Rheumatoid arthritis (RA) is a chronic inflammatory and systemic autoimmune disease characterized by hyperplasia of synovial cells

and angiogenesis [1]. The progression of synovitis in both adjuvant-induced arthritis (AIA) selleck compound and RA is characterized by a pronounced tumour-like expansion of the synovium [2]. Consequently, neovascularization may play a pivotal step during disease progression. Several polypeptide growth factors and angiogenic factors contribute to neovascularization found in RA joints [3]. An important mediator of angiogenesis is endothelial selective vascular endothelial growth factor (VEGF), which also induces vascular permeability. It has been shown by several groups, VEGF is important in the development of RA joint destruction by the significant correlation between serum VEGF at presentation and the magnitude of radiological deterioration [4]. The intensive Veliparib nmr search for markers of prediction and prognosis in RA has been the subject of a large number of studies, and a huge variety of possible markers have been reported. Several lines of evidence support that calcium and membrane binding protein (CaMBP) is one of the

critical cytokines in the proinflammatory and pro-angiogenic cascade [5, 6]. They are involved in numerous functions, ranging from control of cell cycle progression, cell differentiation and enzyme activation to regulation of muscle accumulation at the sites of inflammatory joints, and diseased conditions in RA are responsible for the pathogenesis of diseases

by promoting angiogenesis [7, 8]. During arthritic conditions, expression of VEGF and CaMBP are shown to increase angiogenesis and inflammation [9]. The availability of markers that could help to identify patients with more aggressive, rapidly progressive Orotic acid RA with poorer prognosis would offer a rational basis for early and aggressive treatment. In this way it may be possible to avoid many irreversible clinical complications [10]. The number of disease modifying anti-rheumatic drugs (DMARDs) available has increased in recent years. While the majority of these DMARDs act as immunomodulatory drugs in RA, some also act by inhibiting the angiogenic process [11]. However, the mechanism of the inhibitory effects of DMARDs on angiogenesis remains obscure [12]. The effectiveness, cost and toxicity of the new agents vary widely. The use of monoclonal antibodies (mAbs) in RA has been valuable in assessing the role of various inflammatory mediators and cell-bound molecules in disease pathogenesis [13]. mAbs bind to their targets with high specificity, and therefore have excellent potential as therapeutic agents. Biotechnological advances have allowed the production of large quantities of engineered mAbs for therapeutic use [14]. Recent research in RA has identified important mediators of synovitis.

Of the 20 conserved and non-cross-reactive peptides identified, four were from the NS4A region of the DENV. One of these peptides was from the 2 K region, which lies in between the NS4A and the NS4B region. The

other three peptides were from regions 2–26 aa. Of these, peptide 19 (ILTEIASLPTYLSSRAKL) of DENV-4 was the most frequently recognized peptide of DENV-4. Except for a few peptides in DENV-1 and -4 (peptide buy Idasanutlin 10 in DENV-4 and peptide 20 in DENV-1), the majority of responses to these peptides were from the CD4+ subset of T cells. Therefore, we then proceeded to characterize the HLA restriction of the peptides recognized by the CD4+ subset of T cells. We initially used HLA-DR, -DQ and -DP blocking antibodies to determine which of these molecules were involved in presenting these peptides. We found that all three of these MHC class II molecules were involved in presenting these peptides. Interestingly, the most frequently recognized peptides (peptides 21 and 28 of DENV-3, peptide 19 of DENV-4, peptides 1 and 33 of DENV-2) were found to be restricted through HLA-DP. Of these peptides, peptide 18 of DENV-2 was found LDK378 research buy to include an epitope with restriction through HLA-DQ*06, as complete blocking of the responses to this peptide was achieved by HLA-DQ antibodies in two HLA-DQ*06 homozygous individuals. As responses to peptide 3 of the DENV-3 serotype were found to be blocked by HLA-DR antibodies (Fig. 2a), we proceeded to characterize

further the HLA restriction of this peptide. PBMCs cultured with peptide 3 of the DENV was tested for IFN-γ production using peptide pulsed and unpulsed DRB1*1501 expressing transfected L cells for antigen presentation. Figure 2b shows that peptide 3 was indeed Staurosporine restricted through DRB1*1501. We then proceeded to determine the sensitivity of short-term T cell lines for peptide 3. We found that we could detect responses (mean 81·48, s.d. ± 12·83 SFU/1 million cells) to this peptide even at 0·001 µM/l concentrations of this peptide (Fig. 2c). Ex-vivo IFN-γ ELISPOT assays were used to assess the frequency of memory T cell responses to the peptides in healthy immune and five dengue seronegative

