This includes cases of autoimmune thrombocytopenia (1–3%), thyroiditis (16–30%) and nephritis due to glomerular basal membrane disease (single cases) (Table 1) [10-12,

69]. These SADRs may occur with late onset up to 4 years after treatment cessation [73], which highlights the need for adequate monitoring long after the actual infusion cycles (see above). SADRs from oncological indications, e.g. myelodysplastic changes and tuberculous hepatitis [75, 76], have thus far not been experienced in MS based on available long-term data from applications of CAMPATH-IH in the 1990s [77] or the Phase II trial CAMMS223 [73]. Pathogenesis of secondary autoimmune phenomena remains incompletely understood, but the skewed repopulation with an imbalance of B cells and regulatory T cells may partly account for these SADRs [78]. The prognostic value of serum IL-21 as a risk marker for the development of secondary autoimmunity [79] was not confirmed. Rapamycin concentration Hence, routine blood parameters and urinalysis remain critical regarding patient safety and early detection of SADRs. Daclizumab, used initially in transplant medicine, targets CD25, the alpha chain of the IL-2 receptor

(IL-2Rα) [80, 81]. It is currently investigated on a Phase III level in RRMS after promising Phase II data. Daclizumab was investigated initially in combination with interferon (IFN)-beta [22]. Meanwhile ABT-199 mouse a modified formulation for s.c. monotherapy [daclizumab high-yield process (dac-HYP)] demonstrated clinical and paraclinical efficacy in a Phase II study in RRMS [14]. Inclusion criteria required confirmed

clinical or MRI disease activity [14]. A paediatric study on seven patients showed some efficacy of daclizumab as second-line treatment; however, four children experienced further disease activity [82]. The ongoing dac-HYP Phase III trial DECIDE (Efficacy and Safety of Daclizumab High Yield Process Versus Interferon β 1a in Patients With Relapsing-Remitting Multiple Sclerosis; check details ClinicalTrials.gov NCT01064401) has left the 300-mg dosage in favour of a 150-mg subcutaneous dosage every 4 weeks. The mode of action of daclizumab appears to be pleiotropic despite selective blockade of IL-2Rα: thus, expansion of regulatory CD56bright NK cells [80, 83], reduction of proinflammatory signals [84] and interaction between T cells and antigen-presenting cells (APC) have been described [81]. To date, data on daclizumab show good tolerability and safety (Table 1) [14, 22]. However, the Safety and Efficacy Study of Daclizumab High Yield Process to Treat Relapsing-Remitting Multiple Sclerosis (SELECT) reports a fatal case after a series of events with initial possibly drug-related dermatitis [14]. A single case report on secondary CNS vasculitis has recently been published and was evaluated as linked to daclizumab treatment [85]. Long-term data and data from the Phase III trial are pending.

The specific environmental Nivolumab risk factors leading to the remarkable differences in allergy prevalence between rural and urban communities remain unclear (76–78). The hypothesis that the immunomodulatory effects of parasite infections in rural settings explains it should

be properly investigated. In addition to the downregulation of allergic responses detected during some nematode infections (more evident and better studied in schistosomiasis than in ascariasis (79)), a strong IgE response dominates in human infections by A. lumbricoides, a phenotype that, for a long time, has been interpreted as potentially pro-allergenic and probably related to the complex lifecycle and the antigenic composition of this nematode. Also, high total IgE levels are typical of helminthiasis, which seems to be result of polyclonal B-cell stimulation by parasite products (80,81). The role of such

nonspecific antibodies in immunity to parasites is unknown. Some authors have found that they may prevent cell sensitization by specific IgE (82), but there is evidence that a polyclonal IgE response does not prevent allergic reactions mediated by an actively produced IgE antibody (83,84). Therefore, other mechanisms, probably the immunomodulation on the effector phase of response, are currently considered when analysing the associations of helminth infections and skin tests with environmental allergens. After penetration of the intestinal mucosa, A. lumbricoides larvae Tyrosine Kinase Inhibitor Library clinical trial migrate to the liver, inducing the formation of granulomas, extensive inflammation

