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At least 19 recordsLinked to original sources
PubMed1977

Acceleration of scrapie in mice by target-organ treatment with interferon inducers.

Interferon inducers were used in the target-organ treatment of scrapie in mice. Intracerebral treatments began 24 hr prior to intracerebral inoculation of 10(4.8) LD50 of the Chandler strain of scrapie agent. The treatments included 30 and 0.3 microgram poly(I:C) given weekly 9 times, 45 microgram statolon given biweekly 7 times, or 1.5 HA units of Sendai virus given biweekly 6 times. All treatments except the lower dose of poly(I:C) accelerated death in scrapie-affected mice. Compared to saline-treated control groups, 30 microgram poly(I:C), given weekly, shortened the mean survival time 13.5 days. Groups treated with statolon or Sendai virus had their mean survival times shortened 18.5 and 21.7 days, respectively. Infected mice were also evaluated for signs of disease at approximately weekly intervals using a numerical scoring method. Acceleration was also apparent using this parameter of disease. When treatment occurred only once, Sendai virus was the only inducer to significantly shorten the survival of mice.

Animals↗
PubMed1976

The dynamics of production and the sensitivity to cycloheximide and actinomycin D of interferon-inducing and interferon messenger RNA.

In the process of virus-induced interferon production, two kinds of RNA appear in the cells. One of them induces production by the recipient cells of interferon with the species-specificity of the latter cells (interferon-inducing RNA), and the other is translated by the recipient cells pre-treated with actinomycin D into interferon with the species-specificity of the donor cells of RNA (interferon mRNA). The interferon-inducing RNA appears 20-30 minutes after virus induction and shows maximal activity after 1 hour. Its formation is not influenced by cycloheximide or actinomycin D. This RNA is assumed to be a transcriptive intermediate form of viral RNA. Interferon mRNA appears in the cells 1 hour after virus induction and shows maximal activity after 6-8 hours. Its synthesis is inhibited by cycloheximide and actinomycin D.

Animals↗
PubMed1979

Augmentation of mouse natural killer cell activity by interferon and interferon inducers.

Interferon (IF), in addition to its anti-viral capacity, is increasingly being found to be a regulator of cell division, cell surface antigens, and cell function. To determine whether IF also plays a role in the regulation of natural killer (NK) cell activity in mice, the in vivo and in vitro effects of IF and IF inducers on NK activity were studied. We observed that pyran, lipopolysaccharide, and polyinosinicopolycytidylic acid (poly I:C) as well as crude and purified IF preparations significantly elevated splenic NK levels in normal mice within 3 to 24 hr of i.p. administration. Normal spleen cells treated with poly I:C or IF in vitro also had augmented NK activity. Poly I:C and IF were themselves not cytotoxic and their presence was not required during the lytic process, indicating that IF acts on lymphocytes to activate NK function. The addition of anti-IF in the incubation medium completely blocked the boosting of NK activity by poly I:C or IF. The characteristics of the effector cells activated by IF were consistent with those of NK cells rather than macrophages, since the boosted effector cells were not retained by a rayon column or removed by carbonyl iron. Moreover, they were resistant to treatment with anti-Thy 1.2 serum plus complement, which eliminated mature T cells.

Animals↗
PubMed1977

Cellular origin of interferon induced by bacterial lipopolysaccharide.

Bacterial lipopolysaccharide (LPS) induces interferons with different properties in mouse macrophages and B lymphocytes. Macrophage interferon is labile at 56 degrees C and is neutralized by anti-mouse fibroblast interferon at a dilution of 1:6,142. B cell interferon is more heat stable and is neutralized by the same antiserum only at a dilution of 1:276. Serum obtained early (1 h) after an intravenous injection of 100 mug of LPS resembled macrophage interferon, whereas serum obtained at later times resembled more and more B cell interferon. The diverse cellular origin of LPS-induced interferon may explain the broad hyporesponsiveness produced by LPS in animals.

Animals↗
PubMed1979

Antiviral and interferon-inducing properties of 1,5-diamino anthraquinones.

