cholerae O1/O139, which showed temperature-independent motility between 20 and 42°C, as shown in Figure 1. The difference between C. jejuni and H. pylori motility is clear at 42°C, at which temperature C. jejuni is still motile, but H. pylori motility has declined (Fig. 1). The swimming speed at 37°C was the fastest for C. jejuni (>100 μm/s); the swimming speeds of H. pylori, V. cholerae O1 and V. cholerae O139 were 55.4 ± 6.6, 80.2 ± 8.6 and 75.6 ± 8.9 μm/s,

respectively. The swimming speed of C. jejuni at 42°C was faster than at 37°C (>100 μm/s; the resolution limit of the assay system employed Lapatinib price did not allow precise assessment of speed). The motility of C. coli was very similar to that of C. jejuni (Fig. 1); the swimming speeds at 37 or 42°C were >100 μm/s. Next, correlations between bacterial shape and motility were examined

for C. jejuni. C. jejuni enteritis strains (n = 30) and ATCC33560 all took the form of spiral rods with polar flagella at each buy Gefitinib pole and were highly motile, as shown in Figures 1 and 2a, d. Five of the C. jejuni GBS strains (n = 7) strains took the form of motile spiral rods (as shown in Figs. 1 and 2a, d), whereas one strain (KB3439; belonging to ST22) took the form of a straight rod with polar flagella at each pole (Fig. 2b, e). Interestingly, strain KB3439 was highly motile (Fig. 1), its swimming speed of >100 μm/s (at 37–42°C) being similar to that of a spiral rod, indicating that a spiral body shape is not essential for motility. As expected, the remaining strain (KB3449; belonging to ST4051), which took the form of a straight rod without

flagella (Fig. 2c, f), showed no motility, (Fig. 1). As shown in Figure 3, all C. jejuni strains have cup-like structures (marked by closed arrowheads) at both ends of the bacterial spiral body, irrespective of their bacterial shapes or the presence or absence of flagella. These polar cup-like structures are located inside (and adjacent to) the inner membrane and are 33.8 ± 6.0 nm thick (including the inner membrane) and 206.4 ± 25.5 nm in length (n = 62), as shown in Figure 3a (inset panels in the right and middle lower corner). The space (cytoplasm) within the cup-like structures is less dense than the cytoplasm of the spiral (or straight) bodies (Fig. 3). Motile bacteria have a polar hollow for a flagellum Urease (Fig. 3a, b; indicated by arrows), in contrast to non-motile bacteria (Fig. 3c). Negative staining of C. jejuni cells (Fig. 4a, b) further demonstrated that inner tubular structures extend from the inner membrane and open into a funnel shape on the bacterial cell surface (diameter at the bacterial cell surface, 80.8 ± 10.1 nm [n = 31]); flagella expanding into a funnel shape toward the environment. The inner tubular structure is incompletely shown in Figure 4b, probably due to incomplete penetration of uranyl acetate into the tubular structure from the bacterial surface (funnel shape) side. The funnel shape was also confirmed by thin sections of C.

The authors would like to thank the people of CYC202 cost Um-Zukra village for their continuous cooperation. This study was supported by the Institute of Nuclear Medicine, Molecular Biology and Oncology, University of Gezira, Sudan. Our thanks are also due to the Ministry of Higher Education and Scientific Research for their partial financial support. “
“Thyroid disease is one of the most common endocrine conditions affecting women during reproductive age. A link between thyroid and assisted reproduction outcome is debated. Serum TSH levels, number and scoring of oocytes and embryos, and number of clinical pregnancies were retrospectively recorded

in 164 women undergoing assisted reproduction technologies (ART) at an University–based fertility center, to evaluate the outcome of the first steps of assisted reproduction (ovarian stimulation, oocyte pickup and fertilization, embryo transfer and implantation) in relation to thyroid function and autoimmunity. No significant relationship was found between TSH and all parameters, except clinical pregnancy rate (22.3% in TSH ≤ 2.5 group versus 8.9% in TSH > 2.5 mUI/L group; P = 0.045).

