The possible link between the hygiene hypothesis and the epigenetic imprinting 8 represents an exciting future area of research in mast cell biology. Howard Katz (Boston, MA) described one example of a negative signaling receptor on mast cells – the leukocyte Ig-like check details receptor, subfamily B, member 4 or LILR-B4 – which is critically involved in preventing over-stimulation of various immune cells. The powerful inhibitory potential of LILR-B4 is underscored by two findings: first, animals knocked out for this receptor have enhanced inflammatory diseases and,

second, the co-ligation of LILR-B4 with cross-linked FcεRI efficiently prevents the degranulation of mast cells. LILR-B4 also controls the activity of other innate immune receptors such as the LPS receptor on neutrophils and is rapidly upregulated following exposure to LPS 9. Moreover, the dose

of LPS used during an initial sensitization of animals with Ag in the airways drastically affects the Th profile and the nature of the inflammatory response induced by subsequent airway challenge with Ag, an effect that is also counterregulated by LILR-B4 through its actions on DC 10. The observation that BIBW2992 mw innate immune stimuli targeting TLR can mediate long-lasting changes in the response pattern of innate immune cells, with subsequent effects on adaptive immune responses, subject to counterregulatory Gefitinib datasheet effects from the immune system, has potentially wide reaching implications for vaccine design. This concept applies not only to a variety of pre-clinical vaccine adjuvants which signal through TLR, but also to a human papillomavirus vaccine/adjuvant combination containing the LPS subunit monophosphoryl lipid A which was recently approved by the United States Food and Drug Administration. Francesca Levi-Schaffer (Jerusalem, Israel) described recent findings from her laboratory

regarding the presence and function of the death receptors TRAIL and Fas on mast cells, as well as a series of activating and inhibitory receptors usually present on NK and T cells. She found that mast cells from human lung and cord blood mononuclear cells (CBMC) as well as the transformed human mast cell line HMC-1 all have functional TRAIL receptors. Moreover, human lung mast cells and HMC-1 also express Fas, whereas murine mast cells express only Fas 11. Despite major inter-species differences in death receptor expression and function on mast cells, Dr. Levi-Schaffer and colleagues found that human CBMC, lung mast cells, HMC-1 cells and mouse (BMMC, lung and peritoneal cavity) mast cells express a fully functional CD300a inhibitory receptor. They showed that a bispecific anti-CD300a/anti-cKit antibody inhibits CBMC differentiation, survival and activation.

5C) of IL-32-treated mice than in placebo controls on day 10 after 5-FU injection. This

paralleled a higher marrow cellularity in bone sections (Fig. 5C) with twice the number of cells in 5 μg IL-32-treated mice (Table 3, p=0.046) and three times the numbers of colony-forming cells (p=3.3×10−5). The higher number of BM cells paralleled a higher frequency of SCA-1+c-kit+ cells, which was comparable with non-treated controls (Table 3). Mice that had received 50 μg IL-32 had twice the BM cell count of untreated specimens on day 14 (64.4±10.9×105 cells versus normal saline 32±8.2×105 cells, p=0.024), whereas the values of those treated with 5 μg were between those of the normal saline and the 50 μg IL-32 groups (46.9±8.3×105). Two weeks after 5-FU and IL-32 treatment,

the number of total AZD6244 manufacturer colonies rose to 3.8±1.2×103 in the normal saline-treated control; that was still surpassed by the results in 5 μg IL-32-treated mice (9.5±1.6×103, p=0.006) and in 50 μg IL-32-treated mice (6.4±0.87×103). As we demonstrated, endothelial gene signals of several cytokines were significantly upregulated upon stimulation with IL-1β for 4 h. These included IL-8, IL-32, FGF-18, OPG, CXCL1 to 6, CCL2 to 6 and CCL20. see more Using a complex experimental design, we evaluated the HPC expansion potentials of 11 gene products: FGF-18, IL-8, Gro proteins 1, 2 and 3 (also called CXCL1 to 3), OPG, IL-32, ENA-78 (also called CXCL5), GCP-2 (also called CXCL6) and the chemoattractants CCL2 and CCL20. Although none STK38 of these are known to affect HPC expansion, some of them can induce the proliferation of other cell types. FGF-18, for example, stimulates the proliferation of hypernephroma cells and induces hepatocellular proliferation in vivo 25. As an inflammatory cytokine, IL-8, also called GCP-1, induces the proliferation of cancer cells 26 and ECs in an autocrine fashion 27. Other

