysis where patients are prone to infections, this proposition does not appear very safe and therefore is not very encouraging. Hence, the search for MSC and now T-regulatory T-cells becomes more intense with rekindled hopes of reaching the promised land of tolerance. In kidney transplantation reperfusion injury can cause tissue destruction leading to low glomerular filtration rate initially and affecting long term function by leading to interstitial fibrosis, which cannot be reversed. MSC have been useful in repair of early tissue injury in animal models of kidney, lung, heart and bowel transplantation.[24]

Remuzzi et al. conducted a pilot trial of intravenous administration of autologous BM-derived MSC on the 7th day of RT in two patients. They found that MSC administration was safe and feasible.[25] Ansari et al. used autologous BM-derived MSC in 30 patients with early chronic kidney diseases (CKD) due to systemic lupus eryrthematosus (SLE) and found significant benefits in learn more the form of improved functional status and serum creatinine (SCr) in these patients.[26] Tan et al. conducted a trial using autologous BM-derived MSC in 105 renal transplant (RT) patients. They infused MSC twice,

before anastomosis and 2 weeks after RT. They reported that BM-derived MSC were safe and resulted in better renal function with decreased incidence of infections over one year follow-up.[27] There are ongoing trials in all continents using BM-derived MSC to alleviate tissue injury in autoimmune disorders and transplantation to improve Tenoxicam the long term outcome of grafts. Perico et al. infused autologous MSC 7 days post-renal transplant in two patients who received living related kidneys. These patients received T-cell depletion therapy and were under maintenance immunosuppression of cyclosporin and mycofenolate mofetil and were followed up for about one year. Initially both had rises in serum creatinine; however, at one year, both showed increase in T-regulatory cells (CD4+CD25high FoxP3+ CD127−), with a fall in CD8 + cells and stable graft function.[25] However, barring Ahmedabad group of Trivedi et al. there are no studies available where adipose tissue-derived MSC have been used effectively in inducing and maintaining transplant tolerance.

The airways of cystic fibrosis (CF) patients with chronic Pseudomonas Roscovitine aeruginosa infection represent a complex environment which shapes evolution of the bacteria (Yang et al., 2011). The complexity of the environment is due to differences in the inflammatory process and antibiotic penetration in the

different focal areas of infection which occur in the compartments of the respiratory tree: paranasal sinuses, are conductive and respiratory zones where the bacteria form biofilms (Bjarnsholt et al., 2009; Hoiby et al., 2010). The biofilm mode of growth is the main reason for the failure of antibiotic treatment to eradicate airway infection, allowing the bacteria to persist for decades in the CF lung. It has been shown that P. aeruginosa might survive in the CF lung for more than 200 000 generations, during which evolution through adaptive mutagenesis occurs (Yang et al., 2011). The biofilm mode of growth has been shown to play an important role in the evolution of bacterial diversification (Boles & Singh, 2008). Oxidative stress has been shown to trigger the diversification process both inside (Boles & Singh, 2008; Driffield et al., 2008; Conibear et al., 2009) and outside the biofilm due to inflammation and antibiotic treatment (Ciofu et al., 2005; Kohanski et al.,

2007). As a consequence of bacterial evolution in the CF airways, P. aeruginosa CF strains often exhibit remarkable phenotypic diversity, as documented from the appearance of multiple colony morphology variants, including the mucoid phenotype, the development of hypermutability selleck products and various degree of antimicrobial resistance (Doggett, 1969; Hoiby, 1977; Ciofu et al., 1994; Oliver et al., 2000). It has been proposed that this diversity is associated with specialized adaptation

to the different compartments in the CF airways (Bjarnsholt et al., 2009; Hassett et al., 2010; Mowat et al., 2011). The tolerance of biofilms to antibiotics is a physiological condition that does not involve mutations in resistance genes and allows the bacteria to survive, but not necessarily grow, in the presence of antibiotic concentrations above their planktonic minimal inhibitory concentration (MIC) (Ciofu & Tolker-Nielsen, 2011). Recent research has shown that biofilm tolerance buy Ponatinib is multifactorial, involving restricted penetration, differential metabolic/physiological activity in bacterial subpopulations of biofilms, presence of persisters and activation of biofilm-specific genes (Fux et al., 2005; Williamson et al., 2012). Here we address the question of how the antibiotic tolerance of biofilms is affected by mucoidy, hypermutability and antibiotic resistance of planktonic cells, based on in vitro investigations. A discussion of the therapeutic recommendations in light of the in vitro results is presented.