Dorsomorphin No pregnancy occurred in women with anti-thyroperoxidase autoantibodies, while pregnancy occurred in 23.9% of cycles without autoimmunity (P = 0.02). Further studies must be conducted in order to shed light on the link between infertility and thyroid dysfunction. “
“The

mammalian target of rapamycin (mTOR) is a key regulator of cell growth and metabolism. It associates with multiple proteins and forms two distinct signaling complexes, mTORC1 and mTORC2. Accumulating evidence has revealed critical roles for intact mTOR signaling during T-cell activation and responses to microbial infection. However, the importance of mTOR regulation G protein-coupled receptor kinase in T cells has yet to be explored. The TSC1/TSC2 complex has been shown to inhibit mTORC1 signaling in cell line models. We show here that deletion of TSC1 in the murine T-cell lineage results in a dramatic reduction of the peripheral T-cell pool, correlating with increased cell death. While mTORC1 is constitutively activated, mTORC2 signaling, reflected by Akt phosphorylation and activity, is decreased in TSC1-deficient T cells. Furthermore, TSC1-deficient T cells contain elevated reactive oxygen species (ROS) and exhibit decreased mitochondrial content and membrane potential, which is correlated with the activation of the intrinsic death pathway. Overall, our results demonstrate that TSC1 differentially regulates mTORC1 and mTORC2 activity, promotes T-cell survival, and is critical for normal mitochondrial homeostasis in T cells. The induction of the adaptive immune response is, in part, characterized by the aggressive expansion of an antigen-specific T-cell pool, coincident with the production of cytokines by said population.

3% (251/269). During the study, 25 G-P combinations were detected with G1P[8] in 38.3% (n= 103) and G4P[6] in 5.9% (n= 16) cases. These data provided information on rotavirus in patients with acute gastroenteritis in Seoul, Korea and provided baseline

data to motivate for the implementation of control measures for rotavirus disease. Rotaviruses are recognized as the major etiological agents among infants and young children, and are the leading cause of life-threatening diarrhoeal disease in many countries (1,2,3). The virus is a member of the family Reoviridae and its genome is composed of 11 segments of double-stranded RNA that KU-57788 supplier encode for the six structural proteins that make up the virus particles (viral proteins [VPs]) and six nonstructural proteins (NSPs) (3). The outer capsid is composed of two proteins, glycoprotein VP7 and protease-sensitive VP4 that confer protective immunity (4). Thus, VP7 and VP4 are

used to classify RoVs (3). Semi-nested PCR, based on type-specific primers, is used to determine G and P genotypes. As VP7 and VP4 genes can and do segregate independently, a dual typing system is necessary in order to characterize the strains of RoVs co-circulating during different seasons in different locations (4). It is generally accepted that at least 23 G types [4] and 32 P types (5) are known. Among them, G1–4 are common human genotypes, though increase in prevalence of G12 and G9 strains have been reported worldwide (6). Epidemiological studies have shown that four G (G1-G4) and three P (P[4], P[6], and P[8]) are the most

frequent VP7 and VP4 types (7). The distribution Erlotinib ic50 of different G and P genotypes and RoV strains varies from country and area to area and, therefore, knowledge of the molecular epidemiology of RoVs in circulation is important in the effort to develop a suitable and efficacious vaccine (7). The aims of this study were to investigate the detection rate of RoV infections and the prevalence of the G and P genotypes of RoV strains detected in children hospitalized with acute gastroenteritis in Seoul, Korea in 2009. Between January and December 2009, stool samples were collected from 1,423 patients 650 females, 773 males) presenting to five referral hospitals for the treatment of acute gastroenteritis in Seoul. Patients included in the study had a clinical diagnosis of acute gastroenteritis which check details was defined as more than two episodes of watery diarrhoea within a 24 hr period. The study protocol was approved by the ethics committee of each hospital. The patient’s age ranged from neonates to five year old children. Group A RoV antigen was detected from stool supernatants using ELISA with VP6-group-specific antibody (BioTracer Rotavirus ELISA, Bio Focus, Uiwang-si, Korea) according to the manufacturer’s instructions. Specimens with OD absorbance values greater than 0.4 at a 450 nm wavelength were considered to be positive. Fecal specimens were diluted 1:10 in PBS.