granulocytic chemoattractants like ENA-78 and GCP-2 induce hepatocellular 28 and carcinoma cell 29 proliferation. IL-32, another proinflammatory cytokine, is produced by natural killer cells upon stimulation with IL-2. IL-32 can induce the differentiation of monocytes into macrophages, but reverses GM-CSF-induced macrophage differentiation 30. To our knowledge, this is the first time that the hematopoietic growth factor properties of OPG, Gro 3, and especially IL-32 are demonstrated. In previous studies, several CXC chemokines, such as IL-8, ENA-78 and MIP-2, have been tested in vitro for their BM suppressiveness. That was determined according to a reduced colony-forming capacity of cytokine-treated myeloid progenitors, in which each chemokine was added to a standard cytokine combination in colony assays 31, 32. We chose instead to apply the candidate factors directly to isolated HPCs and assess the cultured cells’ hematopoietic qualities by flow cytometry, colony and cobblestone assays.

Some of these cytokines likely cause podocyte injury and induce proteinuria and hematuria. These pathogenic steps are affected by environmental and genetic factors, some of which act up-stream and/or down-stream of these major hits. New tools, models, and approaches have been developed, including immortalized IgA1-secreting cells from patients with IgA nephropathy and healthy controls, monoclonal and recombinant antibodies specific for Gd-IgA1, high-resolution mass spectrometry workflows, engineering of Gd-IgA1-containing immune complexes in vitro, a model using cultured mesangial cells

for assessment of biological activity of Gd-IgA1-containing immune complexes, and a passive animal model. These tactics have provided unique insights into the nature of pathogenic IgA1-containing immune complexes, their formation, composition, and role in the disease process. Recent progress in high-resolution Syk inhibitor mass spectrometry allowed us to start to define, at the molecular level, the nature of the Gd-IgA1 hinge-region O-glycans. Understanding the heterogeneity of the autoantigen will allow investigators to assess the specificity and heterogeneity

of anti-glycan autoantibodies and thus define the spectrum of the major Gd-IgA1 epitopes in patients with IgA nephropathy. Immortalized IgA1-producing cells from patients with IgA nephropathy have been used to analyze the process and major pathways in the biosynthesis of Gd-IgA1, and to assess cellular responses of these cells to cytokines and growth factors. Comparative studies of IgA1-producing cells from patients with IgA nephropathy vs. those from healthy controls revealed DNA Damage inhibitor differences in O-glycosylation of the secreted IgA1, associated with differential expression and activity of several key enzymes and responses to cytokines, such as IL-6. Specifically, we found elevated expression of N-acetylgalactosamine (GalNAc)-specific sialyltransferase (ST6GalNAc-II) and, conversely, decreased expression and activity of a galactosyltransferase (C1GalT1) and decreased Rebamipide expression of the C1GalT1-associated chaperone Cosmc. These

findings were confirmed by siRNA knock-down of the corresponding genes and by in vitro enzymatic reactions. Expression and activity of these enzymes can be regulated by some cytokines, such as IL-6, that further enhance the imbalance of the activity of the glycosyltransferases and, consequently, enhance the galactose deficiency of the IgA1 O-glycans. Serum levels of anti-Gd-IgA1 autoantibodies correlate with disease severity, manifested as proteinuria. Moreover, elevated serum levels of Gd-IgA1 or anti-Gd-IgA1 autoantibodies are predictive of disease progression. As both components, Gd-IgA1 and the corresponding autoantibodies, are required to form immune complexes, we developed a model to engineer immune complexes in vitro, using Gd-IgA1 and recombinant anti-Gd-IgA1 autoantibody; we then assessed the biological activities of such complexes.

