This effect could be explained

by a specific effect of salts on phospholipids or an interaction between phospholipids and KdpD. Indeed, KdpD autophosphorylation activity was found to be dependent on negatively charged phospholipids, whereby the structure of the phospholipids was of minor importance (Stallkamp et al., 1999). Moreover, the lipid composition of E. coli changes in a K+-dependent manner. The negatively charged phospholipid cardiolipin (net charge −2) was elevated in cells exposed to K+ limitation (Schniederberend et al., 2010). Comparison of various KdpD sequences from different Idelalisib concentration bacteria revealed that the N-terminal domain of KdpD is highly conserved and includes two motifs (Walker A and Walker B) that are very similar to the classical ATP-binding sites of ATP-requiring enzymes. By means of photoaffinity labeling with 8-azido-[α32P]ATP, direct evidence was obtained for the existence of an ATP-binding site located in the N-terminal domain of KdpD (Heermann et al., 2000). Truncated KdpD derivatives lacking this site were characterized by a deregulated phosphatase activity (Jung & Altendorf, 1998b). Therefore, it was proposed check details that binding

of ATP to the N-terminal domain modulates the ratio between kinase to phosphatase activities of KdpD. Because the intracellular ATP concentration is elevated upon an osmotic upshift (Ohwada & Sagisaka, 1987), the internal ATP level is discussed as the third stimulus for KdpD. To sum up, the current model proposes that KdpD perceives and integrates three intracellular chemical stimuli: (1) the K+ concentration; (2) the ionic strength; and (3) the ATP concentration. The secondary structure model of KdpD is presented in Fig. 1. It is based on Gefitinib mouse hydropathy plot analysis, studies with lacZ/phoA fusions (Zimmann et al., 1995), and use of the CDART (Geer et al., 2002; Heermann et al., 2009b). KdpD is anchored with four transmembrane domains (TM1–TM4) in the cytoplasmic membrane, and consists of both a large N- and C-terminal domain. The C-terminal

transmitter domain contains the typical domains of histidine kinases HATPase_c (Histidine kinase-like ATPases; Histidine kinase-, DNA gyrase B-, phytochrome-like ATPases, SMART00387) and HisKA (His Kinase A phosphoacceptor domain, dimerization, and phosphoacceptor domain of histidine kinases, SMART00388); the latter includes the autophosphorylation site His673 (Voelkner et al., 1993). The tertiary structures of the HATPase_c and the HisKA domains have been resolved for the histidine kinase EnvZ (Tanaka et al., 1998; Tomomori et al., 1999). The amino acid similarity between KdpD and EnvZ is high enough to model the corresponding domains of KdpD using the EasyPred3D modeling tool (Lambert et al., 2002) available on the Expasy server. Similar structures as for EnvZ are predicted for the homologous domains of KdpD.

1) is not a result of the decreased activity of these SODs. We next analyzed the expression of KatG, the sole catalase–peroxidase in C. crescentus. Assessed by an in situ assay of H2O2 decomposition, the catalase activity in SP3710 was slightly reduced in exponentially growing cells compared with NA1000,

and the drastic increase in KatG activity seen in NA1000 stationary cells was absent in the rho mutant strain SP3710 (Fig. 4a). These results were confirmed by a learn more biochemical assay for catalase activity by monitoring the decrease of H2O2 A240 nm (Steinman et al., 1997). The decomposition of H2O2 in the exponential phase was 1.7 ± 0.5 × 10−4 μmol H2O2 min−1 μg−1 cell protein for NA1000 and 0.53 ± 0.18 × 10−4 μmol H2O2 min−1 μg−1 cell protein for SP3710. In the stationary phase, the decomposition of H2O2 for NA1000 was 18.5 ± 1.3 × 10−4 μmol H2O2 min−1 μg−1 cell protein compared with only 0.81 ± 0.1 × 10−4 μmol H2O2 min−1 μg−1 cell protein for SP3710. Both exponential- and stationary-phase

