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An experiment was conducted to explore the effects of Fusarium mycotoxins, common animal feed contaminants, on intestinal immune responses to coccidia (Eimeria) in chickens. Effects of feed-borne Fusarium mycotoxins and a polymeric glucomannan mycotoxin adsorbent (GMA) on immune cell populations were studied in the jejunum of broiler breeder pullets using an Eimeria maxima infection model. Birds were fed a control diet, a diet naturally contaminated with Fusarium mycotoxins, contaminated diet plus 0.2% GMA, or control diet plus 0.2% GMA. Contaminated diets contained up to 6.5μg/g deoxynivalenol (DON), 0.47μg/g 15-acetyl-DON and 0.73μg/g zearalenone. Birds received a primary oral inoculation (1000 oocysts/bird) with E. maxima USDA strain 68 at 2 weeks of age and a secondary oral inoculation (30,000 oocysts/bird) with the same strain at 4 weeks of age. Diet-related differences in CD4(+) cell, CD8(+) cell and macrophage recruitment pattern into the jejunum were observed following both the primary and secondary infections. It was concluded that feed-borne Fusarium mycotoxins and GMA have the potential to modulate immune response to coccidial infections.

To develop a model of bovine thymus and lymph node growth in vivo, we have implanted bovine foetal tissues (16–23 weeks gestation) under the renal capsule of severe combined immune deficient (SCID)/beige (BG) mice and assayed for graft growth and characteristics 2–18 weeks after engraftment. Bovine foetal thymus and lymph node grew considerably following engraftment of SCID/BG mice. Growth was optimal if bovine foetal tissues were used before gestation Week 17. Bovine-mouse chimerism was confirmed using glucose phosphate isomerase analysis. Bovine thymus grew during the entire 18 weeks of study. Growth of bovine lymph node was initially rapid, reaching a maximum at 2 weeks after transplantation followed by a progressive decrease in size. Transplanted bovine lymph node and thymus were morphologically similar to age-matched bovine foetal tissue for a limited time period. Fibrosis, degeneration and depletion of lymphocytes were evident 6 weeks after engraftment; changes were more severe in lymph node than in thymus whereas increases in lymphocytes, lymphopoiesis and follicle formation were evident in age-matched bovine foetal tissue. Despite growth and morphological similarities of the transplanted tissue, blood counts suggested there was no peripheralization of bovine leucocytes. Bovine immunoglobulins (IgG1 and IgG2) were detected in serum of some SCID/BG chimeric mice for a limited time. The appearance of bovine immunoglobulins at 2 weeks in SCID/BG chimeric mice depended on the age of the foetal donor (> 18 weeks) and coincided with the appearance of morphologically mature lymphocytes in the donor foetus lymph nodes. The ability to produce bovine immunoglobulins decreased 8 weeks after engraftment, coinciding with the depletion of lymphocytes in the engrafted lymph node. Lymphocyte depletion and loss of function of engrafted tissues appear the result of a lack of lymphoid progenitors normally derived from hematopoietic stem cells in the bone marrow.

Lipopolysaccharide (LPS), a bacterial membrane endotoxin, induces a systemic inflammatory response (IFR) through the activation of blood monocytes and hepatic kupffer cells. These cells secrete pro-inflammatory cytokines, which subsequently activate the hypothalamic–pituitary–adrenal axis (HPAA) to release cortisol, an anti-inflammatory hormone that regulates the IFR and subsequent immune response (IR). The intent of this study was to characterize the acute phase response in female sheep challenged systemically with a range of doses of Escherichia coli endotoxin. Yearling ewes were challenged with an i.v. bolus dose of LPS (0, 200, 400, 600 ng/kg BW) and the acute phase response assessed by measuring serum interleukin (IL)-6 and cortisol concentrations, and the febrile response over time. A follow-up liver biopsy study was performed to determine kinetic differences in the expression of eight candidate hepatic genes between LPS dose groups using real-time RT-PCR. The initial time trail did not follow a linear dose response relationship with respect to the febrile and HPAA response to LPS challenge. Serum IL-6 concentrations increased in the two highest treatment groups but did not correlate with the observed febrile and HPAA response. The expression of Toll-like receptor 4, CD14, IL-6, tumor necrosis factor-α, IL-1β, macrophage migration inhibitory factor, 11-β-hydroxysteroid dehydrogenase (HSD), and tachykinin precursor 1 hepatic genes was dependent on both the dose and the kinetics of the response to LPS.