Finally, FcR γ-chain-deficient mice are devoid of FcεRI and therefore any FcεRI-mediated effects of OVA-specific IgE during the sensitization or challenge phase, either due to mast-cell activation or altered DC function, is absent in these mice. Although the sensitization/challenge model that we used does not require B cells or antibodies, including

allergen-specific IgE, FcεRI, or mast cells 21, 22, it remains possible that in vivo FcεRI facilitated enhanced antigen-uptake or activation of pulmonary DC indirectly through mast-cell activation 23, 24. In contrast to previous studies 13, 14, 17 that employed BMDC and sensitization of FcγR-deficient mice, we aimed to specifically delineate the contribution Nutlin-3 clinical trial of FcγR on lung DC during the challenge phase of the murine asthma model. We first confirmed the expression of FcγR expression on lung DC and compared their function to spleen-derived DC subpopulations, as the importance of considering the phenotypic, functional and anatomical differences of various DC subsets has been supported by several studies 25. Thus, our studies

focus on see more DC populations obtained from lymphoid organs in addition to pulmonary DC to study the function of FcγR. This revealed that lung DC and splenic CD8− DC gave rise to increased CD4+ T lymphocyte stimulation when DC acquired antigen as immune complexes via FcγRI, FcγRIII or FcγRIV. This effect was absent when CD8+ DC or FcR γ-chain deficient DC were used. These observations would be consistent with the view that contamination many of OVA with endotoxins was not responsible for these alterations. Additional results support this interpretation. First, DC of TLR4-deficient mice led to increased T-cell proliferation after exposure to OVA-IC as compared to OVA alone. Second, serum of sensitized mice, which contained anti-OVA IgG, caused increased T-cell proliferation when given together with OVA to WT lung DC. This effect was antigen-specific, as serum of BSA-sensitized

mice did not cause this outcome, and FcγR-dependent, given that FcR γ-deficient DC did not result in increased T-cell proliferation. Several observations support the impact of FcγR on DC during the effector phase of pulmonary hypersensitivity. First, we adoptively transferred Th2-biased antigen-specific CD4+T lymphocytes 4 into antigen-naïve mice, thereby restricting the induction of pulmonary hypersensitivity mainly to the DC–T-cell interaction. Second, pulmonary exposure of mice to OVA-IC dramatically increased eosinophilia in the BALF and cellular infiltration in the lungs, an effect that was not observed in naive mice and thus not induced non-specifically. Third, the increased pulmonary immune reaction induced by OVA-IC was paralleled by a highly significant increase in proliferation of antigen-specific T cells, both in vitro as well as in vivo.

The median age of the cases was 35.0 months (interquartile RXDX-106 in vivo range [IQR], 25.0–52.0), 49.0% were female. The median urinary protein was 1.06 g/day (IQR, 0.28-1.30) and the mean eGFR was 76.5 ± 28.4 ml/min/1.73 m2, with G1 31.9%, G2 37.7%,

G3a 16.7%, G3b 9.5%, G4 3.6%, and G5 0.5%. The median observation period was 5.4 years. In this period, 114 patients reached the renal outcome. Choice of therapy was as follow; conservative theapy 592, steroids therapy 337, and tonsillectomy with pulse methylprednisolone 153. Kaplan–Meier survival curves showed tonsillectomy with pulse methylprednisolone were associated with lower incidence of renal outcome compared with conservative therapy and steroids therapy (log-rank test, P < 0.001 and P = 0.029, respectively). Cox proportional hazard regression analysis, adjusted for the baseline covariates, showed that Saracatinib mouse compared with the patients with tonsillectomy plus pulse methylprednisolone, those with conservative therapy and steroids therapy were more

likely to develop the renal outcome (hazard ratio [HR]: 5.36; 95% confidence interval [95%CI]: 2.14–13.4; P < 0.001 and HR: 2.60; 95%CI: 1.01-6.69; P = 0.047, respectively). This interim analysis seems to indicate the superiority of tonsillectomy with pulse methylprednisolone in terms of improving renal prognosis for the treatment of IgA nephropathy as a whole. However, we are still on the way of the data cleaning. After that, we will clarify proper choice of therapy for the patients with IgA nephropathy adjusted for the clinical presentations of patient including risk stratification. COMBE CHRISTIAN Service de Néphrologie Transplantation Dialyse, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France The

number of patients with advanced CKD is rising in Europe, their mean age is ever increasing: in France the median age at the initiation of dialysis is 70.4 Meloxicam years (1). Similar patterns are found in other European countries, with different therapeutic options offered to patients. For instance, most elderly patients are treated by hemodialysis in France, while the United Kingdom emphasizes the importance of conservative management and palliative care. In younger patients, access to transplantation is variable between countries, with living donor transplantation being more developed in Norway, and less in Southern countries. Nevertheless, in most countries, priority is given to transplantation over other types of renal replacement therapies, since patients with a functioning transplant leave longer, with a better quality of life and less comorbidities. There are wide disparities within each countries on the level of GFR at which dialysis is begun.

