VIP/VPAC1 expression did not vary in BALB/c glands with mouse age and, in contrast with NOD glands, freshly isolated acinar cells seemed not to be prone to apoptosis. Acinar cells from NOD mice could be further induced to JQ1 in vivo apoptosis with a concentration

of TNF-α (10 ng/ml) that was almost ineffective in normal acinar cells. VIP inhibited TNF-α-induced apoptosis in NOD acinar cells through a VPAC1/cAMP/PKA pathway, while neither VPAC2 receptors nor the neuropeptide could be detected in acini, indicating that their expression in whole glands would not correspond to acinar cells. Finally, we found a reduced phagocytic index of NOD macrophages to engulf apoptotic acinar cells compared to normal macrophages, but their basal inflammatory phenotype was suppressed during phagocytosis and VIP stabilized this suppressor regulatory phenotype. It is noteworthy that the time–course of VIP/VPAC1 relative expression decline is similar to the kinetics of nNOS activity loss shown previously and parallels Selleck GDC0068 the reduction in the secretory response to muscarinic acetylcholine receptor stimulation [12]. It also coincided with the loss of acinar cell homogeneous structure of the glands and a higher ductal to acinar cell ratio in the glands at 16 weeks of age [12]. The localization of this enzyme is normally confined

to neural fibres in close proximity to gland epithelial cells where NO contributes to salivary flow. Consistent with this, NOD mice submandibular glands showed a

reduced NOS activation through VIP receptors that coincided with the reduction in salivary flow [15]. While VIP can induce NOS in peripheral and central neurones, VIP expression is regulated by neural NOS activity and knock-out mice for neural NOS isoform express lower neuronal VIP levels [29]. In rat salivary glands VIP is localized in nerve fibres rather than in acinar cells, being mainly released from nerves surrounding acini where it displays trophic effects on epithelial cells [17,18]. In fact, the release of trophic and anti-apoptotic stimuli from nerve terminals with long-term effects on salivary gland parenchyma is the rationale of a newly designed device to restore salivary flow in patients with SS and other sicca-associated pathologies [30]. Acinar cells from both normal and NOD Phosphatidylethanolamine N-methyltransferase submandibular glands express only VPAC1 receptors, as reported previously [16]. In these cells, VIP was able to reduce apoptosis via cAMP/PKA pathway, as derived from the fact that H89 reversed VIP effect on bax expression [16] and Bad phosphorylation, a step previous to the loss of its apoptotic effect through binding to 14–3–3 in cytosol [31]. Evidence shown here indicates that acinar epithelium of NOD but not BALB/c glands present increased apoptosis along with a dysregulated NF-κB basal activation consistent with a predominant apoptosis-to-survival intracellular set-point.

These signals are mainly provided by members of the B7-family including CD80 and CD86. However, macrophages

can also inhibit T-cell activation by release of inhibitory cytokines such as IL-10 and TGF-β or metabolic starvation due to depletion of tryptophan by indoleamine-2,4-dioxygenase 19 and depletion of arginin by nitric oxide synthase (iNOS) or Arg1 Sunitinib 20. In addition, macrophages can suppress T cells by direct cell–cell contact via expression of ligands for inhibitory receptors. B7-H1 (PD-L1) and B7-DC (PD-L2) are two members of the B7-family, which bind to programmed death 1 (PD-1), an inhibitory receptor on T cells. Similar to its effects on cytokine production, chitin may modulate expression Sorafenib of costimulatory ligands on macrophages and thereby regulate the efficiency of T-cell activation, differentiation and proliferation. However, this possibility has not been examined experimentally. To address this point directly, we determined

whether chitin modulates Th2 polarization and T-cell proliferation using adoptive transfers and coculture systems. We observed that chitin reduced the expansion of antigen-specific CD4+ T cells in vivo. Chitin-exposed macrophages upregulated B7-H1 independently of signaling via TLR or Stat6 and blocked T-cell proliferation in a cell–cell contact-dependent manner. Inhibition of T-cell proliferation was not observed with cells from B7-H1-deficient mice which indicates that chitin inhibits T-cell proliferation indirectly by inducing expression of B7-H1 on macrophages. Intranasal administration of chitin particles induces early recruitment of macrophages and neutrophils followed later by basophils and eosinophils 9, 18. As basophils express large amounts of IL-4 and have recently been shown to initiate Th2 differentiation in response to the pro-allergic protease papain, Interleukin-3 receptor we sought that chitin-induced basophil recruitment might result in priming and expansion of Th2 cells in the lung 21, 22. Therefore, we determined whether intranasal chitin administration leads to enhanced Th2-cell differentiation