Elite non-progressors. Affected mothers (to study both mother and infants). Patients with T1D. Healthy control children (to properly age-match). This is a critical resource and knowledge gap and has been traditionally difficult to achieve. There was consensus on a need to begin building a ‘Gold Standard’ Sample Repository immediately, where samples would be collected prospectively through the living biobank effort. This would

allow for later Kinase Inhibitor Library clinical trial validation of an integrated pipeline of biomarker assays and allow sharing of samples for parallel analysis with multiple approaches. The cohort linked with this effort would thus be a ‘validation’ cohort. It was noted that the design of this resource should be protocol-driven, with appropriate equipment and procedures to collect the samples. Participants with background in industry settings suggested that the development of less complex assays and protocols to stabilize samples soon after collection should be paramount here. The repository would not need to be in a single physical location, and some assays could be performed by centralized laboratories to reduce variability; however, it would be helpful to export these assays to other laboratories for a comprehensive analysis. click here An effective strategy would be to create a collection of serum/plasma

samples for non-cell-based assays, and a collection of frozen peripheral blood mononuclear cells (PBMC) for non-live-cell-based assays from the same samples following rigorous standardized protocols [39]. Finally, all data generated could link to a centralized database (see next section) to allow for merging of data from different groups. Highly relevant to the Gold Standard Repository discussion

are efforts in place with the n-POD. There is already a system in place in this network for tissue/sample processing, archiving and efficient distribution to investigators. It was noted that n-POD has begun instituting working groups that study, collaboratively, samples from the same patients 3-mercaptopyruvate sulfurtransferase with a multitude of approaches. Importantly, the design of the approach is discussed collectively, whereby critical details are worked out that allow for maximizing co-ordination and the potential for discovery; for example, co-ordinating tissue sections allows for examinations of multiple parameters by different investigators on the same islets (using serial sections). Results are shared within the groups in real time to guide study progression further and incorporate changes or developments. Finally, n-POD offers the opportunity to correlate emerging biomarkers with pathology in the pancreas (for example, markers of β cell stress, mass, etc.) and a number of ongoing n-POD projects are generating data on these aspects at this time [40]. A central, shared database for the Gold Standard-type biomarker samples was deemed critical to make real progress in the field of T1D.

Specifically, Jijoye cells were treated overnight either with proteasome inhibitors (MG132, epoxomicin and PS-341), tripeptidyl peptidase II inhibitors (butabindide and AAF-CMK), a lysosomal acidification inhibitor (chloroquine), an autophagic process inducer (rapamycin) or IFN-γ, which increases proteasome and ERAP activities as well as HLA class I and TAP expression. All drugs were used at the selected concentrations, which correspond to their known biological effect without effects on cell viability.

As shown in Fig. 6, only partial inhibition of proteasomes leads to an increased recognition of Jijoye cells by HPV-specific CTLs, whereas all other treatments failed to affect target cell lysis. Similar results were obtained with BJAB B95.8 cells, whereas BL cells negative for HLA-B53 and HLA-B35, which were used as a negative control in all assays, were unaffected by these Pritelivir molecular weight treatments (not shown). These results suggest that proteasomes from BL cells, although less efficient in degrading reference substrates than proteasomes from

LCLs, destroy the HPV epitope, which can, however, be generated and presented after partial inhibition of the proteasomes. To evaluate whether proteasomes from BL cells are able to generate the HPV epitope, we analysed the in vitro PD98059 manufacturer degradation of an HPV peptide precursor featuring five amino acids at the C terminus (HPV + 5). Proteasomes were semi-purified from Jijoye cells treated or not with epoxomicin under the same conditions inducing HPV-specific lysis. Subsequently, the in vitro HPV precursor degradation was evaluated at different time-points by HPLC analysis. As shown in Fig. 7, the HPV precursor was degraded in a time-dependent fashion. Orotidine 5′-phosphate decarboxylase Proteasomes isolated from Jijoye cells and treated with epoxomicin were still capable of degrading the HPV precursor, albeit to a lesser extent. Interestingly, the appearance of a single peptide was evident during the HPV + 5 degradation. As this peptide eluted from the HPLC column

with the same retention time as the HPV peptide, it was identified as the HPV epitope, a hypothesis confirmed by mass spectroscopy (not shown). The generation of the HPV epitope by proteasomes isolated from untreated Jijoye cells was maximal after 1 hr and subsequently decreased in a time-dependent fashion, suggesting a further degradation to products that were undetectable under our conditions. In contrast, proteasomes isolated from Jijoye cells treated with epoxomicin still generated the HPV epitope, which was not further degraded because its presence could still be detected after 48 hr. These in vitro findings suggest that BL cells treated with proteasome inhibitors do not degrade the HPV epitope, resulting in its presentation by class I molecules.