Many cytokines, particularly TNF-α and IL-1, are known mediators of endothelial activation and dysfunction (reviewed in [107]). TNF-α acts in part by inhibiting endothelium-dependent

Carfilzomib chemical structure relaxation [13]. In vitro, it reduces expression of eNOS [154] as well as decreases the availability of arginine, the substrate of eNOS, by suppressing the activity of argininosuccinate synthase expression [52]. In addition, TNF-α is associated with an increased expression of a number of powerful vasoconstrictors, including PDGF and ET-1 [54, 82]. ET-1 is elevated in the circulation of women with preeclampsia [17], and in vitro studies show increased PDGF expression by endothelial cells in response to serum from women with preeclampsia [141]. In addition to directly influencing vasodilatation and vasoconstriction, TNF-α can cause endothelial dysfunction by stimulating the production of ROS via NAD(P)H oxidase [46] . The interaction between inflammation and endothelial activation is highly complex in preeclampsia (reviewed in [15]). In addition to displaying altered function when activated by inflammation, endothelial cells play an important role in the induction of the inflammatory response, particularly via selleck chemical the activation and migration of leukocytes [29]. Promotion of

inflammation leads to further endothelial activation and progression of the maternal systemic syndrome. Preeclampsia is also associated with increased production of AT1-AA by mature B cells [146]. AT1-AA stimulates the AT1 receptor to cause a significant increase in vasoconstriction [153]. In the rat RUPP model of preeclampsia, LaMarca and colleagues found that hypertension is associated with an increase in AT1-AA in RUPP rats [70]. In addition, they showed that a reduction in AT1 activation via administration of receptor agonists or B-cell depletion resulted in a decline in blood pressure [69, 70]. AT1-AA may cause endothelial dysfunction through a variety of mechanisms. It is associated with the secretion of IL-6 and plasminogen activator inhibitor-1 (Pai-1)

in humans [14] and promotes Liothyronine Sodium expression of the vasoconstrictor peptide ET-1 in AT1-AA-infused rats [68]. Furthermore, AT1-AA-induced hypertension in rats is associated with renal endothelial dysfunction, characterized by impaired vasodilatation [103]. An increase in AT1-AA is associated with oxidative stress in the placenta of rats [104]. In human VSMC and trophoblasts in vitro, AT1-AA stimulates NADPH oxidase expression and activity, leading to increased ROS formation and activation of NF-kB, which may contribute to inflammation [34]. In addition, AT1-AA may act as a stimulus for the expression of the antiangiogenic factors sFlt-1 and sEng in preeclamptic women [102, 155]. Interestingly, Hubel et al.

These cells are able to present antigens to lymphocytes, and play a role in the up-regulation of homing molecules such as DC [4,5]. In contrast to immune response induction, tolerance is the unresponsiveness of the immune system via suppression of T and B cell activation by regulatory Veliparib chemical structure T cells, deletion or anergy. However, there are many open questions about the function

of the LN, including the migration of cells from the draining area, the role of the LN in the induction of immune responses, the control of parasites or tolerance. It is possible to use knock-out mice, e.g. lymphotoxin α or retinoic acid-related orphan receptor (Ror)-γt knock-out mice to study the function of LN. These mice have reduced or no LN, but they all have further disorders, particularly in the spleen [6,7]. To circumvent the problems of immune

system dysfunction caused by these gene knock-outs, a second method of studying LN function is to remove only the LN of interest. This LN dissection technique permits identification of the role of a specific LN without affecting further organs or areas. Therefore, in this review Doramapimod ic50 different research areas are illustrated where LN dissection was performed to identify the function of LN or the consequences of a missing LN. LN dissection is an experimental surgical technique which has been used for many years not only to Urease analyse the role of LN in the immune system and lymph fluid transport, but also in different diseases in animal models. LN were removed from many different draining sites such as the skin-draining site (for example the axilliary LN [8], the brachial LN [9], the popliteal LN [10–12] or the inguinal LN [13,14]), the head–neck region (cervical LN [15–19]) or the peritoneal area (the mesenteric LN [20–23] and the coeliac LN [24]). For dissection of the mesenteric

LN (mLN), for example, the abdomen was opened and the gut was taken out so that the mLN were visible (Fig. 2a). The mLN were excised carefully in order not to injure the superior mesenteric artery lying behind, whereas the connection of the lymph vessels and small blood vessels to the LN was disturbed. Afterwards, the gut was replaced in the abdomen and the abdomen was closed. LN are integrated as central organs in the lymph vessel system. The afferent lymphatics coming from the draining area, which could be the gut system or the skin, transport fluid, proteins, lipids and different cell populations of the immune system to the LN sinus. The efferent lymphatics leave the LN at the medullar site to greater LN or veins of the blood system. After LN dissection, the lymph vessel system is destroyed and the afferent and efferent system vessels are reconnected.