donors. None of the dengue seronegative donors responded to any of the dengue peptides of the four DENVs. One donor with a past severe DI had a response of 1186·67 SFU/1 million PBMCs to peptide 21 of DENV-3, whereas this donor did not have responses of >100 SFU/1 million to any other peptides. A high frequency of responses (>500 SFU/1 million PBMCs) was also seen of peptide 3 of DENV-3, peptide 16 of DENV-1, peptide 20 of DENV-1 and peptide 19 of DENV-4 (Fig. 3). High responses to these peptides were seen in different donors. Although responses to DENV-1 peptide 1 and DENV-4 peptide 5, which represented the envelope region of the DENV, was detected in individuals, only two individuals responded to each of the peptides. In addition, no ex-vivo responses were detected to DENV-3 peptide 8, which represented the NS5 region.

In an otherwise healthy brain, in the face of systemic inflammation, ‘sickness behaviour’ occurs, which is a reversible state without long-term Selleck H 89 consequences. However, in patients with microglia that have already been primed, for example by ageing and particularly by the early stages of a neurodegenerative process such as AD, the systemic inflammation may lead to irreversible neuronal damage associated with an irreversible exacerbation

of the cognitive deficit. More complete understanding of the intricacies of the interactions between systemic and CNS inflammation is clearly a prerequisite to clarifying the apparently contradictory data from clinical trials of the potential benefits of anti-inflammatory medication in AD. Daniel Lee, David Morgan and colleagues focus on the possibilities of using our rapidly developing knowledge of the subtleties of different states of microglial activation for therapeutic purposes. Intriguing, preclinical studies AZD2014 suggest that in animal models of amyloid-β protein

accumulation, stimulation of microglia by many routes can promote removal of amyloid, but in doing so may exacerbate tau pathology. Of course, this discussion raises the uncomfortable question as to which aspect of human AD pathology CYTH4 should be modelled in mice, at which to aim a therapy: Aβ, tau, both or neither? The recent evidence from animal studies linking microglial activation to tau pathology resonates with the human studies of chronic traumatic encephalopathy as reviewed by Colin Smith in which, in association with microglial activation,

tau pathology seems prominent. New information is eagerly awaited to see if the subtleties of the range of microglial activation states that have been defined so far mainly in peripheral macrophages or in microglia in animal studies apply to the microglia of the human CNS. If so there are considerable future implications including in understanding disease pathogenesis, the ability to image different microglial activation states in the living human brain, and the potential to manipulate microglial activation states for therapeutic purposes.

Recently, a study on Leishmania donovani-infected hamsters has demonstrated a role for TGF-β in induction of lymphocyte apoptosis (45). Regarding the obtained data, no considerable amount of TGF-β has been detected in cell culture supernatants of asymptomatic carriers in comparison with nonhealing cases, and in both study groups, there was no significant difference Alectinib mw in the level of TGF-β between uninfected and infected neutrophils. We, therefore, do not think that TGF-β produced by neutrophil has a major impact failure to cure human leishmaniasis.

We here showed that in vitro-infected neutrophils from nonhealing individuals produce a considerable levels of TNF-α, but not TGF-β over background when stimulated with L. major. These results are in line studies demonstrating that TNF-α mRNA production is significantly higher in Leishmania-infected dogs than in controls (46,47). In conclusion, our observations suggest that in the presence of GM-CSF, neutrophil response to CpG-containing DNA sequences may enhance neutrophil response Birinapant in vivo to Leishmania infection. The neutrophil activation was more effective in the asymptomatic group as compared to nonhealing group. The molecular aspects of this activation system remain to be elucidated and might be interesting to further expand

the data in view of neutrophil extracellular traps contribution in these groups. Induction of NETs and release of antimicrobial components may contribute to the killing of Leishmania parasites before they are engulfed by professional phagocytes (48), although different strains and species of Leishmania induce NET release in a time- and dose-dependent manner (16). In addition, we assessed basal expression levels of three functional human TLR, TLR2, TLR4 and TLR9, and were able to associate nonhealing Leishmania infection with increased expression of TLR 2, 4 and 9 in neutrophils. Our results suggest that innate recognition

