, 2011). Clinically, in the chronic lung infection

associated with cystic fibrosis (CF), see more the majority of aggregated P. aeruginosa are not found attached to pulmonary epithelial surfaces, but within the viscous mucus associated with larger airways (Worlitzsch et al., 2002; Bjarnsholt et al., 2009a). Therefore, although an elemental component of a biofilm is the aggregation of microbial cells, the necessity for attachment to a fixed substratum may be more elastic. Biofilms differ from single cells, and in bacterial systems, research has focused on differences in structure, function, and behavior. Structurally, the amassing of microbial cells has been compared with multicellularity (Stoodley et al., 2002) and constitutes a level of higher organization than single cells. As a strategy to help individual cells withstand diverse environmental conditions, phenotypic differentiation within a larger structure means functionally specialized cells to: (1) stick via different receptor–ligand interactions to a surface or to other cells (homotypic or heterotypic), (2) produce EPS, (3) metabolize slowly or rapidly grow, or (4) stay attached or disperse (Hall-Stoodley

et al., 2004). Definitions of biofilms also include ‘embedded in an extracellular polymeric matrix of microbial Rapamycin origin.’ However, ‘extramicrobial’ host-derived components are particularly important in complex host environments such as dental plaques or intravenous catheter biofilms. Dental biofilms, for example, may use saliva proteins in the surface pellicle to attach to the tooth; bacteria may bind to fibronectin on medical implants; and microbial vegetations in infective endocarditis may be found enmeshed in a mass of fibrin, aggregated platelets, and other host proteins (Parsek & Singh, 2003; Diaz et al., 2006; Moter et al., 2010, Marsh et al., 2011; Stoodley et al., 2011). Restricting a definition of biofilm to ‘microbial or bacterial origin’ therefore ignores infections where bacteria

interact with host molecules and receptors to attach, replicate, and aggregate. Therefore, a more comprehensive definition of a clinically Docetaxel relevant biofilm is: ‘aggregated, microbial cells surrounded by a polymeric self-produced matrix, which may contain host components. Cells in microbial biofilms additionally differ from planktonic cells in two major ways: (1) they are usually more tolerant of antibiotics and antimicrobial treatment, and (2) they may persist in the host, often despite a heavy influx of inflammatory cells and effector functions of the adaptive immune response. This distinction cannot be demonstrated in a diagnostic sample by culture alone, illustrating why better diagnostic markers, which exploit the difference between planktonic and biofilm cells, are needed. The clinical importance is that biofilm infections are typically chronic infections. and the presence of chronic and recurrent infection in a patient should raise the clinician’s suspicion of a biofilm infection.

Interestingly, IgA levels positively correlated with serum C-reactive protein suggesting the involvement of oral infection on systemic inflammation and coronary artery disease prevalence [7]. The primary function of B cells is to produce antigen-specific Ig. Naive B cells present the amazing ability to alter the effector function of Ig molecule by isotype Etoposide order switching, which is a critical component of B cell differentiation and generation of protective humoral immune responses [8]. Recently, it has been demonstrated that some Th-secreted cytokines is essential to stimulate naïve B cells to produce Ig. Interleukin (IL)-21 induces naive

B cells to switch expression of IgA, especially IgA1. In addition, IL-10 amplifies secretion of IgA induced by IL-21 [9], consistent with the role of IL-10 in regulating IgA responses [10]. In contrast, IL-4 dramatically attenuates IL-21-induced switching to IgA secretion while the neutralization of endogenous IL-4 increases the levels of IgM and IgA [9]. In addition to B cell antigen receptor and receptors for cytokines such as IL-4, IL-10, IL-21, the CD40, an integral

membrane protein found on the surface of several cells, upregulates the expression of DNA-editing enzyme called activation-induced cytidine buy Dactolisib deaminase (AID) and triggers the induction of somatic hypermutation (SHM) and class-switch recombination (CSR) from IgM to IgG or IgA [11–13]. It has been proposed that IL-21 in combination with CD40 costimulation is even more effective in inducing IgA production