phenotypes were complemented by the rho gene in trans in the SP3710 (pMR20-Rho) strain (Fig. 4a). This decrease in KatG activity could also account for the sensitivity of the rho mutant to organic hydroperoxide and paraquat. KatG, being a catalase–peroxidase, may have some activity towards alkyl hydroperoxides that are substrates of AhpCF and may be required to decompose the H2O2 produced from SOD-catalyzed decomposition of superoxide from paraquat. selleck kinase inhibitor In fact, oxidative stress phenotypes in null mutants of individual antioxidant enzymes may involve compensatory changes in other antioxidant enzymes acting on the same ROS (Sherman et al., 1996; Loprasert et al., 2003). Nevertheless, a katG null mutant strain (SGC111) did not present a similar sensitivity to hydroperoxides and superoxide (Table 1; Fig. 1), indicating that the lack of Rho in strain SP3710 is affecting pathways of oxidative stress response other than those dependent on the KatG catalase– peroxidase. The basis of this decreased KatG activity was

explored further by analysis of katG expression at the transcriptional and translational levels. Transcription of katG was evaluated by a lacZ transcriptional fusion to the katG promoter. Both NA1000 3-oxoacyl-(acyl-carrier-protein) reductase and SP3710 strains showed increased expression in the transition from the exponential to the stationary phase, as reported earlier (Steinman et al., 1997). However, katG expression continued to increase in strain SP3710 relative to NA1000 such that after 120 h of culture, katG expression in the rho mutant was ∼3-fold higher than the wild type, as judged by the lacZ reporter (Fig. 4b). The observed increase in katG transcription in SP3710 is unlikely to be a result of defective transcription termination, because transcription levels were not affected in the exponential phase. The lacZ fusion data were supported by RT-PCR analysis (not shown). Next, expression of the KatG protein was determined by immunoblotting.

The authors wish to thank Ms Somporn Krasaesub for her statistical consultation; Ms Pavinee Srisawatampai for her assistance on manuscript

preparation; the staff of the CIWEC clinic in Kathmandu, Nepal, for their support on enrollment and specimen processing; and the staff of the Department of Enteric Diseases, AFRIMS, Bangkok, Thailand, for their support on logistic, administration, and all laboratory assays. The views expressed herein do not necessarily represent the views of the Department of Defense or the US Government. The authors state that they have no conflicts of interest to declare. “
“We wish to call readers’ attention to a case that has been published since the publication of our paper, Breastfeeding Travelers: Precautions and Recommendations,1 selleck inhibitor in the January issue of the Journal of Travel Medicine. The Centers for Disease Control and Prevention (CDC) reported that, in 2009, transmission of yellow fever vaccine virus through breastfeeding occurred in an infant (age 23 days) in Brazil whose mother received a primary yellow fever vaccination 8 days prior to the onset of symptoms in the infant.2

The infant was Volasertib mouse diagnosed with encephalitis but recovered completely, and its neurological development and growth were normal through 6 months of age. Yellow fever virus RNA was recovered from the infant’s cerebrospinal fluid and was found to be identical to the 17DD yellow fever vaccine virus. This case was classified as yellow fever vaccine-associated neurologic disease and demonstrated the transmission of the live vaccine virus through breastfeeding. At the time

of publication of our paper, this report had not been published. Our review had found no published data that confirmed the transmission of yellow fever virus through breastfeeding. We noted that (see Table 1 in Ref. 1) “although transmission to infant has not been reported, vaccination should be avoided due to the theoretical risk of transmitting 17D virus to the breastfed infant.” We listed yellow fever vaccine to be used with precaution in breastfeeding women, “but to be considered if risk of infection is substantial.” The Advisory Committee on Immunization Practices also recommends precautions in using the vaccine in breastfeeding women 4��8C and states that “yellow fever vaccination of nursing mothers should be avoided,” except when travel to high-risk areas cannot be avoided or delayed.3–5 In Brazil, yellow fever vaccine has been recommended for everyone in the risk areas where recent yellow fever outbreaks have occurred.2 Presumably, breastfeeding women have been vaccinated during yellow fever vaccine campaigns. However, there are no published studies on this population, and we have found no estimates of the number of women who may have received yellow fever vaccine during any yellow fever vaccine campaigns.

