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Query: HUMANGGP:031927 (cytokine)
 144,509 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a completely serum-free system for primary culture of fibroblasts from explants of adult mouse lung tissue which permits bioassays for cytokine activity to be performed using unselected populations of cells at low passage number, without interference by serum binding proteins or interacting growth factors. Cultures were established on collagen-coated surfaces in medium MCDB 201 containing albumin, transferrin, epidermal growth factor, lipids, prostaglandin E1, vitamin E, and reducing agents. The cells were morphologically and ultrastructurally typical of fibroblasts in culture and demonstrated expression of vimentin and induction of expression of desmin in culture. Proliferation of the cells was reproducible between different primary cultures and was growth factor dependent. Both cycling and growth-arrested cells exhibited increased DNA synthesis when stimulated with epidermal growth factor, platelet-derived growth factor, or basic fibroblast growth factor, which functioned as complete mitogens, but did not respond to insulin, tumor necrosis factor or interleukin-1 beta. Maximal induction of DNA synthesis by epidermal growth factor required the continued presence of the mitogen in the culture medium. These results cannot be satisfactorily explained by the competence-progression model of responses to mitogenic stimuli but support and extend the findings of other studies using diploid fibroblasts.
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PMID:Primary culture of adult mouse lung fibroblasts in serum-free medium: responses to growth factors. 200 52

Murine retrovirus infection induces loss of vitamin E and immune dysfunction with loss of cytokine production by T-helper cells. Therefore interferon-gamma (IFN-gamma) was given during dietary vitamin E supplementation to effectively prevent murine retrovirus-induced immunosuppression, cytokine dysregulation, and development of murine AIDS. Administration of IFN-gamma during vitamin E supplementation significantly prevented development of retrovirus-induced suppression of splenic natural killer cell activity and T cell proliferation. It also significantly slowed retrovirus-induced elevation of T helper (Th) 2 cytokine [interleukin (IL)-4, IL-5, and IL-10] production and monokine (IL-6 and tumor necrosis factor-alpha) secretion by splenocytes. The treatment also prevented loss of Th1 cytokine (IL-2 and IFN-gamma) secretion by splenocytes from retrovirus-infected mice alleviating splenomegaly and hypergammaglobulinemia. The combined therapy had an additive therapeutic impact. It was more effective than IFN-gamma treatment or vitamin E supplementation alone in delaying the development of retrovirus-induced immunosuppression with its cytokine dysregulation.
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PMID:Vitamin E supplementation with interferon-gamma administration retards immune dysfunction during murine retrovirus infection. 749 68

Vitamin E, a lipophilic antioxidant, has effectively inhibited the activation of cytokine-induced nuclear factor kB (NFkB). Since NFkB plays a critical role in the induction of an isoform of nitric oxide synthase (iNOS) gene by lipopolysaccharide (LPS), we investigated the effect of a vitamin E derivative, pentamethyl-hydroxychromane (PMC), which is an extremely potent inhibitor of NFkB activation, on the induction of nitric oxide (NO) synthesis and iNOS mRNA by LPS. PMC inhibited the LPS-stimulated induction of NO production in a concentration-dependent fashion in cultured J774 macrophages and rat vascular smooth muscle cells without evidence of cytotoxicity. However, the addition of PMC to J774 macrophages after the induction of iNOS did not inhibit NO production. Treatment of J774 macrophages with LPS resulted in a significant expression of iNOS mRNA, which was profoundly reduced by PMC. Data suggest that PMC inhibits the induction of iNOS by preventing iNOS gene expression through inhibition of NFkB activation.
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PMID:Pentamethyl-hydroxychromane, vitamin E derivative, inhibits induction of nitric oxide synthase by bacterial lipopolysaccharide. 753 70

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS which is functionally similar to human AIDS. Dietary supplementation, with a 15-, 150- and 450-fold increase of vitamin E in a liquid diet, significantly restored levels of interleukin-2 (IL) and interferon-gamma produced by splenocytes, which were suppressed by retrovirus infection. Retrovirus infection elevated levels of IL-6 and IL-10 produced by splenocytes, which were significantly normalized by all levels of vitamin E supplementation, respectively. Increased levels of IL-6 and tumor necrosis factor-alpha, produced by splenocytes during progression to murine AIDS, were also significantly normalized by all levels of vitamin E supplementation. Vitamin E supplementation restored retrovirus-suppressed splenocyte proliferation and natural killer cell cytotoxicity. Vitamin E supplementation also alleviated the AIDS symptoms: splenomegaly and hypergammaglobulinemia. These data indicate that dietary vitamin E supplementation at extremely high levels was not immunotoxic, and can modulate cytokine release and normalize immune dysfunctions during progression to murine AIDS. It should favorably affect host resistance and thereby retard the development of AIDS.
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PMID:Modulation of immune function and cytokine production by various levels of vitamin E supplementation during murine AIDS. 762 53