and tissue injury. Surviving larvae reach the lungs and generate an inflammatory infiltrate in the airways dominated by severe peri-alveolar eosinophilia (85,86). Antibody production is induced by larvae, and high levels of polyclonal and specific IgE are a hallmark of the infection and, in humans and pigs, immunity is determined by the generation of parasite-specific IgE antibodies against larvae and adult worms (87,88). Experiments show that Ascaris induces sensitization and asthmatic symptoms in humans and infected animals, Loeffler’s syndrome, and IgE-mediated asthma, Celecoxib including immediate-type cutaneous reactivity and airway responses after aerosol challenge with parasite extract (16,89–92). For example, Hagel et al. found that specific IgE levels to A. lumbricoides and positivity of skin test with the nematode extracts were associated with bronchial hyper-reactivity in children from a rural area of Venezuela. Also, the percentage of forced expiratory volume in 1-s (FEV1) predictive values correlated inversely with anti-A. lumbricoides IgE levels. In contrast, in urban children, the same associations were with specific IgE to D. pteronyssinus (16). As already mentioned, epidemiological investigations detected positive associations between A. lumbricoides infection and allergic phenotypes including mite sensitization (13–18).

Regarding how quickly changes in

recognition of HSP20 occur, we observe heterogeneous results in our patient’s population. These observations can reflect various factors, including antigenic stimulus, host genetic factors, cyst status, and the number of albendazole cycles or surgery. The BIBW2992 order incidence of relapse increases with the length of follow-up (17,18). As the monitoring imaging findings during follow-up can be difficult, the events seen in ultrasound need to be matched more closely to immunological events because cysts often undergo relatively small changes that imaging cannot visualise (7). In our preliminary results, HSP20 demonstrated a very good performance as antigen marker for the serological follow-up of human

CE, by contrast to specific antibodies against hydatid fluid and AgB, that remain at high levels over long periods of time after curing (19). As we found weak percentage of patients with CE positive in HSP20-IB, we suggest that more work needs to elucidate the diagnostic potential of E. granulosus HSP20. We postulate that the different antibody specificity showed by the 34 and 50 kDa bands can be explained by the presence of conformational epitopes belonging to the same antigenic molecule in our experimental conditions (polymerisation). As the antibody response to HSP20 could fluctuate over time, the feasibility of quantitative Gamma-secretase inhibitor antibody measurement, such as ELISA, will be addressed in future investigations. It will also be interesting to assess the performance of HSP20 in comparison with other antigens that have been suggested for similar purposes, such

as recP29 (20) and B2t (21). We might anticipate a synergistic outcome by combination of such tools. In conclusion, a comprehensive strategy of proteomic identification combined with further immunological validation appears to provide very useful information on the host–parasite relationship and its associate proteins ensuring the development of novel E. granulosus biomarkers. The identification of panels of parasite Plasmin antigens that elicit an antibody response may have utility in CE screening, diagnosis or in establishing prognosis, and in immunotherapy against the disease. This work was supported by a research grant from the Italian Ministry of Health (Project n°. 8ABF/8). “
“Type 1 diabetes is associated with T-cell responses to β-cell antigens such as GAD65. Single T-cell epitopes have been investigated for immune monitoring with some success, but multiple epitopes may be required to fully characterize responses in all subjects. We used a systematic approach to examine the diversity of the GAD65-specific T-cell repertoire in subjects with DRB1*04:01 haplotypes. Using class II tetramers, we observed responses to 15 GAD65 epitopes, including five novel epitopes. The majority were confirmed to be processed and presented.

Inhaled corticosteroids already increase iTreg cells in asthmatics, and vitamin D analogs could maybe further enhance this effect [156]. Treg-cell expansion could be achieved by using microbial vaccines or products derived from individual microbes such as TLR9 agonists, inactivated Mycobacterium bovis or Mycobacterium vaccae, Helicobacter pylori, or helminth-derived

products [157-159]. Alternatively, specific agonistic antibodies such as the agonistic Ab-stimulating TNFRSF25 (DR3) or CD4 agonistic HIVgp120 have been shown to expand Treg-cell numbers SCH727965 solubility dmso greatly and suppress salient features of asthma [160]. Inhaled drugs increasing the expression of Foxp3 (such as chemically modified Foxp3 mRNA or a cell permeable Foxp3 protein) could similarly achieve this desired effect [161, 162]. Finally active allergen immunotherapy has the ultimate goal of restoring dysregulated immunity in asthma and leads to the expansion of Treg cells (reviewed in [163]). The past few years have seen a renewed interest in the regulation of allergic inflammation, driven by the surge in research on Selleckchem DAPT the role of barrier epithelial cells and innate immune cells in regulating asthma. A complex picture emerges whereby epithelial sensing of exogenous and endogenous danger signals leads to the activation of airway DCs and other innate immune cells such as ILCs and basophils. DCs drive expansion of a mixed Th-cell response that is still dominated

