Objective:  In 50 normotensive pregnancies, we examined the relationship between fetal growth, arterial wave reflection, and microvascular function at 22, 34 weeks gestation, and six weeks postpartum. Methods: 

Arterial wave reflection was determined PD-0332991 research buy by measuring augmentation index (AIx). Changes in skin microcirculation to acetylcholine (ACh) and sodium nitroprusside (SNP) were assessed using laser Doppler imaging. Results:  At 22 weeks, birth weight centile correlated with AIx adjusted for maternal age, MAP, heart rate and timing of reflected wave (r = −0.363, p = 0.012), and with ACh responses (r = 0.317, p = 0.022). ACh responses correlated with adjusted AIx (r = −0.420, p = 0.003). At 34 weeks, birth weight centile correlated with the adjusted AIx (r = −0.301, p = 0.048). ACh responses were borderline

correlated with adjusted AIx (r = −0.323, p = 0.074). At six weeks postpartum, no significant correlations were found between birth weight centile, AIx, and ACh responses. SNP responses did not correlate with AIx or birth weight centile at any time point. Conclusion:  During normal pregnancy, changes in vascular function might reflect important adaptations that are required to facilitate normal fetal growth. This was highlighted in the present study by the findings of a positive correlation between birth weight and endothelial function and a negative correlation between birth weight and arterial wave reflection. “
“To explore the dynamic changes of capillary permeability and the expression of VEGF in cerebral cortex after RIBI. Male SD rats were randomly divided into the RIBI Cyclin-dependent kinase 3 group and control group, and the RIBI group INCB024360 in vitro was randomly subdivided into five groups for analysis on day 1, 3, 7, 14, and 28, respectively. We established

an RIBI model, and then evaluated BBB permeability by EB. We also measured the expression of VEGF with IHC stain and western blot. EB extravasation in injured cortex of RIBI group was increased at five time points compared with the control group. The western blot results and IHC revealed that the levels of VEGF expression in the RIBI groups was significantly increased at day 1 compared with the control group, then rose to a maximum at day 7, and subsequently the levels of expression recovered from day 14 to 28. The increases in both BBB permeability and VEGF expression in the brain cortex of RIBI groups at same time period confirmed the possibility of brain injury following irradiation of 6 Gy. “
“This chapter contains sections titled: Introduction Microcirculatory Alterations Visualized with OPS/SDF Imaging Response of Microcirculatory Variables to Therapeutic Interventions Perspective References “
“The knowledge of the basic principles of lymphatic function, still remains, to a large degree, rudimentary and will require significant research efforts. Recent studies of the physiology of the MLVs suggested the presence of an EDRF other than NO.

In the intestinal mucosae, the ratio of CD138+ cells/total area (7·4 ± 5·3% in wt versus 7·4 ± 5·9% in mutant animals) and the ratio of B220+ cells/total area (3·0 ± 2·3% in wt versus 4·0 ± 1·4% in mutant

animals) did not significantly differ between wt and mutant mice, suggesting that plasma cell differentiation might proceed at a similar efficiency in both mutant and wt mice (Fig. 5c). We wished to block the expression of mIgA during B-cell differentiation by deleting the exon that encodes the membrane-anchoring domain of IgA within the Cα immunoglobulin gene. As expected, early B-cell maturation was normal in homozygous mutant animals, with absolute numbers of B cells accumulating in all of the peripheral lymphoid organs of the homozygous mutant mice, including selleck chemicals this website spleen follicles, marginal zone, lymph nodes, Peyer’s patches and in the peritoneum B1 compartment. Lack of

mIgA expression in peripheral B cells strongly altered but did not abrogate the in vivo production of IgA antibodies, whereas the IgA serum level was cut by about 20-fold. Part of normal serum IgA might therefore come from recently switched and stimulated IgM+ naïve B cells simultaneously undergoing CSR to IgA and plasma cell differentiation, and hence bypassing the need for an IgA class BCR.18,23 Strikingly, the defect appeared much more severe when the IgA level was evaluated in digestive secretions, falling by about 500-fold. This more profound alteration of digestive rather than serum IgA levels indicates that in physiology, IgA production in the gut overwhelmingly relies on mIgA+ memory cells.23,24 Another likely feature of mIgA-driven B-cell differentiation in wt animals is to promote plasma cell differentiation in peripheral organs where mIgA+ cells are abundant, i.e. in the MALT. The propensity of mIgA+ B cells to undergo plasma cell differentiation

