concanavalin-a and Deficiency-Diseases

Arginine deficiency and chronic inflammation may cause immune dysfunction. The authors previously showed that a pharmacological dose of parenteral arginine facilitates ornithine rather than nitric oxide production in subacute peritonitis. Herein, they investigated the effects of different doses of parenteral arginine supplementation on immunocytic subpopulation distribution and function.. Male Wistar rats that underwent cecal punctures for induction of subacute peritonitis were infused with conventional parenteral nutrition solution (1.61% of total calories as arginine) or solutions supplemented with low-, medium-, or high-dose arginine (2.85%, 4.08%, and 6.54% of total calories, respectively) for 7 days. Distributions of T cells, B cells, and monocytes/macrophages and cytokine productions of peripheral blood lymphocytes (PBLs) and splenocytes were analyzed.. There were no significant differences in circulating white blood cell numbers and serum tumor necrosis factor (TNF)-α and interferon (IFN)-γ concentrations among groups. Serum nitrate/nitrite (NOx) and interleukin (IL)-2 levels were significantly decreased by arginine in a dose-dependent manner. Animals supplemented with parenteral arginine had significantly decreased productions of concanavalin (Con) A- and lipopolysaccharide (LPS)-stimulated TNF-α in PBLs and splenocytes, spontaneous IL-6 and LPS-stimulated IFN-γ in PBLs, and LPS-stimulated IL-6 in splenocytes. In addition, low-dose arginine significantly increased production of spontaneous IFN-γ in PBLs and splenocytes. High-dose arginine significantly increased spontaneous TNF-α, and Con A stimulated IL-4 and IL-6 in PBLs.. Parenteral arginine administration at approximately 4% of total calories may alter PBLs and splenocytic immunity, and >6% of total calories might not be of benefit in rats with subacute peritonitis.

Topics: Animals; Arginine; Chronic Disease; Concanavalin A; Cytokines; Deficiency Diseases; Dietary Supplements; Dose-Response Relationship, Drug; Immunity; Inflammation; Inflammation Mediators; Leukocytes; Lipopolysaccharides; Macrophages; Male; Nitrates; Nitrites; Parenteral Nutrition; Peritonitis; Rats; Rats, Wistar; Spleen

Aging is often associated with a dysregulation of immune function. Iron deficiency may further impair immunity in older adults. Published reports on iron deficiency and immune response in humans are inconsistent. Most studies are focused on young children in developing countries and are often confounded by comorbid conditions, infections, and nutrient deficiencies.. Our objective was to determine the relation of iron status with immune function in homebound older women, who often have impairments in both iron status and immune response. The subjects were selected according to rigorous exclusion criteria for disease, infection, and deficiencies in key nutrients known to affect immunocompetence.. Seventy-two homebound elderly women provided blood for comprehensive evaluation of iron status and cell-mediated and innate immunity. Women were classified as iron-deficient or iron-sufficient on the basis of multiple abnormal iron status test results. Groups were compared with respect to lymphocyte subsets, phagocytosis, oxidative burst capacity, and T cell proliferation upon stimulation with mitogens.. In iron-deficient women, T cell proliferation upon stimulation with concanavalin A and phytohemagglutinin A was only 40-50% of that in iron-sufficient women. Phagocytosis did not differ significantly between the 2 groups, but respiratory burst was significantly less (by 28%) in iron-deficient women than in iron-sufficient women.. Iron deficiency is associated with impairments in cell-mediated and innate immunity and may render older adults more vulnerable to infections. Further prospective studies using similar exclusion criteria for disease, infection, and concomitant nutrient deficiencies are needed for simultaneous examination of the effects of iron deficiency on immune response and morbidity.

Topics: Aged; Aging; Concanavalin A; Deficiency Diseases; Female; Humans; Immunity, Cellular; Immunity, Innate; Immunocompetence; Iron; Iron Deficiencies; Lymphocyte Activation; Middle Aged; Nutritional Status; Phagocytosis; T-Lymphocytes

Biotin deficiency is known to affect immune function in both humans and experimental animals. In this study, we determined the effect of biotin deficiency on 4-wk-old Balb/cAnN mice during 20 wk of experimentation. The growth rate of mice slowed significantly during the first 6 wk of consumption of a diet designed to induce biotin deficiency; thereafter, from weeks 7 to 20 there was progressive weight loss in the mice receiving the biotin-deficient diet. In the livers of biotin-deficient mice, the specific activities of two biotin-dependent enzymes--pyruvate carboxylase and propionyl-CoA carboxylase--decreased by as much as 75% and 80%, respectively, and in spleen lymphocytes the specific activities of these two enzymes decreased by 63% and 75%, respectively. With respect to the effects of biotin deficiency on the immune system, we observed statistically significant changes in both the absolute number of spleen cells and in the proportions of spleen cells carrying different phenotypic markers: after 16 wk the percentage of cells expressing surface immunoglobulin (sIg) decreased from 47% (control and supplemented) to 27% (deficient) and CD3+ cells increased from 42% (control and supplemented) to 54% (deficient). The mitogen-induced proliferation of spleen cells from deficient mice was lower than that of spleen cells from the control mice. These findings suggest that biotin could have an important role in lymphocyte maturation and responsiveness to stimulation, and consequently in the capacity of the immune system to respond to an antigenic challenge.

Topics: Animals; Biotin; Body Weight; Carboxy-Lyases; Cell Division; Concanavalin A; Deficiency Diseases; Lymphocyte Subsets; Lymphocytes; Male; Methylmalonyl-CoA Decarboxylase; Mice; Mice, Inbred BALB C; Pyruvate Carboxylase; Spleen

Previously, we documented that bacterial translocation occurs in rats fed an elemental liquid diet (4.25% amino acids plus 28% glucose) for 7 days. Since controversy exists over the protective effect of glutamine on diet-induced bacterial translocation, we compared the effect of two elemental diets, one containing 0% and the other 30% of amino acids as glutamine. After 7 days on the test diets or chow (307 kcal/kg/day), the rats were killed and half the animals had their organs cultured for translocating bacteria; immune function was quantitated in the other half by measuring the blood, splenic, and mesenteric lymph node (MLN) blastogenic responses to the T-cell mitogens phytohemagglutinin (PHA) and concanavalin A (ConA). The incidence of bacterial translocation was higher in the rats fed the glutamine (88%) or nonglutamine (75%) elemental diets than in the chow-fed rats (13%) (p < 0.05). Both elemental diets equally reduced the blastogenic response of lymphocytes harvested from all three lymphoid compartments (blood, spleen, MLN) (p < 0.01 vs. chow). The percentage of reduction averaged 30% to 40% when PHA was used as the test mitogen and 50% to 70% when ConA was used. These results indicate that glutamine does not prevent elemental diet-induced bacterial translocation or immune suppression.

Topics: Animals; Bacteria; Bacterial Physiological Phenomena; Cell Movement; Concanavalin A; Deficiency Diseases; Female; Food, Formulated; Glutamine; Immune Tolerance; Intestines; Leukocyte Count; Leukocytes, Mononuclear; Lymph Nodes; Lymphocyte Activation; Lymphocytes; Male; Mesentery; Phytohemagglutinins; Random Allocation; Rats; Rats, Sprague-Dawley; Spleen