in the lung and draining LN. To visualize Th2-cell differentiation, we used IL-4 reporter mice (4get mice), which were crossed to DO11.10 TCR-tg mice so that the OVA-specific T-cell responses could be analyzed. BALB/c mice were reconstituted with 106 TCR-tg cells from DO11.10/4get mice followed by intranasal administration of OVA protein in the presence or absence of small (20–50 μm) chitin particles. Administration of OVA induced expansion of TCR-tg cells (KJ1-26+ cells) in lung and LN, whereas T-cell expansion was five-fold reduced in mice which received OVA plus chitin (Fig. 1A and B). In addition, Th2-cell differentiation was induced only in OVA but not in OVA/chitin-treated mice (KJ1-26+IL-4/eGFP+ cells in Fig. 1A). Therefore, chitin did not enhance but rather inhibited the Th2 response in the lung and LN.

One of these, the L1007insC frameshift mutation (31% prevalence), results in a truncated NOD2 protein lacking part of the last LRR. Homozygous carriers of this mutation exhibit a much more severe disease phenotype and have a higher Selleckchem Afatinib risk for ileal stenosis and surgical intervention

42. A different subset of CARD15 mutations cause a distinct and highly penetrant autosomal dominant systemic disorder called Blau syndrome (BS) 43. BS mutations almost exclusively target the NBD of the protein and produce a broader distribution of affected tissues than CD. Three-dimensional structure analysis predicted that the NLRP3 R260W mutation and the BS-associated R334W mutation of NOD2 encode a substitution at a homologous, structurally conserved amino acid residue 44. Therefore, as is the case for NLRP3 in CAPS, NBD mutations in BS may produce a protein that is constitutively active, a hypothesis Autophagy activator supported by the finding that R334W NOD2 leads to increased basal NF-κB activation 45. As LRRs are implicated in sensing microbial components, CD-associated mutations in NOD2 may alter the threshold of mycobacterial N-glycolyl muramyl dipeptide recognition and its downstream signalling rather than lead to a constitutively active form as in BS. However, the consensus mechanism by which mutations in NOD2 predispose

to CD remains controversial. Indeed, Segal and colleagues have reported that CD patients, irrespective of their genotype, share a dampened inflammatory phenotype in response to injury or bacterial challenge 46. Enhanced lysosomal degradation

was proposed to be at the basis of the cytokine secretion defect in CD. This raises the question of whether CD is a systemic immune deficiency disease with manifestations in the intestinal tract due to the uniquely high bacterial content of this organ. Only recently did a study reveal the surprising discovery that, unlike its WT counterpart, L1007insC mutant NOD2 actively suppresses the constitutive transcription of human IL-10 Cyclooxygenase (COX) in a peptidoglycan- and NF-κB-independent manner by inhibiting the activity of hnRNP-A1 in monocytes 47. This phenomenon was not found with the mouse orthologues and cautions on the necessity of human functional immunological studies. In this context, it is not surprising that enhanced IL-10 production, which can occur after treatment with certain probiotic bacteria, helps to calm inflammation in CD 48. Such data suggest a complex interaction between NOD2 and a number of other loci controlling innate and adaptive immune function (e.g. IL-23R 49) to confer susceptibility to CD. Nonetheless, these studies provide initial evidence in support of a long-held theory that conjectures that NOD2 normally functions as an innate signal that tolerizes the host’s adaptive immune system to the commensal intestinal flora. Although there are limitations inherent to GWAS design (e.g.

Cases of Aspergillus osteomyelitis in bones after surgery in that area suggest that infection may also be caused by contamination during surgery. In a study published in 2005, 20 cases of osteomyelitis caused by Aspergillus spp. were analysed. Eighteen patients had definite bone involvement diagnosed (spondylodiscitis in 9, sternum/rib osteomyelitis

in 6, and peripheral bone involvement in 5). Fourteen of 20 patients were immunocompromised for various reasons. In seven cases, surgical intervention was required, 57% (four patients) responded well to the surgical therapy, while buy EPZ-6438 in three patients the therapy failed.[47] In a review by Stratov et al. [48], who investigated 42 cases of invasive Aspergillus osteomyelitis, surgery in combination with liposomal amphotericin B increased the success rate to 69% in comparison to 14% cure rate, when therapy consisted of amphotericin B alone, suggesting the important role of surgery in Aspergillus bone infections. Studenmeister et al.