by B cells [14]. Therefore, the presence of IL-21/IL-10/CD40L has been proposed to be critical for isotype switching to IgA by naïve B cells. To date, the possible relationship between the mediators related to Ig production and the levels of IgA was not evaluated in chronic periodontitis subjects. Therefore, the aim of this study was to assess the gingival levels of IL-21, IL-21 receptor (IL-21R), IL-4, IL-10 and CD40 ligand (CD40L) and the salivary levels of IgA in chronic periodontitis subjects, when compared to periodontally healthy ones. Subjects.  Thirty systemically healthy individuals, 15 with chronic periodontitis and 15 periodontally healthy subjects (aged 34–60 years) Etomidate were selected from the population referred to the Periodontal Clinic of Guarulhos University, from January 2009 until July 2010. Subjects who fulfilled the following described inclusion/exclusion criteria were invited to participate in the study. All eligible subjects were informed of the nature, potential risks, and benefits of their participation in the study and signed their informed consent. This study protocol was previously approved by the Guarulhos University’s Ethics Committee in Clinical Research (protocol # 100/2007). Inclusion and exclusion criteria.  All subjects should be >30 years old and present at least 15 teeth (excluding third molars).

Titres HDAC inhibitor by human reference sera and monoclonal antibodies to OMV antigens with known bactericidal titres. Opsonophagocytic activity was measured as respiratory burst [36]. Live meningococci from strain 44/76 and B1723 were used as targets, and human polymorphonuclear leucocytes from

a normal human donor, probed with dihydrorhodamine 123 (Invitrogen, Oslo, Norway), as effector cells. A human serum, different from that used in SBA, served as complement source after passing through a Protein G-column. A positive human reference serum was included as control for complement activity and assay sensitivity. Twofold serial dilutions of the mouse sera were analysed, and respiratory burst

was analysed with a flow cytometer (Partec CyFlow® ML, Partec GmbH, Münster, Germany) gating on the polymorphonuclear population. Opsonic titres were recorded as log2 of the highest reciprocal serum dilution giving ≥50% respiratory burst of the polymorphonuclear leucocytes. Magnetic polystyrene beads (40 mg/ml) (Dynabeads® Talon®; Invitrogen Dynal, Oslo, Norway) were washed with 50 mm Na-phosphate, pH 8.0, 300 mm NaCl and 0.01% Tween-20 according to the manufacturer’s instructions and incubated for 10 min in the same buffer with his-tagged recombinant Omp85. Preliminary experiments showed that 4 mg of beads bound ≤40 μg Omp85, as no Omp85 protein was detected LDE225 after SDS gel electrophoresis of the

supernatant. The recombinant Omp85 protein preparation showed one band in SDS gels of molecular mass about 90 kDa. Due to the small amounts of recombinant Omp85 available, serum pools were used for the adsorption experiments. Differences in antibody levels were analysed with Student’s t-test or Mann–Whitney rank sum test with a SigmaStat 3.1 program (Systat Software, Chicago, IL, USA). Correlations between Phosphoribosylglycinamide formyltransferase SBA and PorA antibody levels were assessed by the non-parametric Spearman’s rank-order correlation test. P-values < 0.05 were considered significant. After induction of transformed meningococci with IPTG, the genetically modified Omp85+ OMVs expressed fivefold higher levels of Omp85 (mean 5.2; range 4.4–7.2 of six determinations) relative to PorA in SDS gels and on blots compared with same levels in the wt 1 and wt 2 OMVs (Fig. 1A,B). The SDS gel also shows that the three OMV preparations contained different levels of the opacity proteins OpcA and OpaJ (Fig. 1A). Omp85+ OMVs expressed negligible levels of both proteins; OpaJ was modestly increased in the wt 2 OMV control, whereas a dominant OpcA band was observed in wt 1 OMVs, as previously reported [33]. These antigens might possibly affect the bactericidal activity of the OMV vaccines. However, OpaJ does not induce bactericidal antibodies in mice [37].