Interleukins 1 and 6 and tumour necrosis factor orchestrate a co-ordinated series of metabolic changes following invasions by pathogens. The changes are designed to destroy the pathogen. The response is characterized by fever, proteolysis in peripheral tissues, acute phase protein and antioxidant synthesis, and enhancement of the activity of the immune system. Cytokine production is enhanced by free radicals. Damage to the host may occur as a consequence. The deterious actions of these molecules are held in check by sophisticated antioxidant defences and systems which exert feedback control on cytokine biology. Nutrients have a profound effect upon the production and actions of cytokines. Protein energy malnutrition, dietary n-3 polyunsaturated fatty acids and vitamin E suppress cytokine production and actions. An opposite influence is exerted by n-6 polyunsaturated fatty acids, poor antioxidant defence, and supplementation of the diet with protein and branched chain amino acids. The synthesis of acute phase proteins and glutathione is dependent upon the adequacy of dietary sulphur amino acid intake. The consequences of the modulatory effects of previous and concurrent nutrient intake on cytokine biology are depletion of resources and damage to the host, which ranges from mild and temporary to severe, chronic or lethal.
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PMID:Malnutrition and the immune response. 2. Impact of nutrients on cytokine biology in infection. 788 48

Highly potent substances are produced by the immune system. These substances include cytokines and oxidant molecules, such as hydrogen peroxide, free radicals, and hypochlorous acid. The purpose of immune cell products is to destroy invading organisms and damaged tissue, bringing about recovery. However, oxidants and cytokines can damage healthy tissue. Excessive or inappropriate production of these substances is associated with mortality and morbidity after infection and trauma, and in inflammatory diseases. Oxidants enhance interleukin-1, interleukin-8, and tumor necrosis factor production in response to inflammatory stimuli by activating the nuclear transcription factor, NF kappa B. Sophisticated antioxidant defenses directly and indirectly protect the host against the damaging influence of cytokines and oxidants. Indirect protection is afforded by antioxidants, which reduce activation of NF kappa B, thereby preventing up-regulation of cytokine production by oxidants. Cytokines increase both oxidant production and antioxidant defenses, thus minimizing damage to the host. While antioxidant defenses interact when a component is compromised, the nature and extent of the defenses are influenced by dietary intake of sulfur amino acids, for glutathione synthesis, and vitamins E and C. In animal studies, in vivo and in vitro responses to inflammatory stimuli are influenced by dietary intake of copper, zinc, selenium, N-acetylcysteine, cysteine, methionine, taurine, and vitamin E. Information from animal studies has yet to be fully translated into a clinical context. However, N-acetylcysteine, vitamin E, and a cocktail of antioxidant nutrients have reduced inflammatory symptoms in inflammatory joint disease, acute and chronic pancreatitis, and adult respiratory distress syndrome. Impaired antioxidant defenses may contribute to disease progression after infection with human immunodeficiency virus. Powerful arguments have been advanced for treatment with antioxidants to slow progression of acquired immunodeficiency syndrome.
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PMID:Nutritional antioxidants and the modulation of inflammation: theory and practice. 792 42

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS, which is functionally similar to human AIDS. Vitamin E effects on immune functions, cytokine production and nutritional concentrations in retrovirus-infected mice were determined. Retrovirus infection inhibited release of interleukin-2 (IL) and interferon-gamma (IFN) and some immune functions, whereas it stimulated secretion of IL-4, IL-5, IL-6 and tumor necrosis factor-alpha (TNF) and immunoglobulin (Ig) production. Furthermore, retrovirus infection induced some nutritional deficiencies in the tissues. A 15-fold increase in dietary vitamin E largely restored concentrations of some micronutrients (vitamins A and E, zinc and copper) in the liver, intestine, serum and thymus. It also partially restored production of IL-2 and IFN-gamma by splenocytes. Retrovirus-induced elevated production of IL-4, IL-5 and IL-6 by splenocytes in vitro was normalized by vitamin E. Elevated release of IL-6, TNF-alpha, IgA and IgG produced by splenocytes in vitro during murine AIDS were also completely or partially normalized by vitamin E. Vitamin E also prevented retrovirus-induced suppression of splenocyte proliferation and natural killer cell activity. These data indicate that vitamin E supplementation during murine AIDS can help to ameliorate the disorders during murine AIDS, suggesting vitamin E usefulness in treatment of AIDS in humans.
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PMID:Nutritional status and immune responses in mice with murine AIDS are normalized by vitamin E supplementation. 793 12