We investigated Ganetespib manufacturer the effect of parameters of classical indication for CRRT on mortality in patients on continuous renal replacement (CRRT) therapy. Methods: We prospectively and consecutively enrolled a total of 519 patients who stared renal replacement therapy. Results: Mean age was 63.4 ± 14.5 years old, and men were 59.5%

in all enrolled patients. Causes of acute kidney injury (AKI) were septic (46.4%), ischemic (19.5%), post-operation (9.1%), and nephrotoxic (6.2%) AKI. Level of pH (hazard ratio (HR) 1.403, 95% confidence interval (CI) 1.181–4.774, 7.20 < pH ≤ 7.25; OR 3.520, 95% CI 1.330–9.316, 7.15 < pH ≤ 7.20; HR 4.315, 95% CI 1.649–11.286, pH ≤ 7.15; P-for-trend 0.001, reference pH > 7.3), weight gain over 2 kg (HR 2.501, 95% CI 1.552–4.032), urine output (HR 2.190, 95% CI 1.408–3.406, urine output ≤ 0.3 ml/min/kg), and phosphorus level (HR 2.136, 95% CI 1.199–3.805, 5.5 < P ≤ 6.5; HR 4.737, 95% CI 2.613–8.590; P-for-trend < 0.001, reference P < 5.5). However, serum creatinine level (HR 0.892, 95% CI 0.824–0.966)

and increased amount of serum creatinine level (HR 1.083, 95% CI 0.930–1.260) were not associated with in-hospital mortality. Diagnostic values of composite of these factors (pH, weight gain, urine output, and phosphorus levels) (area under Palbociclib supplier the curve (AUC) 0.7145, 95% CI 0.656–0.771) was higher than serum creatinine level (AUC 0.449, 95% CI 0.382–0.517), GFR (AUC 0.553, 95% CI 0.485–0.62), and AKIN stage (AUC 0.589, 95% CI 0.521–0.657). Conclusion: These data may suggest that classical indication should be considered for the optimal timing for initiation of CRRT in critically ill patients. HATTORI YUKA1, KIM HANGSOO2, TSUBOI NAOTAKE2, YAMAMOTO AKIHITO1, UEDA MINORU1, MATSUO SEIICHI2, MARUYAMA SHOICHI2 1Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine; 2Department of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine Introduction: Acute kidney injury (AKI) is a critical condition which is

associated with high mortality rates of 30 to 50%. Ischemia-reperfusion injury (IRI) is a major cause of AKI. However, available treatments for AKI are limited. Preclinical studies indicate that administered MSCs ameliorate mafosfamide renal injury and accelerate kidney repair. Recently, stem cells from human exfoliated deciduous teeth (SHED), which are medical waste, have received attention as a novel stem cell source. The purpose of this study is to clarify whether SHED have therapeutic effect on AKI induced by IRI. Methods: SHED were isolated from human exfoliated deciduous teeth as described previously. For all experiments 7- 8-wk-old male C57BL/6 mice weighing 18–22 g were used. Under anesthesia mice were subjected to right heminephrectomy.

Mice were treated i.p. with anti-CCR3 in three different doses (30–300 μg/animal in 500 μl PBS) or isotype control (100 μg/animal in 500 μl PBS, rat IgG2b, clone R35-38; BD-Bioscience Europe, Erembodegem, Belgium) 1 hr before allergen exposure on the first day of exposure. Cytospin preparations from BM and BAL were stained for CD34 using a biotinylated rat anti-mouse CD34 mAb (clone

RAM34; BD Biosciences). Bound antibodies were visualized with a Vector Red Alkaline Phosphatase Substrate kit (Vector Laboratories Inc., Burlingame, CA). The slides Copanlisib cell line were also stained with Luxol Fast Blue and counterstained with Mayer’s haematoxylin (DAKO) to identify these cells as eosinophil-lineage precursors. Five hundred cells were evaluated in random fields of view. Cytospins from BAL were stained with a rat anti-mouse CD34 mAb (clone RAM34; BD Biosciences). A rabbit anti-rat immunoglobulin

(DAKO) was used as a link antibody before incubation with alkaline phosphatase–anti-alkaline phosphatase (DAKO). Bound antibodies were visualized with the Vector Red Alkaline Phosphatase Substrate kit. Slides were then treated with a biotin blocking system (DAKO) and incubated overnight at 4° with a biotinylated rat anti-mouse Sca-1/Ly6 mAb (Clone 177228; R&D Systems). Next day, the slides were washed and incubated with streptavidin-β-galactosidase and X-Gal substrate (β-Gal CFTR modulator staining set; Roche) and counterstained with Mayer’s haematoxylin. Four hundred cells were counted in random fields of view. All data are expressed as mean ± SEM. Statistical analysis was carried out using a non-parametric analysis of variance (Kruskal–Wallis test) to determine the