Clearly, as low vitamin D status and its clinical consequences may be secondary to a host of factors, including advanced age, reduced mobility from disease, reverse causation cannot be excluded. Studies investigating the effect of migration and vitamin D supplementation on PD risk are lacking. There is a clear heritable component in PD. Genetic studies have pointed to a possible role of vitamin D in susceptibility to the disease. Polymorphisms in the VDR gene have been shown to associate with PD risk

in American and Korean cohorts, with the former cohort also showing an age of onset effect [138, 139]. The relatively small sample sizes and the inconsistent replication of SNPs in the VDR gene in discovery and validation sets dampen the impact of these findings. GWAS have identified an increasing number of candidate Cell Cycle inhibitor risk genes in PD, several of which have VDR-binding sites closely associated with them raising the possibility that vitamin D may influence their expression. The biological relevance of a subset of these

susceptibility genes with associated VDR binding on brain function has been well delineated with evidence for roles in nigrostriatal dopaminergic neurotransmission, neurogenesis and neurite outgrowth, and neural ectodermal expression (especially within the marginal and subventricular zones) (see Table 2) [140-144]. Amyotrophic lateral sclerosis (ALS) is a progressive click here neurodegenerative disease affecting both the central and peripheral nervous systems [145]. ALS pathology reveals degeneration of motor neurones and corticospinal tracts, brainstem nuclei, and spinal cord anterior horn cells, with a subset of patients having intracytoplasmic transactive responsive DNA-binding protein inclusions (TDP-43) [146]. Multiple effector pathways are thought to contribute to ALS pathology including neurotrophic factor deficiency, glutamate toxicity, and damage from ROS [54]. Given that many of these effector

pathways are influenced by vitamin D in rodent models, there has been growing interest in the concept that this secosteroid may influence susceptibility to and disease progression in ALS. The epidemiological evidence incriminating vitamin D as a possible risk factor in ALS is sparse. The relatively Thymidine kinase low population prevalence probably contributes but there may be no association. Season of birth observations have been conflicting with a few studies reporting excess births between April and July [147], and others reporting birth excess in between October and December (with a trough between April and July) [148]. A latitude gradient has been suggested, but the results are divergent. An American cohort outlining the geographic distribution of ALS using mortality data demonstrated a north-west to south-east gradient [149], a finding mirrored in a more recent study which found a higher ALS-associated death rate in more northern states [150].

13% to 19.9% for PPMs and from 0.2% to 7.2% for ICDs.2,3,13 Pocket infections occur more often than endocarditis,7 major pathogens include coagulase-negative staphylococci and Staphylococcus aureus, and management

involves both appropriate antimicrobial therapy Erlotinib solubility dmso and device removal.5,7,8,20 The occurrence of postprocedure infections may be reduced by the use of antibiotic prophylaxis prior to the implantation of pacemakers and cardioverter-defibrillators.21 CRMD-associated endocarditis is estimated to account for about 10% of all device-related infection cases and fungi are rarely recovered from such infections, perhaps accounting for only 5% of these episodes.2 When fungi are involved, Candida species are the major pathogens and, for the most part, clinical, management and outcome data relating to CRMD-associated Candida endocarditis can only be gleaned from occasional case reports. In 1997, Joly et al. [12] published a review of PPM-related Candida endocarditis; all culture-positive cases involved C. albicans, adequate clinical information was available for only four of the six cases and it was difficult to derive any meaningful conclusions from the data provided. ICD-related Candida endocarditis is also poorly INCB018424 price characterised in the literature with only a few well-described cases published since 2001.10,22,23 Our

current report, that includes only well-documented cases, serves not only to broaden our understanding of CRMD-associated Candida endocarditis but also to update practitioners concerning recent guidelines relating to the management of this challenging clinical entity. Interestingly, all 15 patients listed in Table 1 were men, four were diabetic, Atezolizumab concentration use of CRMD prior to infection varied from <1 month to 16 years with most developing as late onset infections, and although C. albicans was the most common Candida species recovered, other species were found in half the cases. A major pulmonary embolus occurred in 27% of patients and 2 of 10 patients

died (20%) even when management included antifungal therapy and CRMD explantation. Associated device-pocket infections uncommonly accompany these serious endocarditis events. With reference to current day management of CRMD infections, including cases of endocarditis, we believe that the Mayo Clinic Algorithm as proposed by Sohail et al. [7] is particularly relevant. This algorithm applies only to patients with device explantation and complete lead extraction and includes elements such as obtaining proper cultures, proceeding with a transoesophageal echocardiogram when indicated and utilising targeted antimicrobial agents for specified periods. There are also recommendations pertaining to the reimplantation of a new PPM or ICD should the need for a CRMD remain.