was recently shown in a model where B cells were forced to prematurely express mIgA instead of mIgM and IgD.22 By contrast, in the mutant homozygous mice described herein, the total amount of plasma cells in the MALT was grossly normal in the small intestine lamina propria, as estimated by tissue sections. Although IgA plasma cells were almost absent, they were replaced by plasma cells producing other immunoglobulin classes. Patients with IgA deficiency often show increased Phenylethanolamine N-methyltransferase levels of IgM in mucosal secretions, compensating the lack of IgA, and a similar mechanism probably occurs in the IgA-deficient mice. This may lead to forced differentiation of B cells into IgM plasma cells under conditions that would normally favour the generation of IgA plasma cells. Hence, it appears likely that the abundance of plasma cells within the gut-associated lymphoid tissues rather reflects the local concentration of mediators stimulating plasma cell differentiation, instead of being specifically boosted by signalling peculiarities from the IgA-class BCR.

82,84,85 The SP of boars and humans contains immune-regulatory molecules, including high concentrations of the potent immune-deviating TGF-β (particularly TGF-β1, but also TGFβ2- Selleck TSA HDAC and 3 isoforms), a member of the multifunctional cytokine TGF family.86,87 TGFβ1 concentrations are higher than in other body fluids, as blood plasma or breast milk, and similar to colostrum levels,88 reaching 120–150 ng/mL in boar semen87 or even higher levels in human bulk ejaculates (∼150–200 ng/mL) most of it being the latent (inactive) form and solely 1–2 ng/mL being the short-lived active form.65,89 The origin of the human TGF-β1

latent form is yet discussed, while TGF-β3 is apparently synthetized by the prostate as levels are highest in semen from men with agenesia of the seminal vesicles and lowest in samples there the seminal vesicle secretion dominates (Rodriguez-Martinez H, Kvist U, Ernerudh J, unpublished data). The latent forms can be converted to its active form under acidic conditions (as in the vagina) or by SP acid enzymes upon ejaculation and be then more firmly

attached to the sperm post-acrosomal membrane.87,90 TGF-β seems to induce the differentiation and expansion of the bank of regulatory T (Treg) cells, a 5–10% sub-population of suppressor CD4+ T cells, to reach a state of adaptative functional ABT-263 immune maternal Phloretin tolerance to male antigens.84,91,92 Males differ in their SP contents of TGF-β, without straight relation to fertility.86,89 However, a female could express different levels of endogenous cytokines depending on the exposure to SP from different males, which might thus relate to the often-observed differences in embryo survival among sires (e.g. innate fertility), a real long-lasting effect of the SP on the female.12,93 Whether such mechanism is valid also for humans remains to be fully elucidated, but clinical

evidence exists that fertility after ART is enhanced by accompanying unprotected intercourse or vaginal exposure to homologous SP.12 Interesting is the circumstantial evidence that the latent form of TGF-β2 (as for TGF-β1) could also have a preferential production by the epithelium of the prostate.94 Whether both are activated by PSA in relation to differences among men (or women) is yet to be tested. SP proteomes have been assessed in relation to reproductive outcomes (either fertility levels or (in)fertility), in several species of mammals, particularly domestic animals but also human. SP proteins have been identified as associated with high, respectively, low fertility in bulls,95 isolated as osteopontin (OPN) and lipocalin-type prostaglandin D synthase.96,97 The latter has been always present in the sperm-rich spurts of ejaculates in species (including humans) with fractionated ejaculation.

The mRNA levels of IL-4, IL-10, IL-21, IL-21R, CD40L in the gingival biopsies were evaluated by quantitative real-time polymerase chain reaction. The salivary levels of IgA and the levels of IL-4 and IL-10 in the gingival biopsies were analyzed by ELISA. The mean levels of

