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Biomedical subjects

M Kohase

Publications and source records attributed to M Kohase.

7 recordsLinked to original sources
PubMed1979

Interferon induction with Newcastle disease virus in FS-4 cells: effect of 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB).

DRB is an inhibitor of heterogeneous nuclear RNA (hnRNA) and messenger RNA (MRNA) synthesis. The effect of DRB on interferon production stimulated by Newcastle disease virus (NDV) in the human FS-4 cells was studied. Interferon production in cells primed by treatment with interferon was markedly enhanced (superinduced) in the presence of DRB. This superinduction was essentially due to an inhibition of the rapid decline (shutoff) of interferon production observed in primed cells not treated with DRB. Continuous presence of DRB was required for maximal superinduction. In this and other respects the interferon response induced by NDV in primed cells resembled poly(I). poly(C)-induced interferon production. In contrast interferon production in cells not primed with interferon was virtually abolished by DRB treatment. Since neither virus specific RNA synthesis nor virus replication were significantly affected by DRB, the inhibition of interferon production is likely to result from the inhibitory action of DRB on a cellular, rather than viral, function. Apparently some differences exist in the synthesis or processing of the mRNAs for interferons in primed and unprimed cells and these determine the different sensitivities of these two responses to DRB.

Cell Line↗
PubMed1979

Interferon induction with Newcastle disease virus in FS-4 cells: effect of priming with interferon and of virus inactivating treatments.

Inoculation of human FS-4 cells with Newcastle disease virus (NDV) resulted in the induction of two distinct interferon responses, one that peaked at about 5 hr (early response) and one that reached a maximum between 10 to 24 hr after inoculation (second response). The early interferon response was enhanced by previous treatment of the cells with interferon (priming), whereas the second response decreased after interferon treatment in a dose-dependent manner. The early response diminished with decreasing multiplicities of infection, the magnitude of the second response in unprimed cells was relatively independent of the dose of NDV employed. The early interferon response was sensitive to inhibition by actinomycin D for only 1 hr after inoculation. In marked contrast, the second response remained sensitive to inhibition by actinomycin D until 12 hr after inoculation. The ability of NDV to induce the second response was greatly diminished by irradiation of the virus with ultraviolet light or by its treatment with hydroxylamine, whereas the ability to stimulate the early response was relatively resistant to these virus-inactivating treatments. Treatment of NDV with hydroxylamine abolished the virus to induce the second response at the same rate as it destroyed infectivity. The results suggest the existence of at least two distinct mechanisms of interferon induction by NDV; the early response is triggered either by a virion component or by a product of primary transcription, whereas induction of the second response requires the expression of some functions of the virus not needed for triggering the early response.

Animals↗
PubMed1978

Studies on the enhancement of interferon production in human diploid (FS-4) cells by ultraviolet.

Interferon production stimulated with Polyinosinate-Polycytidylate [Poly (I). Poly (C)] in cultures of human FS-4 cells was enhanced ('superinduced') by the irradiation of cells with UV at the time of induction. UV showed no additional enhancing action on interferon production in cultures already superinduced by the sequential treatment with cycloheximide and actinomycin D; UV doses above 1,000 erg/mm2 inhibited interferon synthesis. In UV-irradiated cells interferon production remained sensitive to inhibition by high concentrations of actinomycin D for at least 3 hr after exposure to Poly (I). Poly (C). Irradiation of induced cells at 4, 5 or 6 hr after stimulation with Poly (I). Poly (C) prevented the rapid decline (shutoff) of interferon synthesis seen in control cultures. All these results support the conclusion that the action of UV protects the interferon mRNA from inactivation. This effect, and the fact that interferon mRNA synthesis can occur after the irradiation of cells with superinducing doses of UV, form the basis of the enhancement of interferon production by UV.

Cells, Cultured↗
PubMed1976

Superinduction of interferon with metabolic inhibitors: possible mechanisms and practical applications.

Ten years have passed since cycloheximide was first shown to enhance endotoxin-induced production of interferon in mice, in the first demonstration of what was later called the superinduction of interferon. Various inhibitors of protein and RNA symthesis, as well as combinations of these inhibitors, have been shown to act as superinducing agents of interferon production stimulated by polyriboinosinic-polyribocytidylic acid. The evidence that superinduction is due to the suppression of a mechanism of post-transcriptional regulation of interferon synthesis is rather convincing. The notion (first proposed about six years ago) that this modification is caused by a protein "repressor" remains the most plausible, albeit still unproved, hypothesis. The availability of systems that translate with fidelity interferon messenger RNA isolated from induced cells should prove most useful in the elucidation of post-transcriptional control mechanisms of interferon synthesis and of interferon superinduction. Meanwhile, superinduction has become a useful tool for the production of large quantities of interferon. In particular, this technique has been successfully applied to the production of interferon from human diploid fibroblasts. The clinical potential of this material remains to be critically examined.

Animals↗
PubMed1975

Binding of polyriboinosinic-polyribocytidylic acid with cultured cells.

Homogenates prepared from polyriboinosinic-polyribocytidylic acid copolymer [poly(rI) - poly(rC)]-treated cells exhibited antiviral activity in chick embryo, L and rabbit kidney cells. The antiviral activity in the homogenate co-sedimented with cellular membrane material and was shown to be poly(rI) - poly(rC) by a hybridization competition test with immobilized polyribocytidylic acid. The results indicate that poly(rI) - poly(rC) binds firmly to cellular membrane. These studies, however, could not differentiate between specific binding leading to the interferon induction and non-specific binding possibly unrelated to the induction of interferon.

Animals↗