Results:  Over-expression of the chemokine receptor CCR7 enables non-metastatic tumor cells to recognise and grow towards LECs (3.9 fold compared with control), but not blood endothelial cells (0.9 fold), in vitro and in vivo in the absence of increased lymphatic clearance. Chemotactic metastasis was inhibited by a CCL21 neutralising antibody (4–17% of control). Furthermore, CCR7 expression in mouse B16 melanomas resulted in in-transit metastasis (50–100% of mice) that was less often seen with control tumors (0–50%) in vivo. Conclusion:  These results suggest that recognition Selleck Alectinib of LEC

by tumors expressing receptors for lymphatic specific ligands contributes towards the identification and invasion of lymphatics by melanoma cells and provides further evidence for a chemotactic metastasis model of tumor

spread. “
“Advances in high‐frequency (15–80 MHz) ultrasound‐based methods for the noninvasive assessment of the microcirculation are described. Well‐established Doppler imaging approaches for vascular imaging are reviewed and their limitations discussed. The use of microbubble (MB) contrast agents with both linear and nonlinear imaging sequences are shown to extend the range of Doppler approaches to the true capillary microcirculation. In particular, nonlinear scattering by MB contrast agents provide a unique intravascular Ulixertinib price signature that can be distinguished from the echoes caused by surrounding tissues. Ultrasound (US) has the ability to selectively eliminate enough the contrast by momentarily increasing US power. Reflow of new contrast then allows local measurement of the microcirculation at reduced power. The characteristic “wash‐in” of MB contrast contains valuable information on the local perfusion and the blood volume of the tissue. Thus, MB contrast agents act as a tracer revealing

the kinetics of tissue blood flow. Examples of wash‐in kinetics for tumor models are presented to illustrate the value of this approach for research in angiogenesis. Further refinement of this approach is described in which hemodynamic measures are mapped on a pixel‐by‐pixel basis to create parametric maps of relative blood volume and perfusion. The strengths and weaknesses of these new methods are discussed and the potential for their use in preclinical animal drug studies, clinical drug trials, and prognostic studies are described. “
“Please cite this paper as: Davis MJ. Perspective: Physiological Role(s) of the Vascular Myogenic Response. Microcirculation 19: 99–114, 2012. The vascular myogenic response is an inherent property of VSM in the walls of small arteries and arterioles, allowing these principal resistance segments of the microcirculation to respond to changes in transmural pressure. Elevated intraluminal pressure leads to myogenic constriction, whereas reduced pressure leads to myogenic dilation.

tropicalis (21%), C. parapsilosis (21%) and C. glabrata (5%). A similar study conducted by Chang et al. [11] in Mato Grosso do Sul, Brazil, detected the presence of C. albicans (45.8%), C. parapsilosis (34.4%), C. tropicalis (14.6%) and C. glabrata (5.2%) in venous blood samples from hospitalised patients. find more A current study conducted by Motta et al. [12] in the largest Brazilian teaching hospital complex demonstrated a similar profile, with C. albicans showing the highest incidence (52.2%), followed by C. parapsilosis (22.1%), C. tropicalis (14.8%) and C. glabrata (6.6%). The incidence of infections due to non-albicans Candida spp. is increasing[4] although

C. albicans remains the species of greatest clinical interest.[13] Currently,

there are about 17 species known to cause invasive or superficial mycoses. Based on a recent study, non-albicans Candida spp. are responsible for 35% to 65% of all candidiasis cases.[14] According to Glolo and Svidzinski [15], the most common species involved in the infectious processes are C. tropicalis, C. parapsilosis, C. krusei, C. kefyr, C. norvegensis, C. rugosa, C. guilliermondii, C. lusitaniae, C. ciferrii, C. haemulonii, C. lypolytica, C. pulcherrima, C. catenulata, C. utilis, C. viswanathii AZD0530 and C. seylanoides. Many factors may predispose an individual to infection, among them the use of broad-spectrum antibiotics, being a transplant patient, prolonged hospitalization and invasive surgical procedures such as the use of vesical catheters, venous catheters and mechanical ventilation.[15, 16] Other second factors, such as extreme age, immunosuppression, renal failure, diabetes, chemotherapy,

radiotherapy, mucosal injury, haemodialysis, previous surgery, corticotherapy and use of dental prostheses, can also play a role.[17-19] The ability of Candida to cause infection also depends on its intrinsic virulence attributes.[20] Yeast of the genus Candida spp. possess several virulence-associated factors that ensure their ability to colonise and cause infection. These include the ability to adhere to host cells, promoting phenotypic changes, converging between yeast and pseudohyphae forms, the ability to form biofilms, producing substances harmful to cells, such as haemolysins, the ability to resist hydrogen peroxide and derivatives and the ability to produce and secrete hydrolytic enzymes. These factors can facilitate the promotion of infections in susceptible hosts and ensure microbial permanence to colonise or invade host tissues.[20-22] Candida albicans has well-known pathogenic potential, due to its ability to adhere to mucosal and epithelial cells, phenotypic transition with the production of hyphae that help tissue invasion, significant thermotolerance and the production of hydrolytic enzymes.[23, 24] In addition, C. albicans forms biofilms that adhere to and colonise surfaces.