High molecular weight genomic DNA was isolated from TMC0356 and 14 reference strains of L. gasseri, including the type strain. The DNA samples were digested with the selected rare-cutting restriction endonucleases SmaI, SacII and ApaI and the resulting fragments separated by pulsed-field gel electrophoresis (PFGE) in a size range between 20 to 290 kb. TMC0356 Doramapimod could be distinguished from the other L. gasseri strains on the basis of the SmaI and SacII macrorestriction patterns. Furthermore, L. gasseri strains isolated from the feces of subjects

who had ingested TMC0356 were identical to TMC0356 in the SmaI, SacII and ApaI macrorestriction fragments of digested DNA. These results suggest that PFGE of genomic DNA digested with SmaI, SacII, could be a practical means of identification of TMC0356. Furthermore, these

results indicate that ingested TMC0356 can survive in, and colonize, the human intestine. Lactobacillus gasseri is one of the primary members of the genus Lactobacillus, the most important group of lactic acid bacteria (1, 2). Among the 50 well-known species of lactobacilli, L. gasseri appears to be one of the principal Lactobacillus species that inhabit the human gastrointestinal tract and have developed a deep symbiotic relationship with humans. L. gasseri is widely used as a probiotic and is believed to be LY2157299 order beneficial for humans by ameliorating intestinal disorders (3), Montelukast Sodium producing bacteriocins (4), enhancing and regulating immune responses (5), and lowering serum cholesterol (6). However, the health-promoting effects of L. gasseri have been found to be strain dependent. Because emerging scientific evidence has indicated that each probiotic, even within

the same taxonomic species, displays individual characteristic effects in host animals, strain-specific evaluation of the potent health-promoting effects of probiotics is very important in both academic and industrial contexts (5, 7). Lactobacillus gasseri TMC0356, a new probiotic strain, was originally isolated from the intestine of a healthy adult. Identification of this bacterium was based on phenotypic and genotypic characteristics, such as carbohydrate fermentation profiles, 16S-rDNA sequences, and DNA hybridization patterns. Cell line studies have also shown that TMC0356 induces production of pro-inflammatory (IL-12) and anti-inflammatory (IL-10) cytokines by macrophages (7). TMC0356 also suppresses the increase in serum IgE concentration that occurs in mice and humans with perennial allergic rhinitis (8, 9). In our previous studies, oral administration of L. rhamonsus GG and TMC0356 significantly inhibited an increase in ovalbumin-stimulated nasal vascular permeability in rats and antigen-induced nasal blockage in guinea pigs with allergic rhinitis (10, 11).

Statistical analyses were performed using GraphPad Prism statistical analysis software. Group differences were analyzed by unpaired, two-tailed Student’s t-test, while a two-way ANOVA with repeated measures was applied when comparing different experimental groups over time. p-values of 0.05 or less were considered significant. The authors thank Dr. Thomas Lane for providing antisera to CXCR3 and CXCL10.

We also thank Dr. Julie Rumble and Dr. Nick Lukacs for critical reading of the manuscript. This work was supported by the National Multiple Sclerosis Society Grant CA 1037A (B.M.S) and by the National Multiple click here Sclerosis Society Grant FG 1985-A-1 (S.J.L.). The authors declare no financial or commercial conflict of interest. As a service

to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information Trametinib solubility dmso (other than missing files) should be addressed to the authors. “
“Antiviral RNA silencing has been recognized as an important defense mechanism in arthropods against RNA viruses. However, the role of this pathway in DNA virus infection remains largely unexplored. A report in this issue of the European Journal of Immunology provides new insight into the role of RNA silencing in antiviral defense against DNA viruses. Huang and Zhang [Eur. J. Immunol. 2013. 137–146] found that the dsDNA virus white spot syndrome PAK5 virus, an agriculturally important pathogen of shrimp, is targeted by the shrimp RNA-silencing machinery via