variance among more than two groups. If significant variance was found, an unpaired two-group test (Mann–Whitney U-test) was used to determine significant differences between individual groups. Wilcoxon signed rank test was used to analyse changes within the same group. P < 0·05 was considered statistically significant. Flow cytometric analysis for CD34+ CCR3+ cells in BM, blood, lung and BAL showed a significant increase of this 17-DMAG (Alvespimycin) HCl cell population in all three compartments of OVA-sensitized/exposed animals when compared with OVA-sensitized but saline-exposed control animals (Fig. 1a). Triple staining for CD34+ CCR3+ Sca-1+ on lung cells was performed to determine if a part of the CD34+ CCR3+ cells also expressed Sca-1. Allergen exposure induced a significant increase in the number of CD34+ CCR3+ Sca-1+ lung cells both in the SSChigh gated population (i.e. eosinophils) and in the SSClow gated cell population (i.e. eosinophil-lineage-committed progenitors) when compared with saline-exposed animals (Fig. 1b). CCR3+, Sca-1+ CCR3+ and CD34+ CCR3+ cells were also increased in the SSChigh and SSClow gated cell populations in allergen-exposed mice when compared with saline-exposed mice (Fig. 1c,d).

Jens Geginat showed that the CCR6+IL-7Rhi T-cell population contains not only Th17 cells but also memory cells that secrete suppressive IL-10 upon suboptimal TCR stimulation and with autologous DC; however, the same cells also produce CD40L, IFN-γ, and IL-2 following optimal TCR stimulation and with a relevant recall antigen, which is similar to the response of conventional memory T cells, suggesting that the cells have a context-dependent regulatory function. A subset of IL-10-producing Th1 effector cells, which suppress T-cell proliferation by an IL-10-dependent mechanism, was also identified in the CD4+CD25−IL-7Rlo T-cell

population. These effector cells express high levels of CTLA-4, and are anergic in vitro but proliferate in vivo presumably in response to persistent antigens. click here As the identified memory and effector-like T-cell subsets show different requirements, kinetics, and stabilities of IL-10 production, Jens Geginat proposed that they have different functions and might inhibit different types of immune responses. Naturally occurring regulatory T cells (Tregs)

have been shown to control immune responses to self and non-self. Muriel Moser (Brussels, Belgium) discussed the regulation of Th1 cells by naturally occurring and adaptive Tregs. It has previously been shown Everolimus datasheet that depletion of natural Treg before immunization with antigen-pulsed dendritic cells (DC) results in increased Th1-type responses characterized by high levels of IFN-γ production and CTL activity. The mechanism by which Tregs control the development of Th1-like responses, including the role of two Th1-prone factors, IL-12 and CD70, has also been examined. In vivo Treg depletion was found to lead to increased IFN-γ production in both wild-type and IL-12 p40-deficient mouse strains, suggesting that the ability of Tregs to down-modulate Th1 responses is largely IL-12- and IL-23-independent. Pregnenolone In marked contrast, neutralizing antibodies to CD70, a membrane-associated TNF family member, prevented the ability of Treg depletion to increase IFN-γ production. In vitro experiments

demonstrated that Tregs inhibit CD70 expression in a contact-dependent manner and, although the suppressive mechanism is still unclear, it may involve a phenomenon of (trans)-endocytosis because CD27−/− Tregs failed to downregulate CD70 in vitro. These observations indicate that natural Tregs control Th1 cell development by predominantly interfering with the CD70/CD27 pathway. Tomáš Brdička (Prague, Czech Republic) presented new data on the regulation of Src-family kinases (SFKs) in leukocytes. SFKs are regulated by phosphorylation of their inhibitory and activatory tyrosines, with the outcome depending on the complex interplay between the activities of several phosphatases, kinases, and adaptor proteins.

LPS is a component of gram-negative bacteria outer-membrane that binds TLR-4. Well known for its pro-inflammatory properties it also dampens immune responses in various experimental setups (e.g. [39, 46, 47]). To test whether Treg are directly involved in the mechanism at the basis of the ‘hygiene hypothesis’, we first tested various protocols of LPS administration PARP inhibitor trial for their capacity to prevent diabetes occurrence in NOD mice. Next, by conducting cellular analysis we revealed that LPS treatment enhances Treg numbers and activity. Finally, by performing adoptive transfer experiments we demonstrated that CD25-expressing Treg are involved in the beneficial effect of LPS

