Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Interferon Inducers”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Results of space experiment program "Interferon". II. Influence of spaceflight conditions on the activity of interferon preparations and interferon inducers ("Interferon II").

The influence of spaceflight conditions on the biological activity of HuIFN-alpha preparations (lyophilized, in solution and in ointment) and interferon inducers was studied. In antiviral activity no difference was observed between the samples kept aboard the spaceship and the controls kept under ground conditions. The interferon inducers poly I:C, poly G:C and gossipol placed in the space laboratory for 7 days maintained their interferon-inducing capacity. The circulating interferon level in mice was the same irrespective of the induction being performed with flight or ground-control samples of inducers.

Animals↗

Interferon-inducible protein 10, monokine induced by interferon gamma, and interferon-inducible T-cell alpha chemoattractant are produced by thymic epithelial cells and attract T-cell receptor (TCR) alphabeta+ CD8+ single-positive T cells, TCRgammadelta+ T cells, and natural killer-type cells in human thymus.

Strong reactivity for interferon-inducible protein 10 (IP-10), monokine induced by interferon gamma (Mig), and interferon-inducible T-cell alpha chemoattractant (I-TAC) was found in epithelial cells mainly localized to the medulla of postnatal human thymus. The CXC chemokine receptor common to the 3 chemokines (CXCR3) was also preferentially expressed in medullary areas of the same thymuses and appeared to be a property of 4 distinct populations: CD3+ T-cell receptor (TCR) alphabeta+ CD8+ single-positive (SP) T cells, TCRgammadelta+ T cells, natural killer (NK)-type cells, and a small subset of CD3+(low) CD4+ CD8+ TCRalphabeta+ double-positive (DP) T cells. IP-10, Mig, and I-TAC showed chemoattractant activity for TCRalphabeta+ CD8+ SP T cells, TCRgammadelta+ T cells, and NK-type cells, suggesting their role in the migration of different subsets of mature thymocytes during human thymus lymphopoiesis.

CD8-Positive T-Lymphocytes↗

Target-organ treatment of neurotropic virus disease with interferon inducers.

Interferon inducers were used against vaccinial encephalitis to study the target-organ treatment of neurotropic disease and to correlate interferon levels and the antiviral state following such treatment. A 45-mug amount of statolon, 30 mug of polyribinosinic-polyribocytidylic acid complex (poly I.poly C), or 0.0154 HA unit of Sendai virus given intracerebrally protected 100% of mice challenged the next day with 1,000 median lethal doses (LD(50)) of vaccinia virus. Significant protection against 1,000 LD(50) of vaccinia virus persisted for 1, 4, or 3 weeks after poly I.poly C, statolon, or Sendai virus (154 HA units), respectively. These doses of poly I.poly C and statolon were also used to study postinfection treatment. Mice challenged with 1, 10, 100, or 1,000 LD(50) were treated intracerebrally with poly I.poly C or statolon 24 or 48 hr later. Significant increases in survival time were seen in mice challenged with 1 to 100 LD(50) of vaccinia virus and treated 24 hr later. At challenges of 10 or 100 LD(50), statolon was more effective than poly I.poly C in increasing survival times. When treatment was delayed until 48 hr after infection, significant increases in survival time occurred only when the challenges were in the range of 1 to 10 LD(50), with poly I.poly C and statolon being equally effective. Interferon was measured by Finter's dye-uptake method, with L-929 cells and Semliki Forest virus. Poly I.poly C, statolon, or Sendai virus, given intracerebrally to mice, produced serum interferon peaks of 5,120 units/ml at 2 hr, 2,560 units/ml at 12 hr, or 320 units/ml at 18 hr, respectively. Corresponding brain interferon peaks were 640 units/g at 2 hr, 640 units/g at 4 to 24 hr, and 960 units/g at 72 hr.

Animals↗

[Broadening of the organ specificity of the action of polynucleotide interferon inducers].

Interferon titers in the blood and brain of mice and their protection from the herpes virus were compared after the animal exposure to poly(G).poly(C) duplex, both native and modified with cis-diammine dichloroplatinum (II). It was shown that the duplex platination especially at the level of the poly(G) strand resulted in sharp rising of the interferon titers in the extracts of the animal brain and rearrangement of the types of interferon induced in the brain to predominance of gamma-interferon. The interferonogenesis indices correlated with the duplex protective activity against the herpes virus. It was concluded that the platinum binding could increase the membrane specificity of the duplex and stimulate its penetration through the hematoencephalic barrier. Possible structural changes in the duplex under the action of platinum (II) resulting in the observed effect are discussed.

Animals↗

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↗

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↗

Interferon-induced proteins. Purification and characterization of a 15,000-dalton protein from human and bovine cells induced by interferon.

Human interferons induce a protein of 15,000 daltons in human and bovine cells. This protein is located in the cytoplasm in a soluble form and is induced by concentrations of interferon which induce the antiviral state. Messenger RNA prepared from interferon-treated human and bovine cells contains a mRNA which yields on translation in vitro a protein similar in size to the 15-kDa protein induced by interferon in vivo. The human protein has been purified to homogeneity from interferon-treated human cells by ion-exchange chromatography and reverse-phase high-performance liquid chromatography. A comparison of the peptides generated by V8 protease from the human and bovine 15-kDa proteins reveals that the two proteins are similar but not identical.