As seen in this case report, the well-being and workability of seafarers was affected not only by the somatic complaints but also by the anxieties and preconceptions that the symptoms caused throughout the crew. This is despite the fact that the disease is long known Sorafenib chemical structure to seafaring and well described in the World Health Organization’s International Medical Guide for Ships, 3rd ed.[10] The appropriate treatment for ciguatera fish poisoning remains unclear. An antidote is not available. Several treatment efforts described in single patients or small numbers of patients seem to indicate some

success in ameliorating the symptoms. Intravenous Mannitol is the most studied therapy for ciguatera fish poisoning (0.5 to 1.0 g/kg body weight over 30–45 min within 48–72 h after the ingestion of toxic fish). The effectiveness of Mannitol was not proven in randomized trials.[2] Intravenous Mannitol treatment rarely is an option in seafaring: The drug is commonly not available Dabrafenib chemical structure on merchant ships to provide timely treatment. As in the Hamburg outbreak most sailors seek clinical care only after returning to their home country or when the next port of

call is reached. Since timely diagnosis and treatment often is not available to sick seafarers, prevention of the disease is of outmost importance. Control measures to prevent further disease on board were: securing the diagnosis, counseling of the seafarers on the natural cause of the disease, and the identification and destruction of the ciguatoxic fish that was stored in plenty in the freezer stores. There is no legal obligation for the ship operator to employ trained cooks on ships. In the experience of the authors (C. S.), there often is a lack of proper training in hygiene and food safety in crew. In this particular case, the cook Alanine-glyoxylate transaminase resisted the liquidation of the frozen fish that looked perfectly fresh to him, not being aware that the ciguatera toxin is tasteless, colorless, odorless,

and not destroyed by either cooking, freezing, salting, pickling, or canning of any sort. The port health officer by his legal power needed to identify and destroy the toxic fish to control a potential threat to the crew and the public health. The series of published case reports on outbreaks of ciguatera fish poisoning in seafarers that caught and consumed fish in at-risk areas while en route points to the necessity to improve the training of ship cooks but also educate the sailors on the risks of fishing in endemic areas to avoid food-borne disease on ships. Beside this, it is the responsibility of the ship management to avoid stocking fish from unsafe sources in the ports of the “ciguatera belt” region. Sailors are an occupational group at risk for ciguatera fish poisoning due to potentially unsafe food sources during international travel.

Although the majority of mutations are usually deleterious to host bacterium, a few

beneficial mutations may also occur, leading to the evolution of a fitter subpopulation that will rapidly take over the rest of the population. At the same time, although the Alectinib research buy presence of mutator genes can be temporally advantageous, in a longer perspective, the overall cost will exceed the income, because accumulation of other, potentially deleterious mutations reduces the fitness of the cells (de Visser et al., 1999; Funchain et al., 2000; Giraud et al., 2001; Notley-McRobb et al., 2002). The long-term effect of the expression of the Pol V homologue on the accumulation of mutations has been studied in Pseudomonas syringae B86-17 carrying the Pol V-encoding rulAB genes in an indigenous plasmid (Zhang & Sundin, 2004). In this experiment, cells were passaged through single-cell bottlenecks with exposure of lineages to UV radiation at the beginning of each cycle. No significant reduction in the overall fitness was detected after 60 cycles were studied. At the same time, the number of loss-of-function mutations was somewhat higher in Pol V-expressing bacteria than in those lacking the functional rulAB genes. To protect themselves, bacteria have evolved several systems to avoid an Dasatinib overload of

deleterious mutations. One of the best-studied examples is a repeated loss and reacquirement of DNA MMR functions during the evolutionary history of E. coli (Denamur et al., 2000). It is not unreasonable to suppose that the spread of mutator genes (e.g. genes encoding error-prone DNA polymerase) within plasmids may be another Janus kinase (JAK) mechanism that allows to accelerate the adaptation of bacteria to a new environment. At the same time, here, the ‘selfishness’

of such genes would become apparent. The plasmidial location might be particularly applied for the persistence of mutator genes that could be doomed with their host to evolutionary extinction if vertical transfer is their only means of inheritance. If the genes encoding highly mutagenic DNA polymerase Pol V are chromosomally located, in a longer perspective, they would most likely become extinct when deleterious mutations accumulate within the genome of the host. Alternatively, being incorporated into a broad-host-range transmissible plasmid, the mutator genes have a chance to escape such cells and continue their existence in other hosts not overloaded by deleterious mutations. Cells have multiple mechanisms for coping with DNA damage. Three major DNA repair pathways are base excision repair (BER), NER and MMR. Additionally, DNA can be repaired by recombination. In addition to avoidance of mutations by removing damage, DNA repair may be associated with DNA synthesis-generating mutations. The possibility of spontaneous mutagenesis resulting from gratuitous repair is the price a cell must pay for having a broad substrate specificity of repair mechanism.