IgA were significantly Tyrosine Kinase Inhibitor Library in vitro higher in the chronic periodontitis compared to periodontally healthy group (P < 0.05). The mRNA levels for IL-21 was higher (P < 0.05) in the chronic periodontitis when compared to the healthy group. However, the expression of IL-21R and CD40L did not differ between groups. The IL-10 was significantly elevated at mRNA and protein levels in chronic periodontitis when compared to periodontally healthy group (P < 0.05). Conversely, the mRNA levels as well as the protein amount of IL-4 were significantly lower (P < 0.05) in chronic periodontitis than healthy ones. In conclusion, the upregulation of IL-21 and Deforolimus cell line IL-10 and downregulation of IL-4 in periodontitis tissues may be collectively involved in the increased levels of salivary IgA in chronic periodontitis subjects. The mucosal immune system generates frontline immune protection at the interface between the host and the environment by forming

a highly integrated system of lymphoid organs collectively known as mucosa-associated lymphoid tissue, which play a crucial role in antibody formation [1]. The antibody immunoglobulin (IgA) is the predominant immunoglobulin secreted by oral mucosal sites, considered one of the most important protein contributing to microbial defence from toxins, viruses, and bacteria by means of direct neutralization or prevention of microbial binding to the mucosal surface [2]. Previous studies have long demonstrated that the humoral immune response, especially Methisazone mediated by secreted IgG and IgA, plays protective role in the pathogenesis of periodontal diseases, including

gingivitis, chronic and aggressive periodontitis. It was previously showed that the levels of salivary IgA directed to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were significantly higher in subjects with deeper periodontal probing depth (PD) compared to healthy subjects [3]. Moreover, the serum IgA- and IgG-class antibody levels against A. actinomycetemcomitans and P. gingivalis were higher in the pathogen carriers compared with the non-carriers, and clearly higher in the carriers with periodontal pockets compared with the carriers without pockets [4]. Also, it was reported that the level of specific salivary IgA antibodies against mycobacterial heat shock protein (HSP) 65 was significantly increased in patients with gingivitis compared to healthy and periodontitis subjects [5].

8A and B). Proliferation of T cells from uninfected mice, however, was unaffected by rIL-2 addition (Fig. 8A and B). All these results demonstrate that the Treg cell-mediated immunosuppression observed during acute T. gondii infection is consequence of a reduced IL-2 availability for T cells. The aim of this work was to evaluate a possible role for Treg cells in the immunosuppression observed during the Selleck GSI-IX acute phase of T. gondii infection in C57BL/6J mice. This suppression has been described using different mitogens and the [3H]-thymidine incorporation assay. In order to determine the cell types affected by the parasite,

we analysed proliferation of mouse splenocytes using CFSE. Our results confirm previous findings showing that T cells are unable to respond to mitogens during acute infection 15, 16, 33

and further show that only CD4+ and CD8+ T cells, but not B cells, were affected. Although suppression of CD4+ T cells has already been reported 33, this is the first report describing suppression of CD8+ T cells during T. gondii infection. Treg cells suppress the proliferation and cytokine production of other cells 34 and have been shown to control immune response in several infection models 29. These properties suggested that these cells could mediate the immunosuppression observed during T. gondii infection. However, we found a reduction in the proportion BAY 80-6946 cost and absolute numbers of Treg cells during the first

two wks of infection, an observation which is in agreement with the recent reports 30–32. Oldenhove et al. recently reported a decrease in Treg cell number during T. gondii infection related to the inhibition of peripheral induction of Foxp3+ T cells in GALT 31 and suggested that an impaired Treg-cell conversion might be involved in this reduction. In order to further characterize the Treg-cell phenotype during infection, we examined the transcription factor Helios which has been recently described as a molecule that can be used to discriminate between natural and induced Treg cells PRKACG 41, and it has already been employed as a marker in murine and human models 42–44. Analysis of this molecule in the residual Treg cells of T. gondii-infected mice showed that the proportion of natural and induced Treg cells was unchanged at 7 dpi, although a slight increase in Helios− cells was observed at a later time point, suggesting that the amount of induced Treg cells is not impaired during the first wk of infection. However, a recent study demonstrated that Helios expression is more related to the method of activation of T cells than to the Treg-cell origin 45. Thus, given that the use of Helios as a definitive marker for natural Treg cells is still unclear, further studies are required to address this issue.