by Th2 cells, but also includes Th17 cells, Th9 cells, and Treg cells, which induce, exacerbate, or limit various aspects of the disease. We need much more Histamine H2 receptor study before we can exploit these novel insights to new therapeutic or preventive strategies for asthma. B.N.L is supported

by an ERC consolidator grant, several EU FP7 grants (MeDALL and Eubiopred grant) a University of Ghent MRP grant (GROUP-ID), and several FWO grants. H.H. is supported by several FWO grants. The authors declare no financial or commercial conflict of interest. “
“It is known that neutralizing species-specific or serovar-specific antibodies are produced in response to chlamydial infection in humans and in some animal species. In a previous study, a strong in vitro neutralizing activity to Chlamydia suis in 80% of sera from C. suis-infected pigs had been observed. In view of the close relationship between C. suis and Chlamydia trachomatis, in the present study, the neutralizing activity against D-K C. trachomatis and C. suis purified elementary bodies (EBs) in sera collected from C. trachomatis-infected patients and C. suis-infected pigs was evaluated. A neutralizing activity of 50–70% was observed in the human sera against the homologous serovar and one to five heterologous C. trachomatis serovars. These sera were also able to neutralize C. suis EBs. The pig sera showed a strong neutralizing activity (70–100%) against C. suis EBs and all eight urogenital C. trachomatis serovars.

Experimentally, however, it is often difficult to discriminate direct effects of antigenic stimulation on recruitment processes from indirect effects selleck kinase inhibitor where a few antigen-specific T cells (‘pioneer

cells’60) are required to boost (non-specific) recruitment of T cells into the tissue. Costimulatory signals (such as those mediated by CD28) delivered to T cells, in conjunction with TCR engagement, are required to sustain T-cell division, differentiation and survival.61–63 Negative costimulators [such as cytotoxic T-lymphocyte antigen 4 (CTLA-4)] counteract these effects, thus promoting homeostatic mechanisms and preventing autoimmunity. These costimulators have been shown to regulate adhesion molecules and intracellular mediators of cytoskeletal rearrangement in vitro.64–70 In vivo, CD28-mediated signals promote the localization of T cells to target tissue following priming. A prominent feature of CD28-deficient immune responses is the inefficient localization of primed T cells to non-lymphoid antigenic sites.61,71,72 We recently reported that intact CD28 signalling is required for primed T cells to leave lymphoid tissue and migrate to antigenic

sites following priming.73 selleckchem TCR-transgenic T cells carrying a mutation in the cytoplasmic tail of CD28 (CD28Y170F) that abrogates phosphatidylinositol-3-kinase (PI3K) recruitment, without leading to defects in clonal expansion,74 failed to localize to target tissue following priming. The mechanism by which CD28 promotes migration of primed T cells to target tissue is unclear. CD28 does not appear to directly mediate adhesion,75 but may favour primed T-cell migration to non-lymphoid tissue by inducing integrin-mediated adhesion.73 The long-term effect of CD28-mediated signals on T-cell migration73 suggests that additional mechanisms, such as transcriptional regulation of chemokine

receptor expression,76 are likely to be involved. Despite sharing these adhesion-inducing and pro-migratory properties in vitro,77 CTLA-4-mediated signals Forskolin lead to effects antagonistic to those induced by CD28 on T-cell migration in vivo. CTLA-4 ligation reduced conjugate formation with cognate DCs and their retention in lymph nodes in response to antigen, suggesting that CTLA-4 engagement may limit the expansion of specific T cells by reducing their cumulative interactions with cognate DCs. In addition, tissue infiltration by a murine HY-specific H2-Kk-restricted T-cell clone was abrogated by CTLA-4 ligation,73 suggesting that CTLA-4 engagement can antagonize recruitment of primed T cells to target tissue mediated by antigen-induced signals. A number of costimulatory molecules other than CD28 and CTLA-4 have been implicated in the regulation of memory T-cell migration.