[49] analysed (2011) 21 cases of vertebral osteomyelitis caused by Aspergillus spp. and found that while most cases were caused by haematogenous spread, one quarter of the patients developed the osteomyelitis after having surgery on the spine, suggesting contamination during surgery. Most of the 21 patients received surgical therapy. Patients who received combined surgical and medical Birinapant supplier therapy had favourable outcome, while antifungal therapy alone resulted in complete response in only two cases. However, reported cases of immunocompetent patients successfully treated with azoles alone – without surgery – suggest that successful nearly outcomes may be possible without surgery in selected cases.[49, 51] The potential of Aspergillus osteomyelitis to spread into the cartilage was reported in a study, in which the therapy of sternal osteomyelitis after open-heart surgery was discussed. In two of 20 patients Aspergillus spp. were isolated from the sternum. Both were presenting with a sterno-cutaneous fistula, needing aggressive surgical debridement,

wire removal and resection of the infected cartilage.[50] A similar case also requiring extensive cartilage debridement was reported recently.[53] Dotis and Roilides investigated 46 cases of osteomyelitis due to Aspergillus spp. in immunocompromised patients with chronic granulomatous disease in 2011. Thirty-one (67.4%) patients underwent surgical debridement, overall mortality was 37%. In 20 of 31 patients, extensive surgical debridement of infected bone material was necessary. The surgical intervention appeared to be a key success factor for the therapy. Twenty-three patients were infected with A. fumigatus and 20 patients with A. nidulans. Of the 23 patients with A. fumigatus, 12 underwent surgery and two died (17%). Of the 20 patients with A. nidulans, 16 underwent surgery and nine (56.3%) died.[51] Horn et al.

In the case of differentiated Th cells, the necessity of this co-stimulation is under debate — there are even reports of so-called self-presenting Th cells specific for haptens, such as nickel, that are activated completely

independently of APCs [37, 38]. A specific activation of Th cells leads to full activation and secretion of cytokines and chemokines; however, the strength of the stimulus and the point in the cell cycle during which specific activation occurs may influence what cytokines are secreted. Namely, antigen-specific T cells shown, by intracellular cytokine staining, to produce either both IL-4 and IL-17, or IFN-γ and JQ1 nmr IL-17, were shown to secrete only IL-4 or IFN-γ, respectively, but not IL-17 after stimulation with their cognate antigen and autologous DCs [8]. However, adding staphylococcal-derived enterotoxins induced the co-expression of IL-17 [8]. These enterotoxins — so-called superantigens — are microbial-derived products that activate T cells independently of their receptor specificity by enhancing the binding of TCR/MHC complexes [39], highlighting the necessity of a strong TCR stimulus

for induction of IL-17 in T cells. The activation state also seems to be important for the cytokine profile of T cells, since resting Th17-cell clones cannot co-express any IL-10, while prolonged TCR stimulation leads to upregulation of anti-inflammatory https://www.selleckchem.com/products/Deforolimus.html IL-10 in a subset of Th17 cells [12]. This highlights that certain functional states of the same cell population, in this case different degrees of activation, can result in different functional outcomes. However, during an immune response in the skin, only a minority of usually less than 10% of all infiltrating T cells is Janus kinase (JAK) actually antigen specific. This has been shown in the

case of patch test-elicited ACD [36] and atopy patch tests to house dust mite or pollen [8]. This raises the question of the role for these nonspecific bystander cells in the inflammatory reaction. Increasing evidence suggests that such cells may be activated nonspecifically by superantigens. As described before, superantigens are strong inducers for IL-17 and IL-22 in T cells [8, 40]. The skin of about 90% of atopic eczema patients is colonized with S. aureus, the source of superantigens, such as staphylococcal enterotoxin B [41]. In contrast, only 25% of the healthy population is colonized with S. aureus, but here the nose and not the skin serves as a bacterial reservoir [42]. Applying superantigens to an atopy patch test reaction was shown to lead to aggravation of the developing eczematous lesion, indicating the importance of these factors in an unspecific amplification of inflammation [8]. Beyond bystander activation through superantigens, the role for bystander Th cells during inflammatory processes is still under debate.