Animals↗

Effect of interferon inducers and interferon on bacterial infections.

The effect of interferon inducers and exogenous L-cell interferon on the infection of mice by Pasteurella tularensis or Diplococcus pneumoniae was investigated. The results indicate that the degree of protection is dependent on the type of inducer used. A variety of defense mechanisms with limited nonspecific activity appear to be involved.

Animals↗

[Relation between interferon-inducing activity of natural interferon inducers and their chemical structure].

The interferon-inducing activity of new derivatives of gossypol, a low molecular weight natural polyphenol, and its model compounds was studied in regard to their chemical structure. The active groups required for development of optimal interferon inductors on the basis of the natural polyphenols were defined. As a result of the studies the new interferon inductor AC-1 which is a condensation product of gossypol, a natural polyphenol, and a cellulose derivative was isolated. The interferon-inducing activity of AC-1 was investigated with respect to its dose and the administration route. High interferon-inducing activity of the interferon inductor after its administration by any route in doses of 10 to 100 mg/kg was demonstrated. The serum interferon titers reached 2560 units/ml.

Administration, Oral↗

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↗

Characterization of virus- and endotoxin-induced interferons obtained from the serum and urine of rabbits.

Interferons induced in the rabbit by Newcastle disease virus or by endotoxin have been further characterized as to their physicochemical stability and molecular size by Sephadex G-100 gel filtration. Endotoxin-induced interferon obtained from serum was more labile than virus-induced interferon. Both endotoxin and virus induced interferons obtained from serum contained two peaks: a minor high molecular weight (>100,000) peak and a major lower molecular weight peak. The molecular weight of the major peak induced by endotoxin was 54,000, and that induced by Newcastle disease virus was 46,000. The gel filtration pattern of interferon recovered from the urine of animals inoculated with virus reflected faithfully the pattern found in serum except that there was proportionately less of the high molecular weight peak. However, the urine interferon from endotoxin-inoculated animals contained only one broad peak with a molecular weight of 35,000. This was not the peak fraction present in the serum of such animals. It is postulated that this may represent the basic unit of endotoxin-induced interferon, and that the serum components are either polymers or conjugates of this basic unit.

Animals↗

Dipyridamole is an interferon inducer.

2,6-Bis(diethanolamino)-4,8-dipiperidinopyrimido-[5,4-d]-pyrimidine (dipyridamole) induced interferon production in vitro in explanted mouse peritoneal leukocytes and to a lower degree in non-lymphoidal cell cultures of mouse (L cells primary embryo fibroblasts) and human (diploid embryo lung fibroblasts) origin. Dipyridamole induced interferon also in mice after intravenous administration. Peak interferon levels in the blood (128 IU/ml) were attained at 49 hr after injection of 0.1 mg dipyridamole per kg body weight and at 24 and 12 hr after injection of 0.6-1.8 and 16.7 mg/kg respectively. By its pH stability, thermostability and antigenic properties the interferon induced in mice, mouse peritoneal leukocytes and L cells corresponded to IFN-alpha and IFN-beta. This interferon-inducing capacity of dipyridamole may account for its broad-spectrum antiviral effect.

Animals↗

Inhibition of macrophage migration by virus-induced interferon preparations.

It was found that a preparation of mouse L cell interferon induced by Newcastle disease virus (NDV) possessed not only interferon activity but also inhibitory activity upon migration of guinea pig peritoneal macrophages (MIF activity). These activities were also observed in a preparation of human leukocyte interferon induced by NDV. The interferon and MIF activities shared common characteristics in the dose response, time course of in vitro production, thermal stability, sensitivity to trypsin and periodate, and elution pattern in CM-Sephadex column chromatography. However, gel filtration pattern with Sephadex G-100 showed two separate peaks. Fractions collected from the first peak, corresponding to a molecular weight of about 45 000, had only the MIF activity, while those collected from the second peak, corresponding to a molecular weight of about 30 000, had both the interferon and MIF activities. A preparation of mouse brain interferon induced by Japanese encephalitis virus had a much weaker MIF activity than the L cell interferon, although these preparations were equal in interferon activity (5000 units/ml).

Animals↗

[Vasodilators as interferon inducers].

Vasodilating drugs, inhibitors of cAMP phosphodiesterase activity (theophylline, caffeine, theobromine, etc.) and other vascular drugs (papaverin, dibasol, no-spa, etc.) were found in experiments in vivo to be capable of inducing interferon the peak of whose production was determined in the blood of animals 24 hours after drug administration (the observation period). The interferon production is critically dependent upon the dose and routes of administration of the drugs. The interferon induced by vasodilating drugs belongs to interferon of the 1st species. It is assumed that both endothelial cells of vessel walls and lymphocytes may take part in interferon production.

Administration, Oral↗

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↗