Exposed brain

was initially sampled at low resolution (512 × 512 pixels, 620 × 620 μm field of view (FOV), 5 μm slices) to identify YFP-labeled cells. Labeled cells were then imaged at high resolution (1024 × 1024 pixels, 155 × 155 μm FOV, or 2048 × 2048 pixels, 310 × 310 μm FOV), with 0.5–1 μm optical slices. Individual dendrites were reimaged 7 and 14 days later. Images were processed for denoising using a novel polynomial interpolation method (Torskey and Smirnakis, in preparation). Dendrites and dendritic spines were quantified and reconstructed in three dimensions using Neurolucida software (MBF Biosciences). A key step in successful P0 intraventricular injection is to precisely target the lateral ventricles with minimal damage to the brain. We have explored a number of different injections, leading us to attain two independent coordinates Navitoclax in vivo for intraventricular virus infusion in neonatal mouse. Targeting of the lateral ventricles was accomplished by inserting the injection needle freehand perpendicular

to the skull surface and penetrating 3 mm deep. One of the sites was located two-fifths of the distance along an imaginary click here line between the lambda and eye; the other was located 1 mm lateral to the sagittal suture midway between the lambda and bregma (Figs 1A and B). To develop accuracy with the technique, a dye solution can be injected in place of virus and the brain harvested immediately to examine localisation and spread. Following correctly targeted injections, dye will be visible throughout the continuous ventricular chambers spanning the brain from the olfactory Carnitine palmitoyltransferase II bulb to the cerebellum. Cross-section of the brain at the level of the rostral striatum should reveal dye restricted to the ventricles, but within these chambers it fills the entire space. Within a few practice sessions, the lateral ventricles can be reliably targeted by freehand injection (Fig. 1D). The other requirement for the successful use of intracranial injection is good survival with minimal injury. We used small-bore injection needles designed to balance

the potential for tissue damage against the possibility of needle clogging; we opted for 32 gauge needles with small neonates such as B6 and 30 gauge with larger strains such as ICR. After injection, ICR pups were returned to their mothers, whereas B6 pups were fostered to ICR females because we found B6 mothers less likely to accept and nurse the pups after being removed from the nest and handled. These approaches yielded survival rates above 95% with consistent transduction patterns and no evidence of tissue damage. We examined the distribution of viral transduction using native fluorescence from recombinant AAV8 encoding eYFP or tdTomato injected into the cerebral lateral ventricles 3–4 weeks before harvest.

gingivalis LPS can result in opposing actions and immunological deregulation. Strategically, this is in line with the manipulation of host innate immune responses by this species, to facilitate its adaptation and survival into the host. A major virulence factor of P. gingivalis is considered to be its capsule, also known as CPS or K-antigen (Schifferle et al., 1989; Holt et al., 1999; Farquharson et al., 2000; Aduse-Opoku et al., 2006; Brunner et al., 2010a, b). Based on the capacity of CPS to generate systemic IgG antibody responses, at least six different serotypes have been identified (Laine et al., 1997; Sims et al., 2001). Encapsulated P. gingivalis strains are shown to be highly invasive, causing

spreading infection in a murine lesion model, whereas nonencapsulated strains induced only localized abscesses (Laine & van Winkelhoff, learn more 1998). Interestingly, immunization with P. gingivalis CPS induced a high IgG systemic response (Choi et al., 1998) and reduced P. gingivalis-induced alveolar bone loss (Gonzalez et al., 2003). Encapsulated strains of P. gingivalis are more resistant to phagocytosis by polymorphonuclear leukocytes than nonencapsulated strains (Sundqvist et al., 1991) and have differential capacities to adhere to gingival epithelial cells (Dierickx et al., 2003).

Moreover, differences in CPS serotypes can reflect differential capacities in chemokine stimulation by macrophages (d’Empaire et al., 2006) or cytokine stimulation by dendritic cells (Vernal et al., 2009). Interestingly, a nonencapsulated P. gingivalis www.selleckchem.com/products/dinaciclib-sch727965.html knockout mutant

