PSA-Nutrition: Feed Additives and Phytase

The developing immune system is particularly sensitive to environmental and hormonal influences. Genders can differ in this sensitivity as well. Because the heavy metal, lead, can suppress Th-1 associated function among perinatal thymocytes and cause a systemic loss of postnatal Th-1 function, we investigated the ability of in ovo administered lead and testosterone to alter thymocyte maturation. Cornell K-strain chick embryos were injected via the air sac on embryonic (E) day 8 with either testosterone (12.5 μg/egg in ethanol) or 15% ethanol in 100 μl volume. The groups then received either lead acetate (200 μg/egg) or sodium acetate (control) on E 12 of incubation by the same route. On E 20, thymuses from 4-5 female embryos per group were harvested in sterile Hanks balanced salt solution on ice, and thymocytes were separated using Ficoll. Tri-color flow cytometry was performed with fluorescent-conjugated antibodies against chicken-CD3, CD4, CD8, TCR1 and TCR2 surface molecules and data were analyzed using the MIXED procedure of SAS. Lead did not induce changes among the cell surface markers measured in this study. However, testosterone administration caused changes in both the CD4+CD8+ and CD4+CD8cell populations (P #8804 0.05). Testosterone treatment followed either by sodium or lead acetate injection caused a statistical increase in CD4+CD8+ cells (73.23 ± 2.77 % and 79.85 ± 2.77 % with sodium or lead acetate, respectively) compared either with ethanol and sodium acetate or ethanol and lead acetate treatments (69.68 ± 2.77 % or 68.98 ± 2.77%, respectively). Additionally, testosterone treatment significantly lowered the percentage of CD4+CD8cells from 7.61 ± 1.3 % (control) to 4.2 ± 1.3% or 4.63 ± 1.3% (for testosterone with either sodium acetate or lead acetate, respectively). Therefore, sex hormonal balance can modulate thymocyte maturation, but cellular validation of lead-induced alterations would require the use of additional Th-specific markers. Supported by USDA grant NE-60/NE-1016.