of Leishmania may be incrementally hypersensitized during the development of leishmaniasis. Given that TLR pathways initiate and maintain inflammatory responses (18), the increases in TLR expression may be Bay 11-7085 associated with the enhanced pro-inflammatory signalling, e.g. TNF-α production, seen in nonhealing subjects. An increase in TLR expression in these subjects may serve to increase innate sensing and responsiveness of the immune system and act as a primary driver for immune activation and disease progression. Experimentally, it has been shown that both TLR4 and TLR9 knockout mice are resistant to parasite-induced damage to the intestinal mucosa, and this is associated with decreased levels of pro-inflammatory cytokines (49). We would like to thank the participation of such nice people that let us sample their blood.

Since the 1980s, the main objective

of VL diagnostics development has been to replace the visual identification of parasites in tissue, a technique that is invasive and requires considerable expertise. Moreover, the use of whole parasite extracts in the serologic tests is limited because of the low reproducibility and low specificity values obtained. Several serological tests have been developed, but none of them are specific for VL, although they have proved to be useful in combination with a clinical case definition (20). So, to obtain a specific diagnosis for VL, some purified recombinant Leishmania antigens have been proposed (21). The present study describes the expression, isolation and purification of two recombinant proteins from L. chagasi, rLci2B and rLci1A that were previously selected from a cDNA library, followed by standardization of an ELISA using South America canine sera, to contribute phosphatase inhibitor library to the diagnostic of dog’s infection provoked by the protozoa parasite. Both proteins were produced in Escherichia coli, and their sequences were registered by the National Institute of Industrial Property – Brazil (INPI) under paragraph PI0900961-2, with the title: ‘Use of antigens of Leishmania in methods for diagnosis, therapy and vaccine for leishmaniasis’. The rLci2B protein has homology with a parasite cytoskeleton protein kinesin, while rLci1A has homology with the heat shock protein 70 (HSP70). The

HSP70 family belongs to Avelestat (AZD9668) a class of proteins highly conserved throughout evolution and has an immunogenic activity

(22). Antibodies to specific recombinant antigens such Belnacasan price as heat shock protein 70 (rHSP70) and kinesin K39 (rK39) have also been shown to be good markers to detect infection (23). Thus, this study will be useful to expand the panel of recombinant antigens for the development of more sensitive and specific serodiagnostic tests for this disease. All reagents used were of analytical grade. Distilled water was filtered and deionized using a Millipore water purification system. The sera used in this study were collected from domestic dogs from three Brazilian regions: Northeast, Southeast and Midwest. The serum samples were collected by venipuncture by veterinaries of three research centres: Centro de Pesquisa Aggeu Magalhães, Pernambuco; Instituto de Pesquisa Evandro Chagas, Rio de Janeiro and Centro Gonçalo Muniz, Bahia, between 2006 and 2008. The sera were stored at −70°C and transferred to our laboratory. The panel of 56 negative sera used for determining the cut-off came from the state of Rio de Janeiro. The multicentre panel of 119 negative sera used in the assay came from the Southeast (79), Midwest (26) and Northeast (14) regions of Brazil. The multicentre panel of 138 positive sera used in the challenge originated in the Southeast (38), Midwest (46) and Northeast (54) regions of Brazil. The panel of 86 negative sera for L.

BALB/C mice lacking Act1 develop systemic autoimmunity resembling systemic lupus erythematosus click here (SLE) and Sjögren’s syndrome (SjS). SLE and SjS are characterized by anti-nuclear IgG autoantibody (ANA-IgG) production and inflammation

of peripheral tissues. As autoantibody production can occur in a T-cell dependent or T-cell independent manner, we investigated the role of T-cell help during Act1-mediated autoimmunity. Act1-deficiency was bred onto C57Bl/6 (B6.Act1−/−) mice and B6.TCRβ−/−TCRδ−/−Act1−/− (TKO) mice were generated. While TCRβ/δ-sufficient B6.Act1−/− mice developed splenomegaly and lymphadenopathy, hypergammaglobulinemia, elevated levels of ANA-IgG, and kidney pathology, TKO mice failed to develop any such signs of disease. Neither B6.Act1−/− nor TKO mice developed SjS-like disease, suggesting that epigenetic interactions on the BALB/C background