strain was found to be a more potent inducer of cytokine synthesis by human gingival fibroblasts, as compared with the corresponding wild-type strain, implying a role of CPS in downplaying the innate immune responses (Brunner et al., 2010a, b). Although it is evident that the presence of CPS, or Megestrol Acetate its individual serotypes, could be determinants of the virulence of P. gingivalis, the potential involvement of this antigen in the overall deregulation of host responses awaits further clarification. The fimbriae of P. gingivalis are thin, filamentous cell-surface protrusions that facilitate its adherence to salivary proteins, extracellular matrix, eukaryotic cells and bacteria of either the same or other species. Through its fimbriae, P. gingivalis can thus attach to early colonizing bacteria, and participate in the developing biofilm structure. Type I (major) fimbriae have important roles in colonization and invasion, whereas type II (minor) fimbriae possess a higher proinflammatory capacity (Lamont & Jenkinson, 1998; Amano et al., 2004; Hajishengallis et al., 2008). Interestingly, however, P. gingivalis strains W50 and W83 that lack major fimbriae are still invasive, as demonstrated in experimental subcutaneous abscess models (Inaba et al., 2008). A particular role of fimbriae is revealed in the induction of bone destruction in experimental periodontitis models.

We used a unilateral chronic constriction injury of the rat infraorbital nerve (CCI-IoN) as a facial neuropathic model. Pain-related behavior of the CCI-IoN animals was tested at 8, 15 and 26 days after surgery (dps). The response threshold to mechanical this website stimulation with von Frey hairs on the injured side was reduced at 15 and 26 dps, indicating the presence of allodynia. We performed unitary recordings in the caudalis division of the

spinal trigeminal nucleus (Sp5C) at 8 or 26 dps, and examined spontaneous activity and responses to mechanical and thermal stimulation of the vibrissal pad. Neurons were identified as wide dynamic range (WDR) or low-threshold mechanoreceptive (LTM) according to their response to tactile and/or PLX4032 mw noxious stimulation. Following CCI-IoN, WDR neurons, but not LTM neurons, increased their spontaneous activity at 8 and 26 dps, and both types of Sp5C neurons increased their responses to tactile stimuli. In addition, the on–off tactile response in neurons recorded after CCI-IoN was followed by afterdischarges that were not observed in control cases. Compared with controls, the response inhibition observed during paired-pulse stimulation was reduced after CCI-IoN. Immunohistochemical studies showed an overall decrease in GAD65 immunoreactivity in Sp5C at 26 dps, most marked in laminae I and II, suggesting that following CCI-IoN the inhibitory

circuits in the sensory trigeminal nuclei are depressed. Consequently, our results strongly suggest that disinhibition of Sp5C neurons plays a relevant role in the appearance of allodynia after CCI-IoN. “
“The dentate gyrus is one of only two regions of the mammalian brain where substantial neurogenesis occurs postnatally. However, detailed quantitative information about the postnatal structural maturation of the primate dentate gyrus is meager. We performed design-based, stereological studies of neuron number and size, and volume of the dentate gyrus layers in rhesus macaque monkeys (Macaca mulatta) of different postnatal ages. We found that about 40% of the total number of granule cells observed in mature

5–10-year-old many macaque monkeys are added to the granule cell layer postnatally; 25% of these neurons are added within the first three postnatal months. Accordingly, cell proliferation and neurogenesis within the dentate gyrus peak within the first 3 months after birth and remain at an intermediate level between 3 months and at least 1 year of age. Although granule cell bodies undergo their largest increase in size during the first year of life, cell size and the volume of the three layers of the dentate gyrus (i.e. the molecular, granule cell and polymorphic layers) continue to increase beyond 1 year of age. Moreover, the different layers of the dentate gyrus exhibit distinct volumetric changes during postnatal development.

fumigatusΔyap1. see more This provided strong evidence that the expression of these proteins (29 in total) was regulated by yap1 in A. fumigatus. The expression of four UFPs was downregulated in A. fumigatusΔyap1 following exposure to H2O2 and future gene deletion studies will be required to dissect the function of these proteins. Finally, the authors observed that although

yap1 was important in A. fumigatus for protection against reactive oxygen intermediates, via the regulation of catalase 2 levels and activity, it was dispensable for virulence in a murine infection model. The identification of resistance mechanisms to antifungal drugs such as amphotericin B and caspofungin (an echinocandin) in A. fumigatus has been investigated by determining the fungal proteomic response to