Splenocytes were fixed and permeabilized using the FoxP3 staining buffer Ruxolitinib molecular weight set (eBioscience, Inc., San Diego, CA), and were then incubated with anti-Bcl-2

or anti-Bcl-xL (Cell Signaling Technology, Danvers, MA). Cells that had undergone apoptosis were detected by flow cytometry using an FITC-annexin V antibody and annexin V staining solution (BioLegend), according to the manufacturer’s instructions. Flow cytometry analyses were performed using a FACS Canto flow cytometer (Becton Dickinson, Franklin Lakes, NJ). The data were analysed using FlowJo software (Tree Star Inc., Ashland, OR). The proliferation rate of T lymphocytes in control and Stat3-deficient mice was measured by in vivo bromodeoxyuridine (BrdU) incorporation assay, as described previously.[21] Briefly, 2 mg BrdU solution (BD Pharmingen, San Diego, CA) in PBS was injected intraperitoneally into control (Stat3fl/fl Lck-CRE−/−) and Stat3-deficient (Stat3fl/fl Lck-CRE+/−) Dabrafenib cost mice. Twelve hours after injection, splenocytes were isolated from both groups of mice. Purified splenocytes were stained with the allophycocyanin-anti-mouse CD3 antibody (BioLegend). Next, the cells were fixed and permeabilized using a FoxP3 intracellular staining kit (eBioscience), and then labelled with an FITC-conjugated anti-BrdU antibody using a BrdU Flow Kit (BD Pharmingen), according to the manufacturer’s instructions. Flow cytometry analyses

were conducted on a FACSCanto flow cytometer. The data were analysed using FlowJo software. Splenic T cells were enriched using a Pan T-cell Isolation Kit (Miltenyi Biotech Inc., Auburn, CA) according to the manufacturer’s instructions. Briefly, non-T cells in a cell suspension from the spleen were magnetically labelled. Then, non-T cells were removed by magnetic selection with an autoMACS Separator (Miltenyi Biotech Inc.). Isolated splenic T-cell purity was over 97% (data not shown). Isolated thymocytes or splenic cells were harvested in a lysis solution (Santa Cruz Biotechnology, Santa Cruz, CA) containing a protease

inhibitor cocktail (Roche, Basel, Switzerland) and a phosphatase inhibitor (Santa Cruz Biotechnology). Total protein samples were separated by SDS–PAGE and transferred to nitrocellulose membranes (GE Healthcare, Glycogen branching enzyme Pittsburgh, PA). The membranes were then probed with antibodies against Stat3, Bcl-2, Bcl-xL, cleaved caspase-3, or β-actin (Cell Signalling Technology) and visualized using SuperSignal West Femto Chemiluminescent Substrate (Thermo Fisher Scientific, Fremont, CA). Total RNA was purified from isolated spleen cells using the RNeasy Plus kit (Qiagen GmbH, Hilden, Germany) and cDNA was synthesized using a QuantiTech Reverse Transcription Kit (Qiagen). Then, cDNA was mixed with QuantiFast SYBR Green PCR master mix (Qiagen) and specific primers. Quantitative reverse transcription-PCR was performed with an Applied Biosystems 7300 Real-Time PCR System (Life Technologies, Carlsbad, CA). Raw data were analysed by comparative Ct quantification.

, 2011). A final diagnosis of R. sibirica ssp. mongolitimonae

was obtained for five samples corresponding to four different patients with a diagnosis of LAR, including a person returning from Egypt (Socolovschi et al., 2010). The samples (three cutaneous biopsies, two eschar swabs) were positive for the set ‘SFG’. A final diagnosis of R. sibirica ssp. mongolitimonae was obtained using conventional PCR followed by sequencing because no specific primer set was available in our laboratory. A final diagnosis of R. australis was obtained for two samples (cutaneous swabs) corresponding to a single patient with a diagnosis of QTT. The samples were positive for both ‘SFG’ and ‘RAUS’. A final diagnosis of R. slovaca find more was obtained for four samples (cutaneous biopsies) corresponding to three different patients with a diagnosis of SENLAT. Three samples were positive for both the selleck chemicals llc ‘SFG’ and the ‘RSLO’ sets. One remaining sample (serum) was positive for the set ‘SFG’ and negative for ‘RSLO’; a final diagnosis of R. slovaca was obtained using conventional PCR followed by sequencing. A diagnosis of TG Rickettsia was obtained for one sample (serum) using the set ‘TG’; this sample corresponded to a patient with a diagnosis of murine typhus. Diagnosis at the species level was obtained by Western blot followed by cross-adsorption. The remaining eight samples (three cutaneous biopsies,

two cutaneous swabs, two total blood and one serum) were positive for the set ‘SFG’, but we could not discriminate at the species level using either molecular or serological techniques. These samples corresponded to eight patients with a diagnosis of rickettsiosis. For these eight samples, the Ct obtained using the set ‘SFG’ was significantly higher compared with the positive samples identified at the species level