the production of virus-derived siRNAs. Furthermore, the authors show that the RNA-silencing pathway, and crucially, Dicer-2, is important for restricting viral infection. This study provides novel insights not only into shrimp antiviral defenses but also potentially into antiviral immunity against DNA viruses in a larger spectrum of hosts, as discussed in this Commentary. Furthermore, this study may contribute to the future development of immune-based therapeutics to combat viral pathogens, not only in aquaculture, but also in insect vectors of human diseases. RNA silencing is an innate antiviral pathway used to target foreign RNA for degradation. This mode of recognition is based on the fact that all RNA viruses produce double-stranded (ds)RNA during their life cycle. Since dsRNAs are not naturally produced in higher organisms, the development of dsRNA-based recognition systems provides a simple strategy for the selective targeting of RNA viruses. Organisms including plants and arthropods use RNA silencing to control both endogenous gene expression and foreign RNAs derived from viruses.

[30] In a phase I trial of tocilizumab (antagonist to IL-6 receptor) in patients with SLE, up to 50% of patients had an improvement in the SLEDAI (Systemic Lupus Erythematosus Activity Index) score of ≥4 points.[31] There was also 47% drop in the median anti-dsDNA levels and reduction in circulating plasma cells in patients Torin 1 mw receiving tocilizumab treatment.[31] Other studies have reported the use of tocilizumab in cases of refractory SLE.[32] Although IL-6 blockade could hamper

proteinuria, lessen the age-related elevation in anti-dsDNA levels and also significantly improve the survival in NZB/W mice,[10, 11] IL-6-directed therapies have not been tested in human for the treatment of acute or severe lupus nephritis. This cytokine belongs to the tumour necrosis factor ligand family and the understanding of this cytokine assumes growing importance due to the recent advancement of SLE treatment related to the manipulation of BLys.[33, 34] BLys is cleaved at the cell surface by furin protease, which leads to the release of a soluble, biologically active molecule.[34] This cytokine is highly expressed on cells of the myeloid lineage and its secretion is promoted by interferon-γ (IFN-γ) and IL-10.[35] It binds to Nivolumab mouse strongly B lymphocytes and is a crucial factor for B lymphocyte proliferation and immunoglobulin secretion.[36]

In BLys-deficient mice, there is significant diminution in mature B lymphocytes, depressed baseline serum immunoglobuin levels and a compromised immunoglobulin response to T cell dependent and independent antigens.[37] Three types of BLys receptors have been identified, namely, BAFFR, BCMA and TACI receptors. BLys can engage to these three receptors on B lymphocytes, whereas a proliferation-inducing ligand (APRIL) can only attach to TACI and BCMA.[38] Among these three receptors, the BAFFR receptor assumes the greatest significance as it mediates most of the B cell effects. A deficiency in BCMA and TACI receptors in lupus

prone mice display no discernible phenotypic or functional abnormalities.[37, 39] In contrast, A/WySnJ mice (which bear a mutated baffr gene) exhibit diminished mature B cell numbers and antibody levels resembling the BLys-deficient mice.[40] BLys-triggered intracellular events are complex and conducted BCKDHB via the interaction of BLys receptors and several TNF receptor-associated factors. Docking of BLys with its receptors activates phospholipase C-γ2 and subsequently the NF-κB pathways,[41, 42] which is followed by prolonged B lymphocytes survival. In BLys transgenic mice (BLys-Tg mice), excessive production of BLys not only results in polyclonal hypergammaglobulinemia but also raised autoantibodies (including anti-dsDNA) titre, circulating immune complexes and renal immunoglobulin deposition.[43] These mice develop autoimmune disorders resembling SLE and Sjogren syndrome.

[9] subsequently reported that T-bet could also promote the differentiation of autoimmune effector Th17 cells by inducing IL-23 receptor expression. Several laboratories have established a role for T-bet in the plasticity of Th17 cells, particularly in their acquisition of Th1-like characteristics to become so called “ex-Th17” cells [10-12]. Fate mapping experiments using IL-17 reporter mice demonstrated that the majority of CD4+ T cells infiltrating the CNS of C57BL/6 mice actively immunized with a peptide of myelin oligodendrocyte glycoprotein (MOG35–55) are ex-Th17 cells [13, 14]. This observation has led some investigators to speculate that the plasticity of myelin-reactive Th17

cells is causally related to their acquisition of encephalitogenic MK-1775 cost properties. If they are correct then T-bet

would be critical for the development of EAE based on its role selleck chemical in facilitating the transition of myelin reactive Th17 cells into ex-Th17 cells. In the current study we directly assess the requirement of T-bet expression in IL-23 polarized, myelin-reactive T cells for the adoptive transfer of EAE. We find that, unlike their WT counterparts, autoreactive T-bet−/− cells resist conversion to an ex-Th17 phenotype upon in vitro or in vivo reactivation. Moreover, these stable Th17 cells trigger the accumulation of myeloid cells in the spleen and CNS, thereby retaining the ability to induce EAE in WT as well as RAG2-deficient hosts. The master transcription factor, T-bet, has been implicated in the pathogenesis of EAE and