in NOD mice, thus providing evidence that CD25+ Treg may play a central role

in the cellular mechanism at the basis of the ‘hygiene hypothesis’. Mice.  Non-obese diabetic (NOD)/Lt and NOD/SCID mice were originally purchased from The Jackson Laboratory (Bar Harbor, ME, USA). All animals were bred and maintained under specific pathogen-free conditions in our animal facilities. Mice experimental protocols were approved by the Instituto Gulbenkian de Ciência ethics committee and by the national authority Direcção Geral de Veterinária. LPS treatment.  In most experiments, 6- to 8-week-old NOD mice were injected i.p. with 10 μg LPS from Salmonella typhimurium (Sigma, Sintra, Portugal) diluted in PBS, once per week until the check details time of analysis. Other experimental groups were: 12-week-old NOD females injected weekly with 10 μg LPS i.p. until time of analysis; 7.5 weeks of age NOD females injected once with 10 μg LPS and 4 weeks of age NOD females injected every 3 days with 10 μg LPS i.p., Ribonucleotide reductase during 1 month. In all experimental groups, PBS-injected age-matched animals served as controls. Diabetes detection.  Diabetes was monitored weekly or biweekly, according to the experiment, by measuring blood glucose levels using ACCU-CHEK Sensor Comfort strips (Roche, Mannheim, Germany). Mice that had values ≥250 mg/dl on two consecutive occasions were deemed diabetic. Cell purification and FACS analysis.  For flow cytometry purification,

thymus, pancreatic (p)LN or spleen cells, according to the experiment, were obtained by forcing the organs through a 100 μm nylon mesh. For isolation of pancreas-infiltrating lymphocytes, whole pancreas (after careful removal of pLN used in the same experiment for FACS staining) were cut into small pieces and incubated in OptiMEM medium (Invitrogen, Madrid, Spain) containing 5% FCS and 450 U of collagenase (Sigma) for 20 min at 37 °C. After filtering through 100 μm nylon mesh, lymphoid cells were isolated on a 40% Percoll gradient. The cells were then washed for posterior FACS staining. For FACS staining, 1 × 106 cells (whenever possible) were preincubated for 20 min with unlabelled mAb to the Fc-γ receptor (clone 2.

Heligmosomoides polygyrus bakeri is a fascinating intestinal parasitic nematode of mice that was isolated in the 1950s by Ehrenford [1] and since then has attracted increasing attention from researchers, particularly in the last two decades and especially from parasite immunologists. H. p. bakeri represents an important model of chronic helminth infection and is phylogenetically related to the ruminant parasites Haemonchus contortus PLX3397 and Teladorsagia circumcincta and the human hookworms Ancylostoma duodenale and Nector americanus

[2]. The parasite has played an important role in helping us to explore and understand many different aspects of infection with helminths, but its pre-eminence is its capacity to cause long-lasting chronic infections in its murine host [3, 4]. Unlike other rodent

intestinal nematodes that became popular laboratory models in the 1960s (e.g. Nippostrongylus brasiliensis, Trichuris muris, Trichinella spiralis, Strongyloides ratti [5, 6]) and which cause limited infections (although note that in some mouse strains, T. muris may develop to patency and cause chronic infections [7, 8]), often restricted click here to 2–3 weeks, and induce strong acquired immunity in their hosts, H. p. bakeri is able to survive for up to 10 months in many commonly used laboratory mouse strains [3, 4]. It is this capacity to cause long-lasting chronic infections

in mice that distinguishes H. p. bakeri from other intestinal nematodes and which makes it a convenient model of chronic nematode infections in humans and our domestic animals [9-12]. This capacity of H. p. bakeri to survive for so long, without inducing rapid expulsion, is facilitated by the mechanisms that this species uses to downregulate local intestinal immune responses primarily in its immediate vicinity, but also in more distant host tissues [13-15]. H. p. bakeri is known to secrete immunomodulatory factors CYTH4 (IMF) that interfere with both the induction and expression of mucosal immune responses [12, 16-18], and one consequence of this is that other parasites residing in the intestinal tract (and elsewhere in host tissues) of concurrently infected animals can benefit by sustaining longer infections than would otherwise be the case. The prolongation of infections with other species has been demonstrated in the laboratory [19-22] and has been detected in the field in wild rodent populations naturally infected with the close relative H. p. polygyrus [23, 24]. The literature on H. p. bakeri is large and has been complicated by taxonomic problems centring on the relationships of H. p. bakeri with another closely related parasite of wild rodents in Europe, which is now more correctly referred to as H. p. polygyrus.