The effect of oxidant stress on human lymphocyte cytotoxicity

Mr, Grever; Thompson, VN; Sp, Balcerzak; Sagone, AL Jr

doi:10.1182/blood.v56.2.284.bloodjournal562284

Cited by 3 publications

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“…Oxidative reactions and an abnormally high level of ROS have been shown to affect the integrity of biological membranes and the function of immunocompetent cells. For instance, it has been found that ROS suppresses mitogen-stimulated T-cell proliferation, mixed lymphocyte reaction, and antibodydependent cell cytotoxicity (Grever et al, 1980;Zoschke and Staite, 1987). Decreased ability of cells to degrade H2@ also impaired chemotaxis (McAllister et al, 1980), microbicidal activity (Serfass and Ganther, 1976), and lymphocyte response to mitogens (Pamham et al, 1983).…”

Section: Se-deficient Groupmentioning

confidence: 99%

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

Lessard

Yang

Elliott

et al. 1991

Journal of Animal Science

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The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Se-deficient Groupmentioning

confidence: 99%

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

Lessard

Yang

Elliott

et al. 1991

Journal of Animal Science

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“…We have found that the lymphoblastic transformation of these cells to PHA could be impaired in vitro as a result of exposure to hydrogen peroxide 141. In addition, oxidant injury alters the membrane characteristics of lymphocytes and impairs their ability to mediate cytotoxicity [5,6]. Further, this impaired cell function was associated with an alteration in the glucose metabolism of the lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

Effect of hyperoxia on the carbohydrate metabolism of human lymphocytes

Sagone

1985

American J Hematol

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Lymphocytes incubated under high oxygen tensions have impaired lymphoblastic transformation to nonspecific mitogens. Since carbohydrate metabolism may be essential for an optimal proliferation of these cells following an antigenic stimulus, we have characterized the effect of hyperoxia on the glucose metabolism of human lymphocytes in vitro. The mean rates of glucose utilization, Krebs cycle activity, and hexose monophosphate shunt activity were determined for unstimulated and phytohemagglutinin (PHA)-stimulated cultures incubated for 3 days. In unstimulated cultures, hyperoxia stimulated glucose utilization and markedly impaired Krebs cycle activity but did not alter HMPS activity. These observations suggest that hyperoxia impairs the mitochondrial activity of lymphocytes and that increased glycolysis compensates for the loss of cellular energy normally produced by this organelle. Under high oxygen tension PHA-stimulated cultures failed to show the burst in HMPS activity and increased Krebs cycle activity characteristic of cultures incubated under physiological oxygen tensions and consumed less glucose. Our results indicate that hyperoxia alters the glucose metabolism of lymphocytes. This metabolic alteration may be related to the impaired function of the cells under hyperoxic conditions.

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“…It is known that oxidants are reactive enough to destroy most biological molecules and are responsible for much of the damage caused by phagocytes on both micro-organisms and surrounding tissues, including vascular endothelium, at sites of infection or inflammation [6]. Moreover, it has been shown that ROS decrease the direct and antibodydependent cytotoxicity of lymphocytes [7], whereas in HIV infection they stimulate CD4 þ T cells in such a way that they prepare these cells to be infected by the virus [8].…”

Section: Introductionmentioning

confidence: 99%

Evidence for non‐adaptive immune response in HIV infection

Tzavara

Vlachoyiannopoulos

Kordossis

et al. 1997

Eur J Clin Investigation

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Increased levels of soluble forms of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1) and E-selectin have been found in the sera of HIV-infected patients and have been associated with disease progression. The aim of the present study was to investigate whether this phenomenon reflects activation of the non-adaptive immune response in HIV infection. Fifty-one patients with HIV infection (42 men, nine women) were classified into two subgroups: those with HIV infection but without evidence of AIDS indicator conditions (HIV infected non-AIDS cases, n = 27) and those with AIDS (AIDS cases, n = 24). The activation of non-adaptive immune response was evaluated as the production of reactive oxygen species that cause lipid peroxidation, which was assessed by measuring thiobarbituric reactive substances (TBARS) using the thiobarbituric acid assay (TBA). Plasma levels of von Willebrand factor (vWF), measured by rocket immunoelectrophoresis, were used to show activation of endothelial cells even in the absence of any other causative agent, in these patients. TBARS levels in non-AIDS cases were significantly higher than in control subjects (n = 17) or AIDS cases (P < 0.001). The mean vWF levels were higher in AIDS cases than in non-AIDS cases or normal subjects (P < 0.05). TBARS levels remained significantly higher in non-AIDS cases after adjusting for age, CD4 T-cell and neutrophil counts, antiretroviral therapy and vWF plasma levels. The above findings indicate that in HIV infection, the virus per se is responsible for the increased oxidative stress that in turn activates various transduction pathways, may be leading to endothelial cell activation and shedding of adhesion molecules from the cell surface.

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The effect of oxidant stress on human lymphocyte cytotoxicity

Cited by 3 publications

References 0 publications

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

Effect of hyperoxia on the carbohydrate metabolism of human lymphocytes

Evidence for non‐adaptive immune response in HIV infection

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