A series of anthraquinones with amino substituents at the 1,5 positions were found to induce interferon in mice. A prototype compound, 1,5-bis[(3-morpholinopropyl)amino]-anthraquinone (Ia), was an effective antiviral agent when administered either orally or parenterally. Peak interferon titers were found 12 to 24 h after drug treatment. The minimum oral dose of Ia required to induce serum interferon or to protect mice against a lethal virus infection was 62 mg/kg. Mice tolerated an oral dose of at least 30 times this minimum effective dose. A single dose of Ia given up to 6 days prior to infection had significant protective activity. Biological properties of Ia were compared with those of three other 1,5-diamino anthraquinones, which also induced interferon and demonstrated antiviral activity in mice. The most active compound was 1,5-bis[[2-(diethylamino)ethyl]amino]-anthraquinone (Ib), which protected mice against virus infection at a dose as low as 8 mg/kg (less than 1/60 its maximum tolerated dose). Mice developed hyporeactivity to interferon induction if the same inducer was injected daily, although by alternating between different inducers the loss of interferon responsiveness could be avoided.

Animals↗
PubMed1979

Regions of the lipopolysaccharide of Pseudomonas aeruginosa essential for antitumor and interferon-inducing activities.

Resistance against ascites tumor development and interferon-inducing activity were demonstrated in lipopolysaccharide derived from the protein-lipopolysaccharide complex obtained from an autolysate of Pseudomonas aeruginosa. Lipid A obtained from the lipopolysaccharide was sufficient to induce interferon in vitro but no antitumor activity was found if lipid A or the polysaccharide derived from lipopolysaccharide was injected into the animal. Chemical modification of the polysaccharide portion or deacylation of the lipopolysaccharide also diminished antitumor activity. In contrast, interferon was induced by these incomplete lipopolysaccharides. These results indicate that both the lipid A portion and covalently linked polysaccharide are necessary for the inhibition of ascites tumor development, whereas incomplete lipid A with amide-linked fatty acids is sufficient to induce interferon in vitro.

Amino Acids↗
PubMed1978

Effect of an interferon inducer, 9-methylstreptimidone, on Candida albicans infection in mice.

The protective effect of an interferon inducer with a low molecular weight, 9-methylstreptimidone (9-MS), against Candida albicans infection in mice was investigated. The antibiotic was effective only when given prophylactically. When administered in such a manner, the growth of C. albicans in the kidneys and brain was inhibited at the initial stage of infection. The growth of C. albicans was not inhibited by the antibiotic in vitro, and no antifungal effect was obtained in a preparation containing induced interferon. These results suggest that the antifungal action of 9-methylstreptimidone in mice might be manifested not by direct antifungal activity but rather by a host-mediated activity that excludes interferon-inducing capability.

Animals↗
PubMed1976

Further studies on the relative antiviral efficacies of interferons induced by poly I:C and Mengo virus.

Mouse serum interferons induced by polyI:C, vesicular stomatitis virus (VSV), reovirus, and Mengo virus were assayed in monolayers of mouse L-929 cells by the plaque-reduction method using both VSV and Mengo as challenge viruses. Titers obtained with Mengo virus as challenge were all lower than with VSV. With the interferons induced by VSV, reovirus, and ployI:C, the reductions were of the order of two- to three-fold. With Mengo virus-induced interferon the reduction was much greater (about 17-fold). This offers an explanation for the observation that, unit for unit (measured by the plaque reduction of VSV), Mengo virus-induced interferon is only about 1/10 as effective as polyI:C-induced interferon in protecting mice against lethal infection with Mengo virus. The data are consistent with the hypothesis that an interferon antagonist is produced in the serum of mice infected with Mengo virus. This antagonist, which is not produced in mice inoculated with polyI:C, or reovirus, effectively blocks the antiviral action of interferon during Mengo virus infections, both in vivo and in vitro.

Animals↗
PubMedDate not supplied

[Interferon inducing activity of rabies cell culture vaccine in humans].

Rabies cell culture vaccines are able to induce circulating interferon in human sera. In 8/15 cases a low peak of interferon appears in the serum about 8 h after the vaccination. The inhibition has been considered as due to interferon because of the resistance to pH 2 and lack of activity on other animal species.

Animals↗
PubMed1978

Interferon inducing activity of polyinosinic acid.

Although poly(I) is generally considered to be inactive as an interferon inducer, we have found several authentic poly(I) preparations to be effective inducers. Their interferon inducing ability varied considerably from one cell system to another. In human diploid fibroblasts, primed with interferon and superinduced by cycloheximide and actinomycin D, all active poly(I) samples proved nearly as effective in inducing interferon as poly(I).poly(C). In primary rabbit kidney cell cultures, the active poly(I) samples were either as active, or 3 to 30 times less active than poly(I).poly(C). In intact rabbits they were 100 times less active than poly(I).poly(C). Except for one particular sample, all active poly(I) preparations were inferior to poly(I).poly(C) when assayed for interferon induction in interferon-treated mouse L cells; in DEAE-dextran-treated L cells, they induced little, if any, interferon. The poly(I) inducers of interferon were considerably more susceptible to degradation by TI ribonuclease, pancreatic ribonuclease and human serum nuclease(s) than was poly(I).poly(C) when assayed under the same conditions. Due to their limited half-life time in biological fluids, poly(I) analogues such as those described here may offer a greater safety margin in clinical use than poly(I).poly(C).

