Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the combination effect of interferon-gamma (IFN-gamma) and cholera toxin and the role of cAMP in the induction of differentiation of a differentiation-insensitive U-937 clone, in which the reactivity to differentiation-inducers was decreased. IFN-gamma (100 units/ml) or cholera toxin (10(-9) M) alone only marginally induced various differentiation-associated characteristics such as NBT-reducing activity, phagocytic activity, a-naphthyl acetate esterase activity and surface markers. However, when combined with each other, they significantly induced these markers. Other cAMP-inducing agents such as prostaglandin E2, forskolin, epinephrine and isoproterenol did not induce NBT-reducing activity, either alone or in combination with IFN-gamma. However, all these cAMP-inducing agents significantly increased intracellular cAMP levels. Tumor necrosis factor, interleukin 6 or granulocyte/macrophage colony-stimulating factor alone did not induce NBT-reducing activity, but they could induce activity when combined with cholera toxin. These results suggest that enhancement of induction of differentiation by cholera toxin in combination with IFN-gamma or other cytokines may not be merely due to increased cAMP levels. There seems to be a transduction signal other than cAMP coupling with cholera toxin to stimulate induction of differentiation of an insensitive U-937 clone.
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PMID:Combination effects of interferon-gamma and cholera toxin on induction of differentiation of an insensitive U-937 clone. 216 23

We used a panel of functional assays to compare directly the pattern and potency of GM-CSF and M-CSF on monocyte activity associated with cell-mediated immune defense. GM-CSF and M-CSF were found to be equivalent both in their capacity to stimulate human monocyte functions in vitro and in their pattern of monocyte activation. The two CSFs were effective in inducing monocyte chemotaxis towards either fMLP or LTB4 at equivalent concentrations across a panel of donors. GM-CSF and M-CSF demonstrated equipotency in the induction of monocyte phagocytosis of heat-killed baker's yeast and in the regulation of the hexose-monophosphate shunt (NBT reduction). Both were also found to be equivalent in preventing steroid (dexamethasone)-induced suppression of monocyte anti-bacterial (Candida albicans) and anti-fungal (Staphylococcus aureus) phagocytic capacities. GM-CSF was somewhat more effective than M-CSF in stimulating monocyte C. albicans killing at a lower E:T ratio.
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PMID:The effects of colony stimulating factors on human monocyte cell function. 759 62

We studied the protective effect of human macrophage colony-stimulating factor (hM-CSF) on fungal infection due to systemic candidiasis in vivo and the activities of macrophages in vitro, in order to demonstrate the usefulness of M-CSF on fungal infection. The effect of hM-CSF on systemic candidiasis was examined by using normal and immunosuppressed mice. In addition, the effects of hM-CSF on the activity of reticuloendothelial system (RES) organ and on the phagocytic activity and NBT reduction activity of mouse macrophage were also examined in vitro. HM-CSF improved the survival rate of systemic candidiasis in both normal and immunosuppressed mice. Combination therapy with hM-CSF and fluconazole showed higher survival rate more than in the therapy with either hM-CSF or fluconazole alone. Furthermore, hM-CSF enhanced the activity of RES organ, phagocytosis by macrophages and NBT reduction by macrophages, significantly. These results indicate that hM-CSF enhances the phagocytic cactivity and candicidal activity by macrophages in vivo, thereby preventing dissemination of fungal infection.
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PMID:[Protective effect of human macrophage colony-stimulating factor (hM-CSF) on fungal infection (1). In vivo effect of hM-CSF on systemic candidiasis and in vitro effect of hM-CSF on macrophages activities]. 775 36