Immune effects of dietary anethole on Eimeria acervulina infection.

The effects of anethole on in vitro and in vivo parameters of chicken immunity during experimental avian coccidiosis were evaluated. Anethole reduced the viability of invasive Eimeria acervulina sporozoites after 2 or 4 h of treatment in vitro by 45 and 42%, respectively, and stimulated 6.0-fold greater chicken spleen cell proliferation compared with controls. Broiler chickens continuously fed from hatch with an anethole-supplemented diet and orally challenged with live E. acervulina oocysts showed enhanced BW gain, decreased fecal oocyst excretion, and greater E. acervulina profilin antibody responses compared with infected chickens given an unsupplemented standard diet. The levels of transcripts encoding the immune mediators IL6, IL8, IL10, and tumor necrosis factor ligand superfamily member 15 (TNFSF15) in intestinal lymphocytes were increased in E. acervulina-infected chickens fed the anethole-containing diet compared with untreated controls. Global gene expression analysis by microarray hybridization identified 1,810 transcripts (677 upregulated, 1,133 downregulated) whose levels were significantly altered in intestinal lymphocytes of anethole-fed birds compared with unsupplemented controls. From this transcriptome, 576 corresponding genes were identified. The most significant biological function associated with these genes was "Inflammatory Response" in the "Disease and Disorders" category. This new information documents the immunologic and genomic changes that occur in chickens following anethole dietary supplementation that may be relevant to host protective immune response to avian coccidiosis.

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 (25-400 ng/ml) induced greater cell proliferation compared with the medium control (P < 0·001). CINN activated cultured macrophages to produce higher levels of NO at 1·2-5·0 µg/ml (P < 0·001), inhibited the growth of chicken tumour cells at 0·6-2·5 µg/ml (P < 0·001) and reduced the viability of Eimeria tenella parasites at 10 and 100 µg/ml (P < 0·05 and P < 0·001, respectively), compared with media controls. In chickens fed a diet supplemented with CINN at 14·4 mg/kg, the levels of IL-1ß, 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 14·4 mg/kg (E. maxima or E. tenella) or 125 mg/kg (E. acervulina) from hatch for 24 d, and orally infected with 2·0 × 10(4) sporulated oocysts at age 14 d. CINN-fed chickens showed 16·5 and 41·6 % increased body-weight gains between 0-9 d 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 controls.

Immunopathology and cytokine responses in commercial broiler chickens with gangrenous dermatitis.

Gangrenous dermatitis (GD) is an emerging disease of increasing economic importance in poultry resulting from infection by Clostridium septicum and Clostridium perfringens type A. Lack of a reproducible disease model has been a major obstacle in understanding the immunopathology of GD. To gain better understanding of host-pathogen interactions in GD infection, we evaluated various immune parameters in two groups of birds from a recent commercial outbreak of GD, the first showing typical disease signs and pathological lesions (GD-like birds) and the second lacking clinical signs (GD-free birds). Our results revealed that GD-like birds showed: reduced T-cell and B-cell mitogen-stimulated lymphoproliferation; higher levels of serum nitric oxide and alpha-1-acid glycoprotein; greater numbers of K55(+), K1(+), CD8(+), and MHC class II(+) intradermal lymphocytes, and increased K55(+), K1(+), CD8(+), TCR1(+), TCR2(+), Bu1(+), and MHC class II(+) intestinal intraepithelial lymphocytes; and increased levels of mRNAs encoding proinflammatory cytokines and chemokines in skin compared with GD-free chickens. These results provide the first evidence of altered systemic and local (skin and intestine) immune responses in GD pathogenesis in chickens.

Immunoenhancing effects of Montanide ISA oil-based adjuvants on recombinant coccidia antigen vaccination against Eimeria acervulina infection.

The current study was conducted to investigate the immunoenhancing effects of Montanide adjuvants on protein subunit vaccination against avian coccidiosis. Broiler chickens were immunized subcutaneously with a purified Eimeria acervulina recombinant profilin protein, either alone or mixed with one of four adjuvants (ISA 70 VG, ISA 71 VG, ISA 201 VG or ISA 206 VG), and body weight gains, fecal oocyst shedding, and humoral and innate immune responses were evaluated following oral challenge infection with live E. acervulina oocysts. Immunization with profilin plus ISA 70 VG or ISA 71 VG increased body weight gains compared with vaccination with profilin alone. Profilin plus ISA 71 VG also reduced fecal oocyst shedding compared with vaccination in the absence of adjuvant. All adjuvants enhanced profilin serum antibody titers. Increased levels of gene transcripts encoding IL-2, IL-10, IL-17A, and IFN-gamma, but decreased levels of IL-15 mRNAs, were seen in intestinal intraepithelial lymphocytes of chickens immunized with profilin plus adjuvants compared with immunization with profilin alone. Finally, increased infiltration of lymphocytes, especially CD8(+) lymphocytes at the site of immunization was observed in birds given profilin plus ISA 71 VG compared with profilin alone. These results demonstrate that vaccination with the E. acervulina profilin subunit vaccine in combination with Montanide adjuvants enhances protective immunity against avian coccidiosis.