Animals↗
PubMed1978

Radioprotective activity of interferon inducers.

The radioprotective activity of interferon inducers (tilorone, Acranil, poly I:C and LPS) was investigated against acute X-ray irradiation and prolonged 60Co-gamma rays irradiation. The endogenous spleen colony formation test and percentage of surviving mice 30 days after irradiation were used as indicators. All interferon inducers investigated proved to have radioprotective activity.

Acridines↗
PubMed1975

Are cytotoxicity and interferon inducing activity of poly(I).poly(C) invariably linked in interferon-treated L cells.

Interferon-treated L cells exhibit a specific enhanced susceptibility to the cytotoxic and interferon inducing activities of double-stranded RNAs such as poly(1). poly(C). These activities remained closely linked through widely varying assay conditions, involving, for example, different time anddosage schedules of poly(1). poly (C),suggesting that there is at least one common step in the mechanisms leading to interferon formation and toxicity in interferon-primed cells exposed to poly(1).poly(C). However, some procedures such as addition of metabolic inhibitors (actinomycin D, cycloheximide) and repeated administration of poly(1).poly(C) suppressed the interferon inducing capacity of poly(1).poly(C) without a concomitant decrease of toxicity. Other procedures such as brief treatment of the cells with interferon or DEAE-dextran permitted full expression of the interferon inducing activity of poly(1).poly(C) without any sign of toxicity. The latter results suggest that the mechanisms underlying interferon production and toxicity of poly(1).poly(C) in interferon-treated L cells diverge from a certain point onward.

Animals↗
PubMedDate not supplied

[Interferon induced in the hamster by subunits of "Nocardia": essay of protection against rabies (author's transl)].

Lipid-free cells of Nocardia opaca and a cell extract (NWSM) are interferon inducers in syrian hamsters: peak interferon appears 2 h after injection as compared to 8 h in the case of interferon induced by inactivated NDV virus. The interferon induced by Nocardia product is inactivated by a treatment for 30 min at 56 degrees C or 24 h at pH 2: NDV-induced interferon is more stable under these conditions. Hamsters inoculated with NWSM before and after infection with rabies virus are partially protected: their survival time is slightly increased.

Animals↗
PubMed1978

The mode of production of endotoxin-induced interferon in rabbit tissue cells. I. Development of priming by pretreatment with interferon.

In vitro production of endotoxin-induced interferon in rabbit tissue cell cultures could be enhanced by pretreatment with interferon. The enhancible state developed from the first hr of incubation at 37 C and a maximal priming effect was attained at 6 hr of incubation. Yields of interferon from unprimed cultures were usually 20-200 units/ml. In contrast, the primed cultures constantly yielded 1,000-2,500 units/ml of interferon. The pretreatment with interferon seemed to cause an earlier appearance of detectable interferon and the primed cells became more sensitive to endotoxin. It turned out that 10--30 units/ml of rabbit interferon were enough to develop the maximal priming. Even when cells were pretreated with higher doses of rabbit interferon such as 1.0 x 10(4) - 1.0 x 10(5) units/ml, the same level of priming effect was always observed without diminution. Various types of homologous (rabbit) and heterologous (human and mouse) interferon preparations showed similar dose-dependent enhancement of interferon production in proportion to the antiviral titers of these preparations as tested with RK-13 cells of rabbit origin.

Animals↗
PubMed1977

Swine cell systems as interferon producers. IV. Comparative studies on the correlation between virulence of different Newcastle disease virus strains and their potency as interferon inducers.

Comparative studies concerning a correlation between virulence of various Newcastle virus strains and their interferon-inducing potency confirmed that such a correlation existed. The nearly avirulent La Sota strain of NDV was the poorest interferon inducer, the virulent Hertfordshire strain manifested a very good inducing potency. However, the most virulent J.B. strain virus was a poorer interferon inducer than the Hertfordshire strain. This should not be viewed as contradictory to the conclusion of the correlation between virulence and interferon-inducing ability of NDV since the highly virulent strain might destroy faster the interferon-producing cells, before the latter produced the maximum interferon quantity which they potentially could produce.

Animals↗