When the same experiments were performed in mice lacking i-proteasomes, there was accumulation of oxidized proteins, and higher levels of BGB324 in vitro apoptosis; and in the EAE model, higher clinical scores of the disease. These data support the hypothesis that i-proteasomes play a protective role against toxic effects induced by protein aggregates formed when cells are subjected to the inflammatory millieu [81]. Nevertheless, the question of whether and how the UPR intersects with i-proteasomes remains open. Both conditions observed in the study (stimulation by pro-inflammatory cytokines and accumulation of misfolded proteins) are potential ER stressors. The protective role of UPR at the face of

protein overload triggered by the innate immune response appears to be conserved through find more evolution.

In Caenorhabditis elegans, protective immunity against Pseudomonas aeruginosa is dependent on PMK-1, an ortholog of the mammalian p38 MAP kinase [82]. Infection by P. aeruginosa causes ER stress, inducing XBP-1 splicing. Infection by these bacteria was lethal for a XBP-1 loss-of-function mutant. Surprisingly, the lethal outcome of the infection in XBP-1 mutants was reversed when PMK-1 was disrupted. Furthermore, hyperactivation of PMK-1 caused larval mortality on the XBP-1 mutants even in the absence of the pathogen. Unexpectedly, mutants for ATF6 and PEK1 (homologue DNA ligase of PERK) developed normally and did not show a detrimental phenotype. The study concludes that although the innate response promotes resistance to this pathogen, it also represents a source of ER stress, demanding a compensatory

activity of the UPR for the development of C. elegans larvae [83]. This hypothesis is further supported by the observation that when C. elegans larvae were stimulated with a pore forming bacterial toxin, PMK-1 was activated as a defense mechanism. The UPR pathway was activated through IRE1/XBP-1 and ATF6. XBP-1 and ATF6 loss-of-function mutants were more susceptible to the toxin, in a SEK1– (MAPKK upstream of PMK-1) and PMK1-dependent manner [84] (Fig. 3). The first report showing that the XBP-1 transcription factor was highly expressed by pre-pro-B cell and plasma cell lines [52] rouse the interest to study the role of XBP-1 in B cell biology. XBP-1 is a necessary transcription factor for B cell terminal differentiation into plasma cells [85]. The disruption of XBP-1 in mice leads to mortality in uterus caused by anaemia due to liver hypoplasia [86]. XBP1−/−RAG2−/− chimera mice develop normally and with normal numbers of T and B lymphocytes. These animals present lower serum immunoglobulin levels when compared with their wild-type littermates. Nevertheless, there are no differences in proliferation and isotype class switch by XBP1-deficient B cells, and no defects in germinal centre formation in XBP1-deficient mice.

e., pitch, vowel quality, timbre, sociolinguistic variation) and production-specific variables (i.e., prosody) that are not associated with lexical contrast

(e.g., there are no English words that differ only by pitch). As these do not cue phonemic or lexical contrasts, much work in speech perception has been devoted to explaining how listeners are able to overcome such variability to arrive at the underlying meaning (e.g., Perkell & Klatt, 1986). Alternatively, it is possible that the auditory system would need to retain, rather than normalize, multiple forms of acoustic information to arrive at the correct categories Selleckchem BIBW2992 (Goldinger, 1998; Klatt, 1979; Pierrehumbert, 2003; Pisoni, 1997). Prior work on this has focused on whether listeners use such detail during online perception (Creel, Aslin, & Tanenhaus, 2008; Goldinger, 1998; Ensartinib order Johnson, 1990; Ryalls & Pisoni, 1997). Importantly, it has been shown that infants might map both indexical and phonetic information of words in

early word learning (Houston & Jusczyk, 2000). This suggests that irrelevant cues, such as indexical information, may help in the acquisition of speech contrasts. Indeed there is evidence that variability along nonphonemic dimensions may help identify the underlying invariant structure of speech. Singh (2008) has shown that variation in the affective quality of speech improves word segmentation in infancy. Hollich, Jusczyk, and Brent (2002) report that word segmentation abilities are improved by multiple-talker familiarization