are responsible for this phenotype in BALB/C.Act1−/− mice. Interestingly, BAFF-driven transitional B-cell abnormalities, previously reported in BALB/C.Act1−/− mice, were intact in B6.Act1−/− mice and largely independent of T cells. In conclusion, T cells are necessary for the development of SLE-like disease in B6.Act1−/− mice, but not BAFF-driven transitional B-cell differentiation. Act1 (Traf3ip2, Ciks) is a negative regulator of CD40 and B-cell activation factor of the TNF family (BAFF)-receptor mediated signaling [1]. As such, B cells from Act1-deficient BALB/C mice and from B-cell-specific Act1-deficient mice (CD19-CRE+/−Act1−/fl) display increased survival in response to anti-CD40 AZD6738 price antibody or BAFF (also known as Blys, THANK) treatment [1, 2]. BALB/C.Act1−/− mice develop signs of systemic Liothyronine Sodium autoimmunity including splenomegaly,

lymphadenopathy and elevated serum anti-nuclear autoantibodies (ANA) starting as early as 3–4 weeks of age [1]. Likewise, both BAFF and CD40L transgenic mice have been shown to develop autoimmunity characterized by spontaneous B-cell activation and autoantibody production [3-5]. BAFF signaling is essential for B-cell maturation and survival as the immature T1 cells differentiate to transitional T2 and T3 B cells in the spleen (reviewed in [6]). In addition, it has been speculated that BAFF may function to maintain the mature pool of B cells [7]. The control of transitional B-cell differentiation is key to the elimination of potentially autoreactive B cells, and deficiency of Act1 in B cells lowers the threshold for B-cell elimination resulting in increased numbers of circulating mature autoreactive B cells [1, 2, 8]. Despite this, previous studies found that some autoantibody production is still measurable in Act1−/−BAFF−/− mice [1], suggesting that among the few B cells that effectively develop in the absence of BAFF signaling a population of autoreactive B cells remain. Act1 is recruited to the CD40 receptor upon binding of CD40 ligand (CD40L, CD154) [1, 9].

This work was funded by IOC and IPEC-FIOCRUZ, PAPES 6, FUNASA/MS, CNPq and FAPERJ, Brazil. M.R.P. is a fellow from Fiocruz-CNPq. We thank to Rodrigo Mexas for the final artwork. Regorafenib cell line A.O.S is recipient of fellowships from CNPq and FAPERJ. Table S1. Percentage of positive cells and CD4/CD8 ratio in healthy control donors and patients with mucosal leishmaniasis. Table S2. Number of positive cells/mm2 tissue in healthy donors and patients with

mucosal leishmaniasis. “
“Recent studies show that proteinase-activated receptor-2 (PAR2) contributes to the development of inflammatory responses. However, investigations into the precise role of PAR2 activation in the anti-microbial

defence of human leucocytes are just beginning. We therefore evaluated the contribution of PAR2 to the anti-microbial response of isolated human innate immune cells. We found that PAR2 agonist, acting alone, enhances phagocytosis of Staphylococcus aureus and killing of Escherichia coli by human leucocytes, and that the magnitude of the effect is similar to that Vorinostat in vitro of interferon-γ (IFN-γ). However, co-application of PAR2-cAP and IFN-γ did not enhance the phagocytic and bacteria-killing activity of leucocytes beyond that triggered by either agonist alone. On the other hand, IFN-γ enhances PAR2 agonist-induced monocyte chemoattractant protein 1 (MCP-1) secretion by human neutrophils and monocytes. Furthermore, phosphoinositide-3 Etoposide concentration kinase and janus kinase molecules are involved in the synergistic effect of PAR2 agonist and IFN-γ on MCP-1 secretion. Our findings suggest a potentially protective role

of PAR2 agonists in the anti-microbial defence established by human monocytes and neutrophils. Proteinase-activated receptor-2 (PAR2) plays a role in the development of allergic diseases of the skin1 and in certain inflammatory disorders.2 The impact of PAR2 activation on inflammation can be pro- or anti-inflammatory, depending on the stage of disease and the primary cell type involved in disease progression.2 During receptor activation, serine protease cleavage of PAR2 unmasks the N-terminal sequence of the ‘tethered ligand’. This unmasked sequence further serves as a receptor activator.3 The PAR2 is activated by trypsin and tryptase, and also by proteases derived from immune cells and pathogens.4 However, serine proteases cause PAR-dependent as well as PAR-independent effects.5,6 As a result, specific synthetic activating peptides are important probes for investigating the role of PAR activation in different processes.

