Improved resistance to Eimeria acervulina infection in chickens due to dietary supplementation with garlic metabolites

The effects of a compound including the secondary metabolites of garlic, propyl thiosulphinate (PTS) and propyl thiosulphinate oxide (PTSO), on the in vitro and in vivo parameters of chicken gut immunity during experimental Eimeria acervulina infection were evaluated. In in vitro assays, the compound comprised of PTSO (67%) and PTS (33%) dose-dependently killed invasive E. acervulina sporozoites and stimulated higher spleen cell proliferation. Broiler chickens continuously fed from hatch with PTSO/PTS compound-supplemented diet and orally challenged with live E. acervulina oocysts had increased body weight gain, decreased faecal oocyst excretion and greater E. acervulina profilin antibody responses, compared with chickens fed a non-supplemented diet. Differential gene expression by microarray hybridisation identified 1227 transcripts whose levels were significantly altered in the intestinal lymphocytes of PTSO/PTS-fed birds compared with non-supplemented controls (552 up-regulated, 675 down-regulated). Biological pathway analysis identified the altered transcripts as belonging to the categories ‘Disease and Disorder' and ‘Physiological System Development and Function'. In the former category, the most significant function identified was ‘Inflammatory Response', while the most significant function in the latter category was ‘Cardiovascular System Development and Function'. This new information documents the immunologic and genomic changes that occur in chickens following PTSO/PTS dietary supplementation, which are relevant to protective immunity during avian coccidiosi

Perceptions of the Cooperative Extension Service: A Community Resource for Youth and Family Programs

PROSPER (PROmoting School-community-university Partnerships to Enhance Resilience) is a prevention partnership involving the Cooperative Extension Service (CES), local schools, and community agencies. PROSPER collaborative teams were formed in 14 communities in Iowa and 14 in Pennsylvania to address risk reduction, competence-building, and positive youth development. The study discussed here examined perceptions of CES personnel compared to other PROPSER team members regarding the CES: as a source of youth and family programming; its commitment to fostering school and community-based prevention programs; and as a leading force in improving the lives of youth and families

Anomalous Gas Exchange in Ascorbate Oxidation by the Myrothecium Enzyme

Manometric studies were employed to assay for ascorbic acid oxidase activity in cell free homogenates from the mycelium of the mold Myrothecium verrucaria. It was found that gas exchange measurements deviated from expected stoichiometry based on the utilization of one-half of a mole of oxygen for every mole of ascorbate oxidized. Oxygen was consumed in excess of the expected amount and carbon dioxide was produced during the course of the reaction. Apparently, the ascorbic acid oxidase reaction which produces dehydroascorbic acid is accompanied by or followed by other reactions involving oxygen consumption and carbon dioxide evolution

Immune-Related Gene Expression in Two B-Complex Disparate Genetically Inbred Fayoumi Chicken Lines Following Eimeria maxima Infection

To investigate the influence of genetic differences in the MHC on susceptibility to avian coccidiosis, M5.1 and M15.2 B-haplotype-disparate Fayoumi chickens were orally infected with live Eimeria maxima oocysts, and BW gain, fecal oocyst production, and expression of 14 immune-related genes were determined as parameters of protective immunity. Weight loss was reduced and fecal parasite numbers were lower in birds of the M5.1 line compared with M15.2 line birds. Intestinal intraepithelial lymphocytes from M5.1 chickens expressed greater levels of transcripts encoding interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-6, IL-8, IL-12, IL-15, IL-17A, inducible nitric oxide synthase, and lipopolysaccharide-induced tumor necrosis factor-α factor and lower levels of mRNA for IFN-α, IL-10, IL-17D, NK-lysin, and tumor necrosis factor superfamily 15 compared with the M15.2 line. In the spleen, E. maxima infection was associated with greater expression levels of IFN-γ, IL-15, and IL-8 and lower levels of IL-6, IL-17D, and IL-12 in M5.1 vs. M15.2 birds. These results suggest that genetic determinants within the chicken MHC influence resistance to E. maxima infection by controlling the local and systemic expression of immune-related cytokine and chemokine genes

Dietary supplementation of young broiler chickens with Capsicum and turmeric oleoresins increases resistance to necrotic enteritis

The Clostridium-related poultry disease, necrotic enteritis (NE), causes substantial economic losses on a global scale. In the present study, a mixture of two plant-derived phytonutrients, Capsicum oleoresin and turmeric oleoresin (XT), was evaluated for its effects on local and systemic immune responses using a co-infection model of experimental NE in commercial broilers. Chickens were fed from hatch with a diet supplemented with XT, or with a non-supplemented control diet, and either uninfected or orally challenged with virulent Eimeria maxima oocysts at 14d and Clostridium perfringens at 18d of age. Parameters of protective immunity were as follows: (1) body weight; (2) gut lesions; (3) serum levels of C. perfringens α-toxin and NE B-like (NetB) toxin; (4) serum levels of antibodies to α-toxin and NetB toxin; (5) levels of gene transcripts encoding pro-inflammatory cytokines and chemokines in the intestine and spleen. Infected chickens fed the XT-supplemented diet had increased body weight and reduced gut lesion scores compared with infected birds given the non-supplemented diet. The XT-fed group also displayed decreased serum α-toxin levels and reduced intestinal IL-8, lipopolysaccharide-induced TNF-α factor (LITAF), IL-17A and IL-17F mRNA levels, while cytokine/chemokine levels in splenocytes increased in the XT-fed group, compared with the animals fed the control diet. In conclusion, the present study documents the molecular and cellular immune changes following dietary supplementation with extracts of Capsicum and turmeric that may be relevant to protective immunity against avian N

