concanavalin-a and Vitamin-A-Deficiency

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.

Topics: Animals; Antibodies, Protozoan; CD3 Complex; CD4 Antigens; CD8 Antigens; Chickens; Coccidiosis; Colorimetry; Concanavalin A; Duodenum; Eimeria; Epithelium; Flow Cytometry; Interferon-gamma; Lymphocyte Activation; Lymphocyte Count; Lymphocytes; Poultry Diseases; Spleen; Vitamin A Deficiency

We have previously reported that vitamin A deficiency resulted in a reduced IgA antibody response to cholera toxin (CT) after per-oral immunization. In the present investigation we have studied the in vivo and in vitro immune response in vitamin A-deficient rats to two parenterally applied antigens, beta-lactoglobulin (beta-LG) and picrylsulphonic acid (TNP)-Ficoll. The serum IgG and IgM antibody responses to the T-cell dependent antigen beta-LG were significantly lower in the vitamin A-deficient rats than in the pair-fed control rats. No such differences were seen with the IgG and IgM responses to the T-cell independent antigen TNP-Ficoll. However, the biliary IgA and the serum IgE antibodies against both antigens were decreased in the vitamin A-deficient rats. In vitro lymphocyte stimulation with concanavalin A (Con A) or beta-LG gave higher T-cell proliferation rates in the vitamin A-deficient than in the control rats. Interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) levels in supernatants from Con A-stimulated mesenteric lymph node cells were also higher in the vitamin A-deficient rats, while IL-6 levels were decreased, which is consistent with an up-regulated Th1 activity. Proliferation studies on purified accessory cells and T cells from the deficient and the control rats, mixed in different combinations, showed that the T cells, but not the accessory cells, were disturbed in the vitamin A-deficient rats. Despite the increased T-cell activity in vitro the vitamin A-deficient rats had a lower delayed-type hypersensitivity (DTH) reaction than the pair-fed control rats. In conclusion, the increased IL-2 and IFN-gamma levels may reflect an up-regulation of Th1 cell function, while the decreased IgA, IgE and IL-6 levels indicate a suppression of Th2 cells. The disturbed T-lymphocyte function is manifested in vivo as a decreased DTH reaction and suppressed antibody production, the latter possibly due to a lack of B-cell switching and proliferation factors in vitamin A-deficient rats.

Topics: Animals; Antigen-Presenting Cells; Cell Division; Cells, Cultured; Concanavalin A; Cytokines; Ficoll; Hypersensitivity, Delayed; Immune Tolerance; Immunoglobulins; Lactoglobulins; Male; Rats; Rats, Wistar; T-Lymphocytes; Trinitrobenzenes; Vitamin A Deficiency

The investigations showed a significant decrease in the alkaline phosphatase activity of retinol deficient liver (48.6%), kidney (65.8%) and spleen (61.9%), as compared to the controls (100%). An increase in Vmax and Km by 12 to 51.5% and 90.4 to 189%, respectively, was observed in all the tissues in the retinol deficient group, as compared to the controls. Subsequent freezing and thawing reduced the activity of alkaline phosphatase by 22.5 to 35.8% in the experimental group; whereas the reduction in the control group ranged from 8.8 to 21.5%. In the presence of lectins and detergents the activity of alkaline phosphatase decreased in both the groups to different levels.

Topics: Alkaline Phosphatase; Animals; Concanavalin A; Detergents; Freezing; Glycoproteins; Kidney; Liver; Male; Microsomes; Microsomes, Liver; Phytohemagglutinins; Rats; Spleen; Vitamin A Deficiency

The immune status of rats fed a vitamin A-deficient diet (-A) was studied before they reached the weight plateau (stage 1), during the first 5 d of the weight plateau (stage 2) and during late stages of vitamin A deficiency (stage 3). Compared to vitamin A-supplemented (+A) animals, there were no significant differences in the relative splenic weights during the early and later stages of deficiency, but the total yield of isolated splenocytes was lower in -A rats during stages 2 and 3. The weights of the cervical and mesenteric lymph nodes were higher during the later stages of deficiency. In the spleen, concanavalin A (Con A)-induced responses were significantly depressed in -A rats at all three stages of deficiency. In stages 2 and 3 splenic pokeweed mitogen (PWM) responses were lower in -A than in +A rats. There were no changes in lymph node responses in stage 1. The Con A and PWM-induced responses of cervical lymph nodes of -A animals were higher in stages 2 and 3. Mesenteric lymph node responses were also higher in -A rats in stage 3. The alterations in the transformation responses of -A rats could not be explained by changes in the relative proportions of T-cell subsets.

Topics: Animals; Body Weight; Concanavalin A; Liver; Lymph Nodes; Lymphocyte Activation; Organ Size; Pokeweed Mitogens; Rats; Rats, Inbred Lew; Spleen; T-Lymphocytes; Thymidine; Vitamin A; Vitamin A Deficiency

The effect of vitamin A deficiency on the response of splenic lymphocytes to mitogenic stimulation was determined in an experimental rat model. Male Lewis rats were divided into three groups. The ad libitum group (AL) was fed unlimited amounts of a vitamin A-supplemented diet. The vitamin A-deficient group (DEF) received a commercial vitamin A-free diet. The pair-fed group (PF) received a vitamin A-containing diet equivalent in amount to that consumed by the DEP group. During the early stages of vitamin A deficiency (determined by cessation of weight gain), the rats were killed and the isolated splenic lymphocytes subjected to mitogenic stimulation. Lymphocytes from DEF rats had one-third the transformation response to the mitogens Concanavalin A, Phytohemagglutinin and E. coli Lipopolysaccharide S of the AL and PF groups. When the DEF rats were supplemented with vitamin A, the transformation response returned to control values within 3 days. In addition to the alterations in the immune response, the DEF rats showed a marked leukopenia, a decrease in the number of circulating lymphocytes and an increase in the number of circulating neutrophils.

Topics: Animals; Blood Cell Count; Body Weight; Concanavalin A; Immunity, Cellular; Lipopolysaccharides; Lymphocyte Activation; Male; Organ Size; Phytohemagglutinins; Rats; Spleen; Vitamin A; Vitamin A Deficiency