(36.71/31.95, P = 0.0023). For one diagnosis of R. honei and five diagnoses of LAR, molecular diagnosis was performed by first screening using the ‘SFG’ set and then sequencing because specific primers and probes were not available. The need to resort to sequencing Methane monooxygenase suggests the genomic databases must be updated regularly to develop new systems of primers and probes. Increased genomic data for Rickettsia species will permit the development of accurate qPCR tools. For eight clinical samples, a diagnosis of rickettsiosis was obtained by systematic screening using the ‘SFG’ set. However, identification at the species level (by different sets of species-specific qPCRs or by conventional PCRs targeting gltA and ompA) remained unsuccessful. We demonstrated that the Ct values for such samples are significantly higher, suggesting that the ‘SFG’ set is more sensitive than conventional PCR (Angelakis et al., 2009); however, molecular tools for diagnosis at the species level are not yet sufficiently sensitive.

(2007) and Gubbels et al. (2008) provide a detailed mechanistic Ensartinib and structural outline of the apicomplexan cell cycle and cell division as it pertains to the different developmental stages (44,49). The genomic revolution has ushered the study of parasite biology into an era where it is now possible to apply high-throughput functional genomics techniques to address pertinent questions regarding the variation in modes of cell cycle and its regulatory mechanisms at different developmental stages, and how these relate to the success of the parasite in the host cell environment. Analyses of global changes in gene expression

have been carried out to define more complex networks of gene interactions on a functional level. It is now beginning to emerge that there are extensive dynamic changes in parasite gene expression that mark the progression through different phases of the replication cycle as well as during transition between host cells (41,50,51). The temporal ordering of global gene expression during the course of the tachyzoite replication cycle has been mapped out using microarray analysis (50). This study measured gene expression at hourly time points during the full replication cycle of synchronized tachyzoites. Over

35% of all Toxoplasma genes were identified to exhibit cyclic expression patterns that are coordinated with the parasite replication cycle. These dynamic expression patterns reflect a functional diversification of gene expression that allows for rapid STAT inhibitor and efficient ‘just-in-time’ transcription of genes that are functionally this website relevant for the different phases of the cycle. There is a coordinated progression from the G1-phase transcription of genes with metabolic and biosynthetic functions to the S/M-phase induction of genes involved in daughter cell maturation and infectivity (50). The transition from one host cell to

another is also marked by a similar pattern of gene expression changes, which is additionally coupled to the parasite cell cycle (51). Parasites in G1 phase of the cell cycle exhibit the highest capacity for egress and reinvasion. Approximately 16% of T. gondii genes are differentially expressed between extracellular and intracellular parasites. The differential expression profiles of extracellular and intracellular parasites reflect their respective biological needs for motility and invasion in the extracellular environment and growth and replication in the intracellular environment. An emerging theme from these studies is the functional diversification of the transcription and translation machinery to temporally coordinate gene expression with parasite cell cycle (50,51). During the asexual phase of its life cycle, T. gondii transitions between two main developmental forms: the actively dividing tachyzoites and the essentially dormant bradyzoites that may persist for the life of the host. Tachyzoite-to-bradyzoite interconversion is important on two levels.

[132] In contrast, Cowley and colleagues have reported that in unpublished studies performed in Han:SPRD rats, the immunosuppressants azathioprine

and cyclosporine failed to attenuate renal disease, suggesting that specific inflammatory pathways may be involved. Although vasopressin V2 receptor antagonists have slowed renal decline in ADPKD patients[153] and have ameliorated interstitial inflammation in renal injury,[139] their effects on inflammation have not been described in any studies in PKD. BUN (42%) SCr (33%) CrCl (85%) BUN (15%) SCr (29%) CrCl (80%) BUN (43%) SCr (41%) CrCl (97%) SUN (∼12%, M) (∼10%, F) SCr (56%) BUN (21%) inflammatory cells (38%) (PAS) MCP-1 mRNA prolif. (38%) PGE2 fibrosis mitosis apoptosis PGE2 release fibrosis MK-2206 concentration (∼20%) In summary, this review has attempted to address the potential mechanisms by which interstitial inflammation arises in PKD. Therefore, is interstitial inflammation the result or cause of cyst growth in PKD, Small molecule library cost or simply an external event correlated with the degree of disease? Given that inflammation is a consistent occurrence in PKD, and that potential confounding factors (e.g. anti-microbial responses) can be reasonably excluded, it is plausible that the genetic abnormalities of PKD cause a predisposition toward an inflammatory renal phenotype, which can be activated and exacerbated by subsequent injury. Renal inflammatory