Cinnamaldehyde enhances in vitro parameters of immunity and reduces in vivo infection against avian coccidiosis

The effects of cinnamaldehyde (CINN) on in vitro parameters of immunity and in vivo protection against avian coccidiosis were evaluated. In vitro stimulation of chicken spleen lymphocytes with CINN (25-400ng/ml) induced greater cell proliferation compared with the medium control (P<0·001). CINN activated cultured macrophages to produce higher levels of NO at 1·2-5·0μg/ml (P<0·001), inhibited the growth of chicken tumour cells at 0·6-2·5μg/ml (P<0·001) and reduced the viability of Eimeria tenella parasites at 10 and 100μg/ml (P<0·05 and P<0·001, respectively), compared with media controls. In chickens fed a diet supplemented with CINN at 14·4mg/kg, the levels of IL-1β, IL-6, IL-15 and interferon-γ transcripts in intestinal lymphocytes were 2- to 47-fold higher (P<0·001) compared with chickens given a non-supplemented diet. To determine the effect of CINN diets on avian coccidiosis, chickens were fed diets supplemented with CINN at 14·4mg/kg (E. maxima or E. tenella) or 125mg/kg (E. acervulina) from hatch for 24d, and orally infected with 2·0×104 sporulated oocysts at age 14d. CINN-fed chickens showed 16·5 and 41·6% increased body-weight gains between 0-9d post-infection (DPI) with E. acervulina or E. maxima, reduced E. acervulina oocyst shedding between 5-9 DPI and increased E. tenella-stimulated parasite antibody responses at 9 DPI compared with control

IL-17A regulates Eimeria tenella schizont maturation and migration in avian coccidiosis

Although IL17A is associated with the immunological control of various infectious diseases, its role in host response to Eimeria infections is not well understood. In an effort to better dissect the role of IL17A in host-pathogen interactions in avian coccidiosis, a neutralizing antibody (Ab) to chicken IL17A was used to counteract IL17A bioactivity in vivo. Chickens infected with Eimeria tenella and treated intravenously with IL17A Ab, exhibited reduced intracellular schizont and merozoite development, diminished lesion score, compared with untreated controls. Immunohistological evaluation of cecal lesions in the parasitized tissues indicated reduced migration and maturation of second-generation schizonts and reduced lesions in lamina propria and submucosa. In contrast, untreated and infected chickens had epithelial cells harboring second-generation schizonts, which extend into the submucosa through muscularis mucosa disruptions, maturing into second generation merozoites. Furthermore, IL17A Ab treatment was associated with increased parameters of Th1 immunity (IL2- and IFN¿- producing cells), reduced levels of reactive oxygen species (ROS), and diminished levels of serum matrix metalloproteinase-9 (MMP-9). Finally, schizonts from untreated and infected chickens expressed S100, Wiskott-Aldrich syndrome protein family member 3 (WASF3), and heat shock protein-70 (HSP70) proteins as merozoites matured, whereas the expression of these proteins was absent in IL17A Ab-treated chickens. These results provide the first evidence that the administration of an IL17A neutralizing Ab to E. tenella-infected chickens inhibits the migration of parasitized epithelial cells, markedly reduces the production of ROS and MMP-9, and decreases cecal lesions, suggesting that IL17A might be a potential therapeutic target for coccidiosis control

Molecular Interactions between MUC1 Epithelial Mucin, β-Catenin, and CagA Proteins

Interleukin (IL)-8-driven neutrophil infiltration of the gastric mucosa is pathognomonic of persistent Helicobacter pylori infection. Our prior study showed that ectopic over-expression of MUC1 in human AGS gastric epithelial cells reduced H. pylori-stimulated IL-8 production compared with cells expressing MUC1 endogenously. Conversely, Muc1 knockout (Muc1−/−) mice displayed an increased level of transcripts encoding the keratinocyte chemoattractant (KC), the murine equivalent of human IL-8, in gastric mucosa compared with Muc1+/+ mice during experimental H. pylori infection. The current study tested the hypothesis that a decreased IL-8 level observed following MUC1 over-expression is mediated through the ability of MUC1 to associate with β-catenin, thereby inhibiting H. pylori-induced β-catenin nuclear translocation. Increased neutrophil infiltration of the gastric mucosa of H. pylori-infected Muc1−/− mice was observed compared with Muc1+/+ wild type littermates, thus defining the functional consequences of increased KC expression in the Muc1-null animals. Protein co-immunoprecipitation (co-IP) studies using lysates of untreated or H. pylori-treated AGS cells demonstrated that (a) MUC1 formed a co-IP complex with β-catenin and CagA, (b) MUC1 over-expression reduced CagA/β-catenin co-IP, and (c) in the absence of MUC1 over-expression, H. pylori infection increased the nuclear level of β-catenin, (d) whereas MUC1 over-expression decreased bacteria-driven β-catenin nuclear localization. These results suggest that manipulation of MUC1 expression in gastric epithelia may be an effective therapeutic strategy to inhibit H. pylori-dependent IL-8 production, neutrophil infiltration, and stomach inflammation