). Expression of the anti-apoptotic genes Bcl-2 and Bcl-xL was markedly decreased in the T-cell-specific Stat3-deleted group compared with the control group (Fig. 6a). Stat3, Bcl-2 and Bcl-xL protein levels were reduced; accordingly, the expression of cleaved caspase-3 was enhanced in purified T cells from T-cell-specific Stat3-deficient mice (Fig. 6b). Furthermore,

expression of both Bcl-2 and Bcl-xL in splenic T cells was considerably reduced in Stat3-deficient mice, as shown by flow cytometry analyses and immunofluorescence assays (Fig. 6c,d). These data collectively suggest that Stat3 plays a crucial role in maintenance of the T-cell population by inducing Bcl-2 and Bcl-xL expression. We demonstrated that Stat3 contributes to T-cell homeostasis by inducing the expression of Bcl-2 family genes. Stat3 deficiency may

enhance the susceptibility of PI3K inhibitor T cells to apoptosis by attenuating the expression of Bcl-2 and Bcl-xL, resulting in the breakdown Selleckchem Wnt inhibitor of T-cell homeostasis in lymphoid organs. In the present study, we successfully generated T-cell-specific Stat3-deficient mice, as described previously[17] (Fig. 1). These mice were born healthy and presented no obvious abnormalities. The study in which T-cell-specific Stat3-deficient mice were first generated showed that these mice had no abnormalities in T-cell development.[17] Instead, it demonstrated that Stat3-deficient T lymphocytes have impaired proliferation in response to IL-6 treatment and defective IL-2-mediated selleckchem IL-2 receptor α chain expression.[16, 17] However, a recent study reported that the spleen and lymph nodes of T-cell-specific Stat3-deficient mice were smaller than those of wild-type littermates.[18] We also found that the spleens of T-cell-specific Stat3-deficient mice were considerably smaller and that their cell numbers were reduced (Figs 1c,d, and 2b). These findings were attributable to the deficiency of T lymphocytes, rather than non-T

cells, in Stat3-knockout mice (Fig. 2a,c). We demonstrated that both the per cent population and absolute numbers of CD4+ and CD8+ T cells were reduced in Stat3-deficient mice (Fig. 2d–f). The maintenance of Foxp3+ regulatory T cells has also been reported to be attributable to the common γ chain cytokine signalling in which Stat3 and Stat5 are involved.[24, 25] Consistently, the population and the number of cells of CD4+ Foxp3+ T cells were notably decreased in Stat3-deficient mice when compared with the control group (Fig. 2g,h). Next, we investigated whether the reduction of CD4+ or CD8+ T lymphocytes was mainly a result of the decrease of naive or memory/effector T cells. The population of CD44low CD62Lhigh naive cells in both CD4+ and CD8+ T lymphocytes was significantly reduced in splenocytes and lymph node cells from Stat3-deficient mice, whereas that of CD44high CD62Llow effector/memory cells was unchanged (Fig. 3a–c).

Cells from spinal cord were restimulated in vitro with MOG peptide and stained intracellularly for IL-17 and IFN-γ. As shown in Fig. 4, MOG-specific T cells from inflamed Talazoparib cell line spinal cords belonged to Th1, Th17, and Th17/Th1 subsets. However, the percentage of CD4+ T cells from LFA-1+/+ and LFA-1−/− mice producing these cytokines was absolutely comparable on the level of antigen-specific cells. In addition, the amount of cytokines

produced did not differ (MFI for IL-17: 20 020±1457 (LFA-1+/+) versus 21 460±1080 (LFA-1−/−), p=0.436; MFI for IFN-γ: 15 436±2127 (LFA-1+/+) versus 14 940±804 (LFA-1−/−), p=0.832). The same results were obtained for IL-2 and TNF-α. However, it is important to note that the increased total number of antigen-specific cells finally results in a higher absolute number of cytokine-producing CD4+ T cells. Interestingly, there was also no correlation between EAE score of an individual animal and cytokine production on the single cell level. Again, only the number of infiltrating CD4+ T cells correlates with disease severity (see above). Polyfunctional Th1 cells producing multiple effector cytokines at the same time are believed to be particularly

destructive in inflammation 12. Therefore, we also analyzed whether the frequency of IL-2, IL-17, IFN-γ double selleck chemical or triple producers was altered between WT and KO mice, but did not find any significant differences (data not shown). Alternatively, a change in Th2 or anti-inflammatory cytokines could influence the severity of disease. Therefore, we tested for the production of IL-4 and IL-10. Only