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS which is functionally similar to human AIDS. Retrovirus infection targets the thymus producing altered T-cell differentiation via the dysregulation of thymocyte cytokine production. Therefore the effects of dietary vitamin E at various levels were determined on cytokine production by ConA-stimulated thymocytes from uninfected (normal) and retrovirus-infected mice. Dietary supplementation, with a 15-, 150- and 450-fold increase of vitamin E in the diet modulated interleukin-2 (IL) production in both uninfected mice and retrovirus-infected mice. The 150- and 450-fold vitamin E supplementation significantly reduced IL-4 secretion by thymocytes from the uninfected, normal mice. Supplementation at all levels also significantly reduced IL-4 production by thymocytes, which was elevated by the retrovirus infection. Vitamin E significantly reduced IL-6 and interferon-gamma production increased during the progression to murine AIDS. The effects of dietary vitamin E on conA-induced proliferation of thymocytes were consistent with the finding on changes of IL-2 secretion. No effect of dietary vitamin E on thymus weight was observed in both uninfected and retrovirus-infected mice. These data indicate that dietary vitamin E supplementation at extremely high levels can modulate cytokine production by thymocytes. This could affect T-cell differentiation, especially during murine AIDS when cytokine production was partially normalized by vitamin E supplementation.
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PMID:Vitamin E supplementation at various levels alters cytokine production by thymocytes during retrovirus infection causing murine AIDS. 794 Jun 43

Mg deficiency results in loss of red blood cell glutathione and was thought to be due to decreased Mg-dependent synthesis. The effects of vitamin E, D-propranolol, and chloroquine on red blood cell glutathione levels in Mg-deficient rats were examined. Feeding the rats a Mg-deficient diet for 3 wk resulted in an approximately 80% decrease in serum Mg and a 55% loss of red blood cell glutathione; concomitantly, plasma thiobarbituric acid reactive (TBAR) materials rose 240%. All three drug treatments had no effect on the plasma Mg levels but significantly inhibited the rise in TBAR content and attenuated (60-80% effective) the loss of glutathione. Red blood cell ghost membranes from the Mg-deficient rats also exhibited 2.3-fold higher TBAR content, which was attenuated by vitamin E treatment. With isolated red blood cells from Mg-sufficient rats, loss of glutathione could be induced by a chemical oxyradical system. Direct protective effects were afforded by alpha-tocopherol and D-propranolol but not by chloroquine. The data suggest that 1) the loss of glutathione during Mg deficiency was due to increased oxidative degradation, 2) both vitamin E and D-propranolol protected by a membrane antiperoxidative action, and 3) chloroquine probably protected by diminishing prooxidant activity secondary to its inhibition of cytokine induction during Mg deficiency.
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PMID:Loss of red blood cell glutathione during Mg deficiency: prevention by vitamin E, D-propranolol, and chloroquine. 797 98

A 15-fold increase in dietary vitamin E (160 IU/liter) normalized hepatic and serum levels of vitamin E normally reduced by retrovirus infection. It also significantly retarded development of splenomegaly and hypergammaglobulinemia induced by retrovirus infection, while significantly restoring release of interleukin-2 (IL) and interferon-gamma by splenocytes which are suppressed by retrovirus infection. Retrovirus infection elevated production of IL-4 and IL-6 by splenocytes, but this elevation was inhibited by vitamin E. Increased levels of IL-6 and tumor necrosis factor-alpha produced by splenocytes during progression to murine AIDS were also inhibited by vitamin E. Vitamin E supplementation also helped restore retrovirus-suppressed splenocyte proliferation. These data indicate that vitamin E supplementation can help overcome retrovirus-induced reduction in tissue vitamin E, modulate cytokine release, and normalize immune dysfunctions during progression to murine AIDS.
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PMID:Long-term dietary vitamin E retards development of retrovirus-induced disregulation in cytokine production. 802 Jan 95


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