We also performed the following mutations for the amino acid residues surrounding the tryptophans. Because some of the amino acids adjacent to the three tryptophan residues carry electrical charges, we changed the charge in each amino acid residue. We changed two residues, E306 and D308, from acidic to basic amino

acids by replacement with arginine (E306R and D308R). We replaced the residue K310 with glutamic acid in order to change from basic to acidic type (K310E). We also substituted the residue V312 with alanine to maintain hydrophobicity and no electric charge (V312A). We constructed mutant toxins in which we replaced residue N302, the most amino-terminal domain side in the tryptophan-rich region, with alanine (N302A). Wild-type and mutant alpha-toxins were expressed

in E. coli BL21 and purified by affinity chromatography. SDS–PAGE detected every purified mutant toxin at the expected positions find more and each of their secondary structures was similar to that of wild-type toxin according to far-ultraviolet (190–260 nm) circular dichroism LY2606368 mouse spectral analysis (data not shown). As shown in Table 3, the cytotoxic activities (EC50) of mutant toxins were compared with that of wild-type toxin. We found that the EC50 of W307F/W309F/W311F and W307A/W309A/W311A were >640 ng/mL, indicating that the cytotoxic activity of alpha-toxin decreased remarkably to below the limit of detection. The

mutants of W307A, W309A and W311A also had marked reduction of cytotoxic activity. Although replacements of W307 and W311 with phenylalanine decreased the cytotoxic activities (207 and 113 ng/mL), they did not completely abolish them. Interestingly, replacement of W309 with phenylalanine did not greatly reduce cytotoxic activity. The mutant of W309F retained the same activity as the wild type. In the case of amino acid substitutions surrounding the three tryptophan residues, only D308R caused a decrease in cytotoxic Elongation factor 2 kinase ability (127 ng/mL). The cytotoxic activities of E306R, K310E, K310R, V312A and N302A did not change in comparison with that of the wild type. To determine whether the tryptophan-rich region plays an important role in the binding of alpha-toxin to cell membranes, we used a toxin overlay assay to examine the binding activities of mutant toxins to detergent-insoluble proteins from Vero cells. After lysis with 1% Triton X-114, we separated Vero cells into detergent-soluble and -insoluble fractions by centrifugation. As shown in Figure 2a, we observed a specific band with a molecular mass of about 34 kDa in the detergent-insoluble fraction using a toxin overlay assay with wild-type alpha-toxin. In previous studies, we reported that alpha-toxin selectively binds to GPI-anchored proteins detected in the detergent-insoluble fractions from various cell lines [12, 25].

This work was supported by the 04/UR/08-05 Research Unit, from the Ministry of Health, Tunisia. The authors declare that they have no conflict of interest. “
“Astragalus verus Olivier, Fabaceae has been used against ringworm in Kurdish ethnomedicine throughout millennia. selleck chemicals The objective of this study was to evaluate the effects of A. verus extracts against Trichophyton verrucosum on in vitro and in vivo guinea pig model of dermatophytosis. The skin of albino guinea pigs was infected with T. verrucosum (1.0 × 107 conidia) and animals were divided into five groups (n = 5 for each): negative control (NC), received a vehicle; positive control (PC), received topical terbinafine

1.0% and three other groups: AE10%, AE20% and AE40% which received topical 10%, 20% and 40% aqueous extract of A. verus, respectively. Evaluation of clinical efficacy was performed 72 h after completion of a 7-day treatment regimen. Higher significant antifungal activities were observed in aqueous extract in the concentration 320 mg ml−1 compared with acetone and methanol NVP-BGJ398 order extracts. The aqueous extract showed

minimum inhibitory concentration at 160 mg ml−1. Lower clinical scores indicate improved efficacy compared with NC. The lesion scores significantly declined in AE20%, AE40% and PC groups in comparison with NC group. The lesion scores in AE10% and AE20% groups were significantly higher than that of PC group. The AE10% group (18.3%) and AE20% group (39.43%) and AE40% group (66.19%) showed clinical efficacies compared with PC group (76.05%). In conclusion, aqueous extract showed promising antidermatophytic activity. “
“Screening Dimethyl sulfoxide of 217 soil samples of different habitats, such as PG study centre, garden, farmhouse, nursery, roadside, hostel, animal habitat, bird habitat, marriage garden, temple, vegetable market and house dust, was carried out for the presence of dermatophytes