One important facet is the circulatory system dysfunction, which includes capillary bed plugging. This review addresses the mechanisms of capillary plugging and highlights our recent discoveries on the roles of NO, ROS, and activated coagulation in platelet adhesion

and blood flow stoppage in septic mouse capillaries. We show that sepsis increases platelet adhesion, fibrin deposition and flow stoppage in capillaries, PLX3397 cell line and that NADPH oxidase-derived ROS, rather than NO, play a detrimental role in this adhesion/stoppage. P-selectin and activated coagulation are required for adhesion/stoppage. Further, platelet adhesion in capillaries (i) strongly predicts capillary flow stoppage, and (ii) may explain why severe sepsis is associated with a drop in platelet count in systemic blood. Significantly, we also show that a single bolus of the antioxidant ascorbate (injected intravenously at clinically relevant dose of 10 mg/kg) inhibits adhesion/stoppage. Our data suggest that eNOS-derived NO at the platelet-endothelial interface is anti-adhesive and required PD0325901 mw for the inhibitory

effect of ascorbate. Because of the critical role of ROS in capillary plugging, ascorbate bolus administration may be beneficial to septic patients whose survival depends on restoring microvascular perfusion. “
“Please cite this paper as: Wijnstok N, Hoekstra T, Eringa E, Smulders Y, Twisk J, Serne E. The relationship of body fatness and body fat distribution with microvascular recruitment: The Amsterdam Growth and Health Longitudinal Study. Microcirculation 19: 273–279, 2012. Introduction:  Microvascular function has been proposed to link body fatness to CVD and DM2. Current knowledge of these relationships is mainly based on studies in selected populations of extreme phenotypes. Whether these findings can be translated to the general population remains to be investigated. Aim:  To assess the relationship of body fatness and body fat distribution with microvascular function in a healthy population-based cohort. Methods:  Body fatness parameters were obtained by anthropometry and whole-body dual-X-ray absorptiometry (DEXA) in 2000 and 2006. Microvascular

recruitment (i.e., absolute increase in perfused capillaries after arterial occlusion, using nailfold capillaroscopy) was measured in 2006. Linear regression analysis was used to examine the Olopatadine relationship of (changes in) body fatness and body fat distribution with microvascular recruitment. Results:  Data were available for 259 participants (116 men). Capillary density was higher in women than in men (difference 7.3/ mm2; p < 0.05). In the total population, the relationship between total body fatness and microvascular recruitment was positive (β = 0.43; p = 0.002), whereas a central pattern of fat distribution (trunk-over-total fatness) showed a negative relationship (β = −26.2; p = 0.032) with microvascular recruitment. However, no association remained apparent after adjustment for gender.

Using multi-parameter flow cytometry and intracellular cytokine staining for IFN-γ, TNF-α and IL-2, we found double and single cytokine-producing CD4+ as well as CD8+ T cells to be the most prominent subsets, particularly IFN-γ+ TNF-α+ CD8+ T cells.

The majority of these T cells comprised effector memory and effector T cells. Furthermore, CFSE labeling revealed strong CD4+ and CD8+ T-cell proliferative responses induced by several “immunodominant” Mtb DosR antigens and their specific peptide epitopes. These findings demonstrate the prominent presence of double- and monofunctional CD4+ and CD8+ T-cell responses in naturally protected individuals and support the possibility of designing Mtb DosR antigen-based TB vaccines. Host defense against mycobacteria critically depends Selleck MK-3475 on effective innate and adaptive immunity, culminating in the activity of Mycobacterium tuberculosis (Mtb)-specific https://www.selleckchem.com/products/AC-220.html T cells and in the formation of granulomas that contain Mtb bacilli. Both CD4+ and CD8+ T-cell responses are involved, and it is undisputed that Th1- and Th17-like cytokines (IL-12, IFN-γ, TNF-α and IL-17) are crucial for optimal host immunity 1, 2. Tuberculosis (TB) continues to claim almost 2 million lives each year,