very few (<2%) antigen-specific CD4+ T cells in the spinal cord produced these two cytokines. However, Amylase we did not observe any significant differences between LFA-1+/+ and LFA-1−/− T cells (data not shown). To analyze the general capacity of T cells to produce certain cytokines, we additionally used an antigen-independent stimulation with PMA and ionomycin. Also, with this kind of stimulation, none of the analyzed cytokines differed between KO and WT mice (data not shown). Taken together, these results clearly show that loss of LFA-1 does not alter the cytokine pattern of autoreactive CD4+ T cells. Therefore, only the increased total number of antigen-specific, cytokine-producing cells in LFA-1−/− mice can be accounted for the increased severity of EAE. Treg play an important role for the suppression of chronic inflammation 8, 13. They control the expansion as well as the function of autoreactive effector T cells. Utilizing intracellular staining for the lineage-specific transcription factor FoxP3, we analyzed Treg in the spinal cord of LFA-1−/− and LFA-1+/+ mice after EAE induction. The absolute number of Treg was the same in both groups (Fig. 5).

The trypanosome lytic factor (TLF) that protects many higher primates from veterinary pathogenic trypanosomes is a subset of high-density lipoproteins that is specifically bound and endocytosed by BSF trypanosomes (45–47). Once localized to the acidic lysosome TLF exerts CT99021 in vitro a membrane-disrupting activity that results in cell lysis. Acid pH facilitates lytic factor–membrane interaction by neutralizing electrostatic repulsion and allowing TLF to bind the anionic lysosomal membrane (48). This may also be the case for neuropeptides. Alternatively, or in addition to, it may be that protonation of the peptides

increases their hydrophobicity thus driving intercalation into the lysosomal bilayer. Trypanosome Obeticholic Acid nmr lytic factor is also the origin of an unusual AMP that kills trypanosomes through a novel mechanism of membrane rigidification (Figure 1). One unique component of TLF is haptoglobin-related protein (Hpr). This protein is unusual in that it is secreted without cleavage of its N-terminal signal peptide (49). Purified, delipidated Hpr is toxic to BSF trypanosomes (50); however, recombinant Hpr that lacks the signal

peptide shows no toxicity (51). Recently, we have shown that a synthetic small hydrophobic peptide (SHP-1) corresponding in sequence to the Hpr signal peptide specifically kills both veterinary and human pathogenic BSF T. brucei (24). Trypanocidal activity is not limited to SHP-1, the signal peptide

of another apolipoprotein (termed SHP-2), paraoxonase-1, which is entirely different in primary structure, but similar in terms of its length, charge and hydrophobicity profile is also toxic to BSF trypanosomes. The SHPs are not toxic to PC T. brucei or mammalian cell lines nor do they induce haemolysis of human erythrocytes at concentrations orders of magnitude higher than necessary to kill BSF trypanosomes. Studies with model liposomes suggest that the specificity of SHP-1 is because of the high degree of lipid fluidity in the BSF plasma membrane. Procyclic trypanosomes have a more rigid plasma membrane, consistent with the hypothesis that lipid fluidity mediates susceptibility to SHPs (24). The phenotype of death superficially resembles formaldehyde-fixed trypanosomes; cells retain their slender, elongated shape but are motionless. Death is preceded Digestive enzyme by dramatic changes in cell motility, with an initial hyper-activation of the cell followed by decreased motility and subsequent motionlessness (24). The lack of swelling or intracellular vacuolization suggests that membrane permeabilization is not involved in the mechanism of killing. A direct effect of SHP interaction with BSF trypanosomes is rigidification of the plasma membrane (24). It is likely that membrane rigidification is the mechanism of toxicity. The BSF of African trypanosomes offers an attractive target for membrane rigidifying peptides as trypanocidal agents.

The wECV/TBW ratio was determined by ‘classical’ wrist-to-ankle whole body bioimpedance spectroscopy (wBIS); in addition, a novel whole body model (WBM) based on wBIS was used to predict normal hydration weight (NHWWBM). Results:  Twenty-one haemodialysis patients were studied; 11 ± 6 measurements were performed STA-9090 per patient. Nine patients reached DWcBIS (DWcBIS group), while 12 patients remained fluid-overloaded (non-DWcBIS group). Change in wECV as measured by wBIS

accounted for 46 ± 23% in DWcBIS group, which was higher than in non-DWcBIS group (33 ± 48%, P < 0.05) of actual weight loss at the end of study. In both groups the wECV/TBW ratio did not change significantly between baseline and study end. Mean predicted NHWWBM at baseline was 3.55 ± 1.6 kg higher than DWcBIS. The difference in DWcBIS and NHWWBM was 1.97 ± 1.0 kg at study end. Conclusion:  WBM could be useful to predict a target range of normal hydration weight particularly for patients with substantial fluid overload. The cBIS provides an accurate reference for the estimation of DW so that combined use of cBIS and WBM is promising and warrants further studies.