Kenilworth, NJ, USA), voriconazole (VOR; Pfizer Central Research). In vitro susceptibility testing was performed using the broth microdilution method for filamentous fungi, according to CLSI document KPT330 M38-A2.15

Stock solutions of antifungal drugs had a concentration of 3200 μg ml−1, while pure substance (powder) of AMB, ISA, ITR, POS, VOR, and ANI were dissolved in dimethyl sulfoxide; for stock solutions of caspofungin and micafungin, sterile distilled water was used. Test concentration solutions were produced using filter-sterilised (0.22 μm filter) RPMI 1640 medium with l-glutamine (Difco, Breda, The Netherlands). For susceptibility testing, strains were re-grown from cryo-preserved cultures on SGA tubes at 30 °C, until colonies revealed strong sporulation (up to 14 days). Inocula were produced by streaking with a sterile cotton swab wetted with 0.9% NaCl + 0.05% Tween 20 solution over the sporulating fungal colonies. Spores were transferred

in a 0.9% NaCl solution + 0.05% Tween 20 to reach a turbidity of approximately 0.5 McFarland. Afterwards, inoculum was adjusted to a light transmission of 68–71% at 530 nm, using a spectrophotometer. Spore solutions were then diluted 1 : 50 in sterile RPMI 1640. Candida parapsilosis (ATCC 22019) and C. Selleck IWR 1 krusei (ATCC 6258) were included as quality control strains. Results were read after an incubation time of 72 h at 37 °C. MIC Sirolimus for AMB, ITC, ISA, POS, and VOR was read visually, whereas MEC for ANI, CAS, and MICA was read microscopically. When susceptible to the antifungal agent, hyphae were shorter, more rounded and compact, deformed than those in control wells, and the cell walls of susceptible

hyphae were thickened and the hyphae appeared deformed. Geometric mean MICs and MECs was computed using Microsoft® Office Excel 2003 SP3. For MIC geometric mean calculations, concentrations ≤0.125 μg ml−1 were set as 0.062 μg ml−1 and concentrations ≥16 μg ml−1 were set to 32 μg ml−1. For MEC geometric mean calculations, concentrations ≤0.062 μg ml−1 were set as 0.031 μg ml−1 and concentrations ≥8 μg ml−1 were set to 16 μg ml−1. For MIC50 and MIC90 calculation, MIC data of each antifungal and for all strains belonging to the same species were sorted in ascending order, then median and 90th percentile were determined. The AFLP-electropherograms of clinical isolates (n = 60) were compared with those of the included type strains (Fig. 1). Based on this analysis, they were identified as: P. apiosperma (n = 6), S. aurantiacum (n = 1), P. boydii (n = 15), S. dehoogii (n = 1), P. ellipsoidea (n = 3), S. prolificans (n = 34). No P. angusta, P. minutispora, and P.

The mRNA data however tells us only that production of the receptors is depressed. It cannot tell us about functionality. One factor that can further reduce the response of cells to TNF-α is their ability to shed their TNF-α receptors from the cell membrane, as competitive antagonists 31. This

effect is most pronounced for TNFR2. We therefore tested plasma from the samples for the presence of TNF-α and soluble TNFR2 by ELISA. The sensitivity of the ELISA for circulating TNF-α protein was low, with many samples from all cohorts below the limit of detection. Although there were more TNF-α-positive samples in TB patients, the number of samples with undetectable TNF-α was too high for the results to be meaningful (data this website not shown). In contrast, soluble TNFR2 was readily detectable and there was significantly increased soluble TNFR2 receptor in both household contacts and TB patients, compared with CC and further, high throughput screening assay significantly more soluble TNFR2 in patients than contacts (Fig. 2), suggesting increased inhibition of TNF-α