and causes active (infectious) TB disease in over 9 million new cases per annum. Control of TB is further impeded by the strong increase in TB morbidity and mortality due to HIV co-infection, and the rise of multi-drug resistant and extensively drug-resistant Mtb strains 3. At least 2 billion people are latently infected with Mtb, representing a huge reservoir of latently infected

individuals from which most new TB cases arise. While 90–98% of all Mtb-infected individuals are able to contain infection Cytidine deaminase asymptomatically in a latent state, 2–10% of these Mtb-infected individuals will progress towards developing TB during their lifetime. Despite strong international efforts in TB vaccine development, Mycobacterium bovis Bacillus Calmette-Guérin (BCG) continues to be the only available TB vaccine. BCG vaccination induces effective protection against severe TB in young children and protects against leprosy, but does not provide sufficient protection against the severe and contagious form of TB; pulmonary TB in adults 4, 5. Moreover, BCG does not protect against TB reactivation later in life. Ideally, not only improved preventive vaccines with pre-exposure activity but also therapeutic vaccines with post-exposure activity during late-phase infection are urgently required 2, 6. Such vaccines should prevent reactivation of TB from latency by inducing and maintaining robust immunity to Mtb antigens that are expressed by persisting Mtb bacilli during latent infection. Such immune responses may not only help controlling but perhaps also eradicating persisting bacilli.

To verify Vα usage for DbNPCD8+ and DbPACD8+ T cells, PCR was performed with a panel of Vα primers: Vα1, Vα2, Vα3, Vα4, Small molecule library manufacturer Vα5, Vα6, Vα7, Vα8, Vα9, Vα10, Vα11, Vα13, Vα14, Vα16, Vα17, Vα18, Vα19, and Vα20 41. PCR products were cloned into a vector pCR2.1-TOPO, and colonies containing inserts were sequenced. The authors thank Dina Stockwell for technical assistance, Ken Field for FACS sorting and Serrin Rowarth for providing the A7 mice. This work was supported by Australian National Health and Medical Research Council (NHMRC) Project Grants to KK (AI454312) and PCD (AI454595), an NHMRC Program

Grant # 567122 (to PCD and SJT), and NIH grant AI170251. K. K. is an NHMRC RD Wright Fellow and S. J. T. is a Pfizer Senior Research Fellow. S. A. V. is a recipient of the Australian Postgraduate Award and E. B. D. of the NHMRC Postgraduate Biomedical Scholarship. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“Caribbean hair sheep are more

resistant to gastrointestinal nematodes than conventional wool breeds, but mechanisms that confer resistance are not fully understood. This study compared immune effector cell populations and antibody learn more concentrations in 12 hair and 12 wool lambs infected with the abomasal parasite Haemonchus contortus and sacrificed at 3 or 27 days Molecular motor post-infection (p.i.) and 14 uninfected animals of each breed. Faecal egg counts were over 2·5-fold higher (P = 0·12) and packed cell volumes approximately 8% lower (P < 0·10) in infected wool lambs. Abomasal lymph nodes were heavier in infected animals (P < 0·05) and infected hair sheep had larger lymph nodes than infected wool sheep (P < 0·05). Tissue eosinophil concentrations were likewise larger (P = 0·07) in hair compared with wool sheep at 3 days p.i. Circulating levels of IgE and IgA in uninfected lambs were higher in hair sheep

(P < 0·05) and during infection, hair sheep had higher serum IgA than wool sheep at 3, 5, and 21 days p.i. (P < 0·05). Serum IgE in infected lambs did not differ between breeds, but concentrations of IgE in lymph nodes were higher (P < 0·01) at 27 days p.i. in infected hair sheep. Haemonchus contortus, a blood-feeding, abomasal parasite, is the most common and problematic of the gastrointestinal nematodes (GIN) of sheep in humid temperate and subtropical climates. The prevalence of GIN that are resistant to anthelmintic treatment is increasing, with almost all farms in the southeastern US having GIN that are resistant to one or more anthelmintics (1). In addition, consumers are driving the livestock industry to produce chemical-free products. Therefore, other methods of parasite control are needed. Caribbean hair sheep have greater resistance than conventional wool sheep to GIN parasites (2–4).