and related fungi in relation to soil pH. A total of 461 isolates belonging to 26 genera and 34 species were recorded. Soil pH values vary from 3 to 10.5. Trichophyton verrucosum, Microsporum audouinii and M. canis were isolated for the first time in Jaipur from pH range 7.0 to 9.0. Chrysosporium tropicum (46.08%) was the most predominant fungus isolated from pH range 6.5 to 9.5. Trichophyton mentagrophytes (24.88%) was the second most common fungal species isolated from pH 6.5 to 9.5. Most of the keratinophilic fungi were isolated from pH 6.5 to 8.5. Only one isolate of Fusarium moniliforme was reported from a highly acidic site at pH 3. Roadside and garden soils were found to be the most suitable sites for almost all keratinophilic fungi. “
“Repeated and prolonged use of fluconazole in treating candidosis leads to drug resistance.

However, the precise role of LFA-1 in the pathogenesis of EAE has so far remained unclear. We describe here the disease development in LFA-1−/− mice compared with WT controls. Ablation of LFA-1 resulted in more severe EAE with increased demyelination and increased numbers of myelin oligodendrocyte glycoprotein-reactive CD4+ T cells in the CNS. However,

the production of the selleck pro-inflammatory cytokines IL-17 and IFN-γ was unchanged on the level of antigen-specific T cells. Interestingly, LFA-1-deficient mice showed a clearly reduced frequency of Treg in the inflamed CNS. Moreover, Treg counts in spleens and thymi of unimmunized LFA-1−/− mice were lower in comparison to the WT controls, indicating an impairment of Treg generation. In combination,

these results suggest a substantial role of LFA-1 in Treg generation and subsequent expansion of effector T cells and highlight the importance of Treg in limiting EAE. EAE is a T-cell-mediated inflammatory disease of the CNS and serves as an animal model for multiple sclerosis. The autoimmune phenotype can be induced in rodents sensitized to proteins such as myelin basic protein or myelin oligodendrocyte glycoprotein (MOG). The disease is initiated by infiltration of peripheral lymphocytes and macrophages into the CNS and is characterized by local AZD4547 cost inflammation and demyelination. The migration of leukocytes into the CNS is facilitated by interactions of cell-surface adhesion molecules and their endothelial ligands 1. The family of β2-integrins is involved in leukocyte–vascular cell interactions as well as in the communication between T cells and antigen-presenting cells. The αLβ2-integrin LFA-1 (CD11a/CD18) is widely expressed by leukocytes including peripheral blood lymphocytes, monocytes, and NK cells 2. Among the members of TCL the β2 family of integrins, only LFA-1 is expressed by CD4+ T cells and CD4+ CD25+ Treg 3. Interestingly, CD18-deficient mice, which do not express

β2-integrins, showed an impaired development of thymic and peripheral Treg, but it remained unclear which of the β2-integrins is responsible for this phenotype 3. The function of LFA-1 in EAE has been extensively studied. However, in part controversial and conflicting results have been obtained. For example, treatment with anti-LFA-1 Ab led to either protection against EAE 4 or more severe disease development 5. More recently, a deficiency for LFA-1 was suggested to dampen EAE upon active induction of an autoimmune response 6. On the other hand, adoptive transfer of WT encephalitogenic T cells into LFA-1−/− mice profoundly exacerbated the EAE course in comparison to WT mice, indicating an anti-inflammatory role of LFA-1, which would limit disease progression 7. It remained, however, elusive how LFA-1 exerts its immunosuppressive effects.

[31] Also, the survival

of thymocytes has been suggested to be regulated by Bcl-x protein.[32] These findings imply that the survival of thymocytes may be largely regulated by Bcl-2 and Bcl-xL expression, which is promoted by Stat3 activation. To determine whether T-cell deficiency in Stat3-deleted mice was attributable to the dysregulation of thymic selection and development; we assessed expression patterns of various T-cell receptor vβ chains (see Supplementary material, Fig. S3). The T-cell receptor vβ expression pattern was generally unvarying between wild-type littermates and Tanespimycin concentration the Stat3 knockout group, which implies that Stat3 does not influence the thymic selection process. To investigate whether the T-cell deficiency in Selleckchem MS275 Stat3-knockout mice resulted from increased susceptibility to apoptosis, we performed annexin V staining and TUNEL assays. The numbers of Stat3-deficient T lymphocytes undergoing apoptosis were increased considerably compared with controls (Fig. 5a,b). Several studies performed using T-cell-specific Stat3-deficient mice have suggested that the expression of Bcl-2 family genes, including Bcl-2 and Bcl-xL, was significantly attenuated in T cells upon

