PubMed · 491240
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Y Tofuku, M Kuroda. 1979-06-29. [Pyrazinamide suppression test].. https://pubmed.ncbi.nlm.nih.gov/491240/
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IL-12 is a heterodimeric cytokine produced by phagocytic and other cells with important physiologic and pathologic properties. Regulated IL-12 production is crucial for the generation of protective Th1 responses to infectious agents. In contrast, IL-12 excess contributes to the pathogenesis of a variety of autoimmune and inflammatory disorders. To further understand the processes regulating IL-12 production, we determined whether IL-11 regulated monocyte/macrophage production of this cytokine moiety. IL-11 did not alter the IL-12 (p70) production of unstimulated THP-1 monocytic cells or human blood monocytes. It did, however, inhibit, in a dose-dependent fashion, the IL-12 production of IFN-gamma plus Staphylococcus aureus Cowan strain 1-stimulated THP-1 cells and stimulated blood monocytes. This inhibition of IL-12 protein production was associated with a proportionate decrease in IL-12 p35 and p40 mRNA accumulation. Nuclear run-on assays revealed comparable decreases in IL-12 p35 and p40 gene transcription. IL-11 did not similarly regulate monocyte/macrophage production of IL-8 or macrophage inflammatory protein-1alpha (MIP-1alpha) and IL-6 did not similarly inhibit IL-12 elaboration. These studies demonstrate that IL-11 is a potent inhibitor of monocyte/macrophage IL-12 production and that this inhibitory effect is, at least in part, transcriptionally mediated. They also demonstrate that this inhibition is not the result of a generalized suppression of macrophage effector function and that the ability to inhibit monocyte/macrophage IL-12 production is not a generalized property of all IL-6-type cytokines.
Tumor necrosis factor alpha (TNF-alpha), an important cytokine produced mainly by activated macrophages, plays a critical role in certain physiological immune systems. But it causes severe damage to the host when produced in excess. Therefore, TNF-alpha can be regarded to possess both favorable and unfavorable effects. These pleiotropic effects indicated that TNF-alpha production-enhancers in some cases and TNF-alpha production-inhibitors in other cases would be useful as biological response modifiers (BRMs) under various circumstances. A possible lead compound is thalidomide, which had been used as a hypnotic/sedative agents but was withdrawn from the market because of it's teratogenicity. Thalidomide is a specific inhibitor of TNF-alpha production, and this effect has been shown to be useful for the treatment of various immunodiseases. Recently, we found that the regulation of TNF-alpha production by thalidomide and related hthalimides was both inducer-specific and cell-type-specific, i.e., (I) the compounds enhance 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced TNF-alpha production by HL-60 cells, while they inhibit TPA-induced TNF-alpha production by another human leukemia cell line THP-1, and (II) the compounds inhibit TNF-alpha production both by HL-60 and THP-1 cells when the cells are stimulated with okadaic acid. We also found that in a optically active phthalimide analogues of thalidomide the inducer specific bi-directional regulation of TNF-alpha production is separated. This implies that the target molecule(s) of the two systems are different each other.
Some commercially manufactured disinfectants tested (Desur, Dezox, Diesen forte, Lysoformin 3,000, Sokrena, Topax 91) depressed Pseudomonas aeruginosa virulence factors (elastase and proteinase), Nobacel did not. The degree of inhibition was directly proportional to the disinfectant concentration. The most effective concentrations were 1/4 of the MICs. Topax 91 most significantly suppressed proteinase activity (20.3%), Dezox was the most efficient in case of elastase (47.8%).