in older infants. However, both studies looked at broad segmentation abilities, not at the perception of a single phonetic feature (e.g., voicing) in a highly ambiguous context. This was explicitly tested in Experiment 3. The exemplar set used in Rost and McMurray (2009) was highly variable in noncontrastive aspects of the signal (such as vowel quality or pitch), but the range of variability within these dimensions did not differ between /buk/ and /puk/. If infants Fludarabine datasheet use highly variable information to isolate relatively invariant elements of the signal, they should succeed at the switch task when exemplars contain lots of variability, but minimal within-category variability in contrastive cues. Recruitment and exclusion criteria were the same as in Experiment 1. Twenty-three infants participated, and data from seven were excluded from analysis for experimenter error (4), fussiness (2), and failure to habituate (1). Sixteen infants (9 boys; M age = 14 months 8 days, range = 13 months 5 days to 15 months 1 day) were included in the experimental analysis. Stimuli consisted of the original set of 54 exemplars recorded from 18 speakers from Rost and McMurray (2009). These were modified to maintain variation in all of the noncriterial (indexical and prosodic) cues but eliminate within-category variation in VOT.

16,31,32 The up-regulation of β-tubulin-specific IL-10 production by splenocytes suggests the possibility that hASCs may induce IL-10-producing Treg cells31,33 in EAHL mice. We therefore examined the possibility that this suppression was mediated by the production of Treg cells in vivo. We found a significantly elevated percentage of CD4+ CD25+ Foxp3+ cells from EAHL mice exposed to hASCs compared with the PBS control groups. Also, these hASC-induced Treg cells potently inhibited the proliferative response of autoreactive T cells in vitro, and these effects were significantly abrogated

by anti-IL-10 antibodies. Therefore, hASC treatment might induce IL-10-secreting selleck screening library β-tubulin-specific CD4+ CD25+ Foxp3+ Treg cells in mice with EAHL that mediate T-cell tolerance. In summary, the present study demonstrated that hASCs display a therapeutic potential and suggests that hASCs may provide a novel therapeutic approach for AIED. Mechanistically, our results indicate that the hASCs inhibit the Th1/Th17 cell responses through the generation of IL-10-secreting Treg cells with the capacity to suppress autoreactive T-cell responses, thereby maintaining self-tolerance. We thank RNL-bio (Korea) for providing

the funding for this research project. The authors declare no financial conflicts of interest. “
“Because regulatory T (Treg) cells play an important role in modulating the immune system response against ABT-199 concentration Oxymatrine both endogenous and exogenous antigens, their control is critical to establish immunotherapy against autoimmune disorders, chronic viral infections and tumours. Ribavirin (RBV), an antiviral reagent used with interferon, is known to polarize the T helper (Th) 1/2 cell balance toward Th1 cells. Although the immunoregulatory mechanisms of RBV are not fully understood, it has been expected that RBV would affect T reg cells to modulate the Th1/2 cell balance. To confirm this hypothesis, we investigated whether RBV

modulates the inhibitory activity of human peripheral CD4+ CD25+ CD127− T cells in vitro. CD4+ CD25+ CD127− T cells pre-incubated with RBV lose their ability to inhibit the proliferation of CD4+ CD25− T cells. Expression of Forkhead box P3 (FOXP3) in CD4+ CD25− T cells was down-modulated when they were incubated with CD4+ CD25+ CD127− T cells pre-incubated with RBV without down-modulating CD45RO on their surface. In addition, transwell assays and cytokine-neutralizing assays revealed that this effect depended mainly on the inhibition of interleukin-10 (IL-10) produced from CD4+ CD25+ CD127− T cells. These results indicated that RBV might inhibit the conversion of CD4+ CD25− FOXP3− naive T cells into CD4+ CD25+ FOXP3+ adaptive Treg cells by down-modulating the IL-10-producing Treg 1 cells to prevent these effector T cells from entering anergy and to maintain Th1 cell activity.