stimulation with IL-2 or IL-6, or in mouse models of autoimmune disease, such as mice with experimental colitis.[11, 16, 17] Our data provide striking evidence that Stat3 also regulates Bcl-2 family genes in T cells without any prominent GPX6 cytokine stimulation or induction of autoimmunity (Fig. 6). These results suggest that Stat3 plays a critical role in both maintenance of the resting naive T-cell population and T-cell clonal

expansion in response to pro-inflammatory signals through regulation of pro-survival Bcl-2 family genes. Stat3 also promotes T-cell expansion by enhancing the expression of both pro-survival and proliferative genes.[11, 17] Hence, we examined whether proliferative potential was decreased in Stat3-knockout cells. Unexpectedly, neither the proportion of cells that were proliferating (Fig. 5a) nor the expression levels of genes that promote cell division, such as cyclins D and E, was significantly decreased in T cells from Stat3-deficient mice (data not shown). Mature SP T lymphocytes are known to enter a ‘resting’ state in which they are quiescent and relatively resistant to apoptosis.[33] This suggests that most naive T cells are quiescent. Hence, their maintenance may depend largely on pro-survival signals rather than on stimuli that promote cell division. Our data suggest that Stat3 does not contribute to T-cell proliferation under resting conditions, but could provide resistance against apoptosis by up-regulating Bcl-2 and Bcl-xL gene expression in naive T lymphocytes.

(28). All procedures were approved and carried out in accordance with the Animal Care Committee of Virginia Tech. Equal numbers of female and castrated male lambs were represented in each breed. Lambs were born in January, weaned at approximately 70 days of age and maintained on native pastures until the start of the study in June. Mean body weights in June averaged 19·9 and 27·5 kg for hair and wool lambs respectively. These pastures were known to be contaminated with H. contortus and provided prior

exposure to the parasite. Measurements taken in this study therefore reflect acquired rather than innate immune responses. Levels of parasitaemia were not quantified before the start of the study, but signs of Roxadustat manufacturer AZD6244 chemical structure clinical haemonchosis were not observed. In addition, lambs were infected with 3000 H. contortus infective third stage larvae (L3) weekly for four consecutive weeks prior to the start of the experiment to further standardize previous exposure to the parasite. One week after receiving the last dose of infective larvae (i.e. at day −11 relative to experimental parasite challenge), lambs were moved to drylot

and treated with levamisole (8 mg/kg body weight) and fenbendazole (10 mg/kg body weight) on days −11 and −8 to remove existing worms. No eggs were detected in lamb faecal samples taken immediately prior to experimental infection. Small numbers of coccidial oocysts were seen throughout the study, but symptoms

of coccidiosis were not apparent. Twelve lambs of each breed were randomly assigned to receive experimental parasite infection and were moved to raised indoor pens on day −4, de-wormed again at day −3 to remove any remaining worms and orally infected with 10 000 H. contortus L3 larvae on day 0. These lambs remained in these pens until the end of the study. For reasons of space limitations, the 14 control lambs of each breed remained in drylot for an additional 2 weeks. Control lambs were moved to indoor pens on day 7 relative to infected animals and de-wormed on day 8 to approximate treatment of infected animals. However, control lambs were accidentally infected on day 11 and therefore required additional de-worming on days 12 and 14 to prevent establishment of Ergoloid infection. At all time points assessed, no parasitic nematode eggs were present in the faeces of control animals, but this accidental transient exposure to L3 larvae changes interpretations of responses in control lambs in ways that will be discussed below. Infected animals of each breed (n = 6) were euthanized at 3 or 27 days post-infection (p.i.). These days were selected to represent responses to larvae (day 3) and adult worms (day 27). Control animals of each breed were sacrificed on days 17 (n = 4), 27 (n = 6) and 38 (n = 4), relative to day 0 of infected animals, corresponding to days 6, 16 and 27 following exposure to the parasite and subsequent immediate de-worming.