cells are a cardinal feature of PKD, and may be drawn into the interstitium by chemoattractants. Isotretinoin Chemoattractants and cytokines such as TNF-α probably originate from CEC, and may serve an autocrine function in stimulating further CEC proliferation (refer to Fig. 1). Defective cystoproteins can control the production of pro-inflammatory chemoattractants and cytokines through downstream signalling pathways. Reciprocally, pro-inflammatory cytokines may disrupt cystoprotein

function (summarized in Fig. 2). Thus, the evidence points toward a ‘positive-feedback’ relationship, in which interstitial inflammation is influenced by the pathological and molecular features of PKD and vice-versa. This review has also examined the possible harmful and beneficial effects of interstitial inflammation in PKD. Although macrophages possibly have reparative roles in PKD, several anti-inflammatory therapies have reduced cystic growth and improved renal function, suggesting that inflammation probably has a largely detrimental effect in this disease. Some therapies such as methylprednisolone, have reduced both cystic disease and inflammatory cell infiltration. Other drugs with known anti-inflammatory properties (e.g. pioglitazone), have attenuated disease in PKD, though their respective studies have not published evidence of decreased inflammation. Interestingly, several of the anti-inflammatory drugs that have successfully reduced cyst area and improved renal function, are inhibitors of NF-κB.

, 2000). Direct influence of bacterial toxin on the BBB alone or in combination with host’s inflammatory mediators such as nitric oxide, TNF-α, and IL-1 enhances BBB permeability (Mun-Bryce & Rosenberg, 1998). Increased permeability of BBB by pertussis toxin (PT) of Bordetella pertussis is recently reported. Authors speculate the role of PT-dependent hyperpermeability that may facilitate entry of Bordetella and other coinfections like E. coli via ‘Trojan horse’ mechanism (Seidel et al., 2011). Subunits encoded by ptx and other associated genes form PT secretion system. In the last years, increasing

attention has been given to this secretion complex to unfold its role not only in the translocation of Bordetella, but also in coinfections.

Small Molecule Compound Library Inversely, role of type III secretion system in the translocation of Salmonella enterica serovar Typhimurium has been ruled out recently (van Sorge et al., 2011). BMEC invasion by Salmonella seems to be dependent on actin cytoskeleton rearrangements only. Earlier, we have described that bacteria exploit host fibrinolytic components, plasminogen/plasmin, to increase the permeability of BBB. Plasmin-binding protein (PAM) of Streptococcus pyogenes attracts plasminogen, which is successively activated by streptokinase, and this active plasminogen remained bound to streptococcal surface (Berge & Sjobring, 1993). Plasminogen is also exploited by M. tuberculosis through PF-562271 with the help of various plasminogen-binding and activating molecules like 30-kDa, 60-kDa, and 66-kDa cell

wall proteins (Monroy et al., 2000) (Table 1). Some bacteria alter the expression of TJ proteins and thus the permeability of the BBB. This mechanism is described for Chlamydiophila pneumoniae. Chlamydiophilae increase the expression of the zonula adherens proteins (beta-catenin, N-cadherin, and Ve-cadherin) and decrease expression of the tight junctional protein occludin. These events may lead to junctional alterations and BBB breakdown (MacIntyre et al., 2002). In contrast to other meningitis-causing bacteria, interestingly, C. freundii is able to multiply within human BMECs. This may be a mechanism whereby C. freundii traverses the BBB via transcellular route (Huang et al., 2000). Like Borrelia, S. pyogenes, and M. tuberculosis, C. albicans also exploits host plasminogen system. It is shown that interaction between Candida enolase and plasminogen results in the invasion and traversal through BMECs (Jong et al., 2003) (Table 1). Fibronectin, laminin, and vitronectin have also been shown to participate in the adherence of C. albicans to ECM (Klotz & Smith, 1991; Forsyth et al., 1998; Spreghini et al., 1999). Previously, it was demonstrated that expression of the agglutinin-like ALS1 protein is responsible for the adherence to HUVEC and epithelial cells (Fu et al., 1998).