function in infected individuals. In addition to its role as an activating factor, TNF-α plays an important role in immunopathology 39 and cell death 40. Cell death by apoptosis has been postulated as a potentially important method by which infected macrophages are removed in TB 41. We therefore examined some of the other factors involved in the FADD pathway of cell death, which is activated by FasL and TNF-α. As shown in Fig. 3A and B, both Fas and FasL are upregulated on cells in the blood of TB patients (Fig. 3A and B) and FasL expression is augmented in contacts. When we looked at cells separated on the basis of CD14, there was no difference in mRNA on a per-cell basis for Fas between the clinical cohorts (Fig. 3C and E). However, FasL mRNA was higher in both CD14+ and CD14− cells from TB patients, suggesting a broad upregulation

of this molecule in this cohort. This observation is consistent with earlier reports from human and murine M. tuberculosis infections 38, 40, 42–44. The start of the extrinsic apoptotic cascade is the conversion of pro-Caspase 8 to the active form, Caspase 8. This process is inhibited by the short and long forms of FLIP (FLIPS and FLIPL). Thymidylate synthase As shown in Fig. 4A, expression of the Caspase 8 precursor was significantly upregulated in TB patients and their contacts, on the level of whole blood, but no significant difference was seen at the per-cell level, in either the monocytic or non-monocytic compartment (Fig. 4B and C). The inhibitors of Caspase 8 conversion (FLIPS and FLIPL) are induced by TNF-α through NF-κB activation 45. TB patients produce very high levels of TNF-α; so as might be predicted, both genes are upregulated in TB patients – FLIPS not quite significantly and FLIPL very significantly (Fig. 5A and B), though a lack of cDNA prevented us from quantifying this at the CD14+/− level.

“
“A simple medium for

identification and melanin production of Cryptococcus neoformans was developed using cowitch (Mucuna pruriens) seeds. “
“Dysphonia in patients with bronchial asthma is generally ascribed to vocal-cord abnormalities or steroid CP-690550 in vitro myopathy secondary to inhaled corticosteroids. Herein, we report the case of a 55-year-old male patient – a diagnosed case of bronchial asthma being on inhaled corticosteroids – who presented with dysphonia and was diagnosed to be suffering from Aspergillus laryngotracheobronchitis. “
“Lichtheimia brasiliensis was recently described as a novel species within the genus Lichtheimia, which comprises a total of six species. L. brasiliensis was first reported selleck compound from soil in Brazil. The aim of the study was to determine the relative

virulence potential of L. brasiliensis using an avian infection model based on chicken embryos. Mucormycosis is a rare disease caused by fungi of the Mucorales order affecting immunocompromised hosts. The Mucorales genera most commonly isolated from patients are Mucor, Rhizomucor and Rhizopus.[1-5] However, approximately 5% of mucormycoses worldwide are caused by Lichtheimia species.[1] Within Europe, Lichtheimia species even range as the third to second most-common agent of mucormycosis.[2, 6] The genus Lichtheimia Vuill. (syn. Absidia pro parte, Mycocladus) consists of saprotrophic and predominantly thermotolerant species, which inhabit soil and decaying plant material. By 2010 five species of the genus were described: L. corymbifera (Cohn) Vuill. (syn. MYO10 Absidia corymbifera, M. corymbifer), L. ramosa (Zopf) Vuill. (syn. A. ramosa, M. ramosus), L. hyalospora (syn. A. hyalospora, M. hyalosporus), L. ornata (A.K. Sarbhoy) Alastr.-Izq. & Walther (syn. A. ornata) and L. sphaerocystis Alastr.-Izq. & Walther.[7] Microscopically, these species are characterised by erect or slightly bent sporangiophores, apophysate collumellae, which frequently forms

one to several projections. Giant cells are abundant. Suspensor cells of zygospores lack appendages. Equatorial rings surround occasionally the zygospores.[8-10] Themotolerance is an important factor for differentiating Lichtheimia from Absidia. While Absidia is mesophilic and grows below 37 °C, Lichtheimia is thermotolerant having its optimum growth temperature at 37 °C.[8] L. corymbifera and L. ramosa grow up to 49 °C, whereas the maximum growth temperature for L. ornata is 46 °C. Lichtheimia sphaerocystis and L. hyalospora grow at 37 and 40 °C, respectively, but fail to grow at temperatures above 40 °C.[7] Recently, two specimens of a novel Lichtheimia species (L. brasiliensis A.L. Santiago Lima & Oliveira) were isolated from soil in semiarid and littoral dune areas in the northeast of Brazil.[11] The strains were characterised based on the morphological, physiological and molecular data (5.8S and LSU rDNA sequences).