Effect of vitamin A deficiency on host intestinal immune response to Eimeria acervulina in broiler chickens.

The effects of vitamin A (VitA) deficiency on the host intestinal immune response and disease susceptibility to coccidiosis were investigated in broiler chickens following oral infection with Eimeria acervulina (EA). Day-old male broilers were fed milo-soybean meal diets either with 8,000 IU VitA/kg feed (CONT) or without added VitA (A-DEF). At 25 d, a group of randomly selected birds from each treatment was inoculated orally with EA-sporulated oocysts. Intestinal immune response was assessed by the changes in the duodenum intraepithelial lymphocyte (IEL) subpopulations using flow cytometry at 35 d in in fected and noninfected birds. Concanavalin A (ConA)-induced spleen lymphocyte proliferation was tested using dimethylthiazol diphenyltetrazolium bromide colorimetric assay. Whether challenged or not with EA, A-DEF birds had fewer IEL expressing the surface markers CD3, CD4, CD8, alphabetaTCR, and gammabetaTCR. Without EA challenge, A-DEF birds had more surface IgA-expressing cells than CONT birds. Upon challenge, A-DEF chickens showed lower CD4+ IEL than CONT chickens. Following EA infection, CD8+ IEL increased in the CONT group, whereas no change was found in CD8+ IEL of A-DEF birds. A higher number of EA oocysts was recovered from A-DEF birds than from CONT birds (9.2 x 10(8) vs 5.4 x 10(8), respectively; P < or = 0.05). Serum samples taken 10 d post challenge showed higher antibody level against a recombinant coccidial antigen in A-DEF birds than in CONT birds. The A-DEF birds showed depressed ConA-induced lymphoproliferation response and produced lower serum interferon-gamma than CONT birds. These data show that VitA deficiency compromised local immune defenses of challenged birds, as reflected in lymphocyte profiles, oocyst shedding, and interferon-gamma levels in A-DEF birds.