drug exposure (Gautam et al., 2008; Cagas et al., 2011). Differential expression (at least a twofold difference in expression) of 85 proteins (76 upregulated http://www.selleckchem.com/products/abt-199.html and nine downregulated) was detected, compared with normal growth conditions, when A. fumigatus was exposed to amphotericin B. These were identified by MALDI-ToF/ToF MS as cell stress proteins, transport proteins and enzymes involved in ergosterol biosynthesis (a key amphotericin B target). Concomitant microarray analysis of the fungal response to amphotericin B was also undertaken and the expression of 295 genes was found to be differentially expressed, whereas that of 165 genes was upregulated and 130 downregulated. It is notable that 142/265 genes encoded hypothetical proteins, and that Aspartate few of these were detected by proteomic analysis. This points to the usefulness of integrated genomic and proteomic strategies, where possible, for such studies – which

may be facilitated in future by RNaseq, as opposed to microarray technology (Sheppard et al., 2006). Expressions of three genes, a Rho-GDP dissociation inhibitor, a secretory-pathway GDI and Mn SOD, were detectable at both microarray and proteomic levels. An unexpected alteration in the enzyme levels involved in protein secretion was evident; however, the biological significance of this finding requires further study. Cagas et al. (2011) have quantitatively evaluated the proteomic response of A. fumigatus to caspofungin by subcellular fractionation (for localization) and MALDI-ToF/ToF MS identification. Postcaspofungin exposure, subcellular fractionation was achieved by differential centrifugation to yield secreted, cell wall/plasma membrane (CW/PM), microsomal and cytoplasmic fractions; however, only CW/PM and secreted fractions were subjected to quantitative proteomic analysis. In the CW/PM fraction, an altered expression of 56 proteins was evident (26 up- and 30 downregulated), 81% of the upregulated proteins were ribosomal proteins, the most highly upregulated protein was a UFP and chitinase was the most significantly downregulated protein (12-fold).

, 2006; Sansom et al., 2008). The ecto-nucleoside triphosphate diphosphohydrolase family (ecto-NTPDases) is constituted by eight members (NTPDase1–8) that hydrolyze nucleoside di- and triphosphates to the monophosphate form. Nucleoside monophosphates may then be catalyzed to nucleosides such as adenosine by the action of ecto-5′-nucleotidase. Purine salvage and the regulation of blood clotting, inflammatory processes and immune reactions are among the major roles played by these enzymes to date (Sansom et al., 2008; Burnstock & Verkhratsky, 2009). The adenosinergic check details signalling can be controlled by adenosine uptake via bidirectional

transporters, followed by intracellular phosphorylation to AMP by adenosine kinase or deamination to inosine by adenosine deaminase (ADA; EC 3.5.4.4). ADA participates in the purine metabolism, where it degrades either adenosine or 2′-deoxyadenosine, producing inosine or 2′-deoxyinosine, respectively

(Franco et al., 1997). A phylogenetic study demonstrated the existence of different ADA-related members, which include ADA1, ADA2 and a similar deduced amino acid sequence named adenosine deaminase like (ADAL) (Maier et al., 2005). Despite its intracellular location, ADA1 may occur on cell surface, anchored to two proteins, CD26 and A1 receptors, acting PLX3397 cell line as an ecto-ADA cleaving extracellular adenosine (Franco et al., 1997). ADA has been described in mammalian cells and tissues, blood-feeding insects, mollusks and parasites, Plasmodium lophurae, Trichinella spiralis, Fasciola gigantica and Hyalomma dromedarii (Franco et al., 1997; Gounaris, 2002; Mohamed, 2006; Ali, 2008). The characterization and expression of S-adenosylhomocysteinase

were described in T. vaginalis, which catalyzes the reversible hydrolysis of S-adenosylhomocysteine to homocysteine and adenosine (Minotto et al., 1998). Those authors have previously reported the absence or the poor activity of ADA. It is important to mention that T. vaginalis is dependent Dichloromethane dehalogenase on salvage pathways to generate de novo nucleotides (Heyworth et al., 1982, 1984). Munagala & Wang (2003) demonstrated that adenosine is the primary precursor of the entire pool of purine nucleotides in T. vaginalis, and activities of ADA, IMP dehydrogenase and GMP synthetase were identified in trichomonads, suggesting a metabolic pathway able to convert adenine to GMP via adenosine. Our group has investigated the purinergic system in T. vaginalis throughout the extracellular nucleotide hydrolysis, and NTPDase and ecto-5′-nucleotidase activities were described (Matos et al., 2001; Tasca et al., 2003, 2005). Considering that (1) extracellular nucleotides and nucleosides, such as adenosine and inosine, act as DAMPs playing a role in cell signalling that contribute to inflammation and immune responses (Bours et al., 2006; Sansom et al.