“
“Aim:  The relationship between abnormalities of tubular architecture and tubulointerstitial nephritis antigen (TIN-ag) in juvenile nephronophthisis (J-NPH) was evaluated. Methods:  https://www.selleckchem.com/products/pexidartinib-plx3397.html Sixteen J-NPH patients were examined. Nephrocystin-1, TIN-ag, type IV collagen, Fas antigen and the C5b-9 complement complex were stained by immunohistochemical methods. Results:  Renal tubules of patients with J-NPH showed morphological abnormalities of tubular basement membranes (TBM) and frequent apoptosis of tubular epithelial cells. Additionally, the C5b-9 complement complex was deposited within the TBM in the absence of immunoglobulin deposition, suggesting complement-dependent TBM injury.

Localization of TIN-ag in the TBM of J-NPH patients disclosed a partial defect or discontinuity in 14 of the 16 patients, while type IV collagen immunoreactivity was relatively preserved. These findings suggest that tubulogenesis is selleck kinase inhibitor disturbed during nephronogenesis in J-NPH patients because of a defect in nephrocystin, an NPHP gene product. TBM defects induce further morphological abnormalities such as cystic dilation of tubules; as tubular function impairment advances, the incomplete tubules may be injured by C5b-9 complement complexes, followed by apoptotic cell death. Conclusion:  TIN-ag, which is important in early nephrogenesis, lacks normal activity, and vulnerable and incomplete tubules with deficient TIN-ag expression are formed. Removal of these defective tubules by apoptosis combined with the C5b-9 complement complex could be the primary reason for progression to end-stage renal disease in J-NPH patients.

albicans and 12 C. parapsilosis strains to human buccal epithelial cells and the expression of fungal cell surface carbohydrates using lectin histochemistry. Adherence assays were carried out by incubating epithelial cells in yeast suspensions (107 cells ml−1) and peroxidase conjugated lectins (Con A, WGA, UEA I and PNA at 25 μg ml−1) were used for lectin histochemistry. The results showed that adherence was overall greater for C. albicans than for C. parapsilosis (P < 0.01) and that the individual strain differences correlated with a high content of cell surface α-l-fucose residues as indicated by the UEA I staining

pattern. Based on the saccharide specificity of the lectins used, these results suggest that l-fucose residues on cell surface glycoconjugates may represent recognition see more molecules for interactions between the yeast strain studied and the host (r = 0.6985, P = 0.0045). In addition, our results indicated the presence of α-d-glucose/α-d-mannose, N-acetyl-d-glucosamine/N-acetylneuraminic acid and d-galactose/N-acetyl-d-galactosamine in fungal cell wall. “
“Cutaneous Malassezia is an exacerbating factor in patients with atopic dermatitis. We analysed the Malassezia microbiota of adult patients with head and neck atopic dermatitis of different severities (mild, moderate and severe). Of the nine human-associated Malassezia species, the number detected was similar

(3.5–4.2 species per case) among the members of all severity groups. However, the ratio of the two major Malassezia species, M. globosa and second M. restricta, was different in the severe group. “
“Volatile Selleckchem Akt inhibitor metabolites of Aspergillus fumigatus and Candida species can be detected by gas chromatography/mass spectrometry (GC/MS). A multi-capillary column – ion mobility spectrometer (MCC-IMS) was used in this study to assess volatile organic compounds (VOCs) in the headspace above A. fumigatus and the four Candida species Candida albicans, Candida parapsilosis, Candida glabrata and Candida tropicalis in an innovative approach, validated for A. fumigatus and C. albicans by GC/MS analyses. For the detection of VOCs, a special stainless steel

measurement chamber for the microbial cultures was used. The gas outlet was either attached to MCC-IMS or to adsorption tubes (Tenax GR) for GC/MS measurements. Isoamyl alcohol, cyclohexanone, 3-octanone and phenethylalcohol can be described as discriminating substances by means of GC/MS. With MCC-IMS, the results for 3-octanone and phenethylalcohol are concordant and additionally to GC/MS, ethanol and two further compounds (p_0642_1/p_683_1 and p_705_3) can be described. Isoamyl alcohol and cyclohexanone were not properly detectable with MCC-IMS. The major advantage of the MCC-IMS system is the feasibility of rapid analysis of complex gas mixtures without pre-concentration or preparation of samples and regardless of water vapour content in an online setup.