Genetic selection for aflatoxin B1 resistance influences chicken T-cell and thymocyte proliferation.
Studies were conducted with two lines of chickens that were selected for high and low plasma protein concentrations in response to aflatoxin B1 (AFB1) exposure. The experiments were designed to determine genetic differences in the responses of T cells and thymocytes to the toxin. Chicks were orally administered AFB1 at a rate of 0, 100, or 500 micrograms/kg body weight up to 21 days of age. At 4 weeks of age, concanavalin A (Con A, 2.5 micrograms/mL) stimulated T-cell proliferation was similar for untreated chicks from the low line (LL) and the high line (HL). However, AFB1 reduced the responses of T cells with HL cells being more sensitive. In a second experiment, immature chickens were bled and peripheral blood lymphocytes were cultured with Con A and either 0, 3.125, 6.25, 12.5, or 25 micrograms/mL AFB1. T cells from LL had greater responses to Con A than those from HL, and LL T-cells were also more resistant to in vitro AFB1 exposure. Furthermore, thymocyte proliferation was greater for LL chicks; but when thymocytes were cultured with 25 micrograms/mL AFB1, 3H-thymidine incorporation was similarly reduced in both lines. Cell cycle analysis indicated that there were more LL thymocytes in S phase, and the percentages for both lines decreased with AFB1 treatment. Although there were no differences between the lines for percent G2/M cells, AFB1 treatment increased the percentages of thymocytes in G2/M. These studies showed that selection for plasma protein response also changed T-cell and thymocyte proliferative activity.
Scott
T R
TR
Department of Poultry Science, Clemson University, SC 29634.
Rowland
S M
SM
Rodgers
R S
RS
Bodine
A B
AB
D016604:Aflatoxin B1 / Q000378:metabolism / Q000494:pharmacology / Q000633:toxicity*; D000818:Animals; D001798:Blood Proteins / Q000032:analysis; D002453:Cell Cycle / Q000187:drug effects; D002478:Cells, Cultured; D002645:Chickens / Q000097:blood / Q000235:genetics / Q000276:immunology*; D003208:Concanavalin A / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology; D007111:Immunity, Cellular / Q000187:drug effects; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology; D007153:Immunologic Deficiency Syndromes / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology; D008658:Inactivation, Metabolic; D007178:Inbreeding; D008213:Lymphocyte Activation / Q000187:drug effects; D012641:Selection, Genetic; D013601:T-Lymphocytes / Q000187:drug effects*
D001798:Blood Proteins; D003208:Concanavalin A; D000431:Ethanol; D016604:Aflatoxin B1