MS [15-18]. We revisited the role of T-bet in EAE by comparing the clinical courses of C57BL/6 T-bet−/− and WT mice following subcutaneous immunization with an emulsion of MOG35–55 in CFA and intraperitoneal injection of inactivated Bordetella pertussis toxin. Ninety percent of T-bet−/− mice succumbed to moderate to severe EAE, although disease onset was slightly delayed compared with that of their WT counterparts (Fig. 1A). Examination of cytokine expression by CNS mononuclear cells pooled from representative mice in each group, and by splenocytes harvested from individual mice at peak EAE, revealed skewing toward an IL-17+IFN-γ− profile in the T-bet−/− cohort (Fig. 1B and C). Splenocytes from immunized T-bet−/− mice produced significantly higher levels of Liothyronine Sodium IL-17 and lower levels of IFN-γ than splenocytes from WT mice in response to in vitro challenge with MOG35–55 (Fig. 1D). Collectively, these data suggested that in the absence of T-bet, inflammatory demyelination was mediated by myelin-reactive Th17 cells that resist conversion to ex-Th17 cells. In support of this hypothesis, MOG-primed T-bet−/− CD4+ T cells predominantly exhibited an IL-17+IFN-γ− profile following a 96 h culture with antigen plus recombinant IL-23 and IL-1β, while a significant percent of WT CD4+ T cells cultured under the same conditions were IL-17−IFN-γ+ (Fig. 2A).

flavus and the zygomycete species. In conclusion, PMN-induced HD decreases with increasing biomass.

This effect is both species-dependent and E : T ratio-dependent. “
“Candida species are common pathogens causing superficial mycoses primarily affecting the mucosa and the skin in humans. Crucial steps during pathogenesis of superficial candidiasis comprise fungal adhesion, colonisation and subsequent penetration of the respective tissues. Exploring these pathological events and perhaps fungal and tissue responses towards drug treatment is imperative in the management of this infection. Unfortunately, pathological biopsies of superficial candidiasis do not exhibit the early changes Enzalutamide datasheet in the host–pathogen interaction as the tissues are already invaded by the fungi. In vivo

experimental assessments of pathological processes of superficial candidiasis are also limited because of the difficulties in providing reproducible and comparable conditions in the host environment. Conversely, in vitro models have helped studying fungal–host interactions under more defined and controlled conditions. Some common in vitro models used to simulate superficial candidiasis are chick TGF-beta inhibitor chorioallantoic membrane, mucosal explants and single layer or multiple layer cell cultures. Interestingly, these experimental approaches share advantages as well as disadvantages when compared with in vivo conditions. Hence, this review intends to discuss about the experimental superficial candidiasis produced in various tissue models Fluorometholone Acetate and their advantages as well as disadvantages with a particular reference to further improvement of validity and reliability of such experiments. “
“Species identification of yeasts is based on biochemical (e.g. API ID 32 C®, bioMérieux) and molecular biological approaches. As an alternative to DNA-dependent methods, mass spectral analysis based identification of micro-organisms has become increasingly recognized. In a number of studies, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) has been applied for

the rapid classification and identification of micro-organisms. In this study, the applicability of MALDI-TOF MS for identifying yeasts isolated from dermatological patients was analysed and compared with the results from the API ID 32 C® system. Furthermore, sequencing the internal transcribed spacer (ITS) regions of the ribosomal DNA was employed as reference method. Candida (C.) albicans was isolated in 41.9% of all cases, C. parapsilosis in 20.3%, C. glabrata in 10.8%, and C. krusei in 6, 8.1%. Rarely isolated yeasts were Candida colliculosa, famata, guilliermondii, lusitaniae, and tropicalis as well as Geotrichum candidum, Rhodotorula mucilaginosa and Trichosporon mucoides. The MALDI TOF results were equal to the results gained by ITS sequence analysis in 94%, whereas API ID 32 C® provided the correct diagnosis in 84.3% (of all cases).