A new dimension of functional genomics has been introduced by next-generation sequencing technologies. Ceritinib purchase The high-depth sequencing achievable by such methods as RNA sequencing (RNA-seq) will enhance transcriptome

profiling and gene identification. Proteomic studies have been essential for validating gene annotations in Toxoplasma and for better characterizing proteins from distinct subproteomes. While significant effort has gone towards studying tachyzoite proteins, proteomic data for other developmental stages such as the bradyzoite and the sporozoite are notably lacking. Future proteomic studies directed at these life stages should provide a basis for better understanding the functional differences between them. Beyond simply cataloguing parasite proteins, proteomic studies should be able to begin complementing transcription analyses to better define the timing of protein expression during development. “
“Progress in our understanding of the role of the maternal immune system during healthy pregnancy will help us better understand the role of the immune system in adverse pregnancy outcomes. In this review, we discuss our present understanding of the ‘immunity of pregnancy’ in the context of the response to cervical and placental infections and how these responses affect both the mother and the fetus. We discuss novel selleck products and challenging concepts that help explain the immunological aspects of pregnancy and how

the mother and fetus respond to infection. “
“Interleukin 17A IL-17A is a crucial immunomodulator in various chronic immunological diseases including rheumatoid arthritis and inflammatory bowel disease. CYTH4 The cytokine has also been demonstrated to control the pathogenesis of the Mycobacterium tuberculosis by dysregulating production of cytokines and chemokines and promoting granuloma formation. Whether IL-17A regulates innate defence mechanisms of macrophages in response to mycobacterial infection remains to be elucidated. In the current

report, we investigated the effects of IL-17A on modulating the intracellular survival of Mycobacterium bovis bacillus Calmette–Guérin (BCG) in RAW264.7 murine macrophages. We observed that IL-17A pre-treatment for 24 hr was able to synergistically enhance BCG-induced nitric oxide (NO) production and inducible nitric oxide synthase expression in dose- and time-dependent manners. We further delineated the mechanisms involved in this synergistic reaction. IL-17A was found to specifically enhanced BCG-induced phosphorylation of Jun N-terminal kinase (JNK), but not of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase. By using a specific JNK inhibitor (SP600125), we found that the production of NO in BCG-infected macrophages was significantly suppressed. Taken together, we confirmed the involvement of the JNK pathway in IL-17A-enhanced NO production in BCG-infected macrophages.

At the systemic level, serum IgA peaked around 3 weeks post-infection (WPI) and decreased thereafter (Figure 3). Serum IgG quickly increased to a asymptote around three WPI and remained consistently high throughout the infection (Figure 3). Changes in serum IgA and IgG were significantly different between treatment

(infected and controls) and the interaction between treatment and WPI, RG 7204 when the analysis was corrected for the random effect of the host and the nonindependence of sampling the same individual over time (Table 4). Mucus IgA and IgG patterns exhibited similar trends: values were significantly higher in the infected, compared to controls, and decreased from section 1 to section 4 of the small intestine; mucus IgG also increased with sampling time in infected rabbits (Table 4). Graphidium strigosum: Infected rabbits mounted a strong somatic IgA and IgG response at the systemic level but the local antibody response was relatively low to both adult and L3 stages (Figures 4 and S2).

Specifically, serum IgA and IgG significantly differed between treatments and increased with infection time in infected individuals (Table 5). Mucus IgA and IgG were higher in the infected compared to the controls, and Doxorubicin purchase for the infected, values increased with the course of infection showing stronger response in the fundus compared to the antrum section of the stomach (Table 5). Together these findings suggest that rabbits develop an effective systemic and local antibody response to T. retortaeformis but an inefficient mucosal response to G. strigosum. Trichostrongylus Amoxicillin retortaeformis: Total white blood cell

and lymphocyte counts were significantly higher in infected hosts compared to the controls and consistently increased over the course of the infection (Figure 5). No significant trend was recorded for eosinophils and neutrophils, corrected for the random effect of the host and the dependence of sampling the same individual over time (Figure 5). However, a more detailed analysis showed that during the second-to-fifth WPI, coinciding with the peak in antibody response, a strong eosinophilia, anaemia (haemoglobin) and high total white blood cells were recorded in infected compared to control rabbits (Table 6). Graphidium strigosum: A consistent increase in the concentration of eosinophils, lymphocytes, total white blood cells and haemoglobin was observed with the progression of the experiment but no significant differences were recorded between the infected and the controls (Figure 6, Table 6). In line with T. retortaeformis infection high eosinophilia, neutrophilia and total white blood cell concentrations were found during the second-to-the fourth WPI in infected compared to the controls; no significant development of anaemia was observed during this infection.