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I Cerutti

Publications and source records attributed to I Cerutti.

At least 37 records · Page 2Linked to original sources
PubMed1986

Aspartate-assisted immune stimulation: its importance in antitumor and antiviral protection.

Immune stimulators such as Corynebacterium parvum (CP) are useful for antitumoral and antiviral therapy. However, the immune trigger cannot be reactivated without adversely affecting the disease. We have tried to amplify the results yielded by a single injection of CP by using either interleukin-2 (IL2) or aspartate salts (ASP). In the present report, we show that IL2 has no detectable clinical effect. In contrast, the addition of an ASP salt increases the antiviral and antitumoral protection afforded by the CP-induced trigger. Moreover, treatment using only ASP slightly protects against tumor development and significantly increases antiviral resistance during experimental encephalomyocarditis (EMC) infection. This ASP-assisted CP immune stimulation improves antitumoral resistance even when ascitic tumors have already developed. In the latter case, tumor regression can even be detected. Since ASP increases T-cell cytotoxicity in vitro and aggravates spontaneous T-cell lymphomas in AKR mice, the involvement of T-cell-mediated immunity may explain antitumoral and antiviral effects. We propose the use of this therapeutic model for human cancer therapy, and possibly for treating AIDS.

Adjuvants, Immunologic↗
PubMed1986

Role of VSV G antigen in the development of experimental spongiform encephalopathy in mice.

The ts G31 VSV mutant induced spongiform encephalopathy without any inflammatory response when injected i.c. into the mouse. In electron microscopy, no virions could be detected in spongiform lesions. In contrast, with the wild VSV strain inflammatory lesions were seen, which contained viral particles in great abundance. As previously shown in vitro, when using the ts G 31 mutant at the nonpermissive temperature, the G antigen can spread from membrane to membrane to distant sites, fusing a great number of cells even in the absence of virus multiplication. Therefore, we postulate that a comparable mechanism is responsible for extensive brain lesions originating probably from a relatively small number of G antigen-producing cells. Indeed, the spongious regions seen mainly in the grey matter contained vacuoles, whose walls were clearly stained by peroxidase-labelled immune serum to G antigen, without detectable virions or inflammatory lesions. The vacuoles probably represent altered and swollen dendritic cell membranes. The relationship between spongiosis development and antigen diffusion in the absence of significant virus replication is discussed.

Animals↗
PubMed1985

Importance of coordinated immune stimulation in experimental antitumor treatment.

We have proposed an antitumor therapeutic model in mice grafted with Crocker 180TG cells. The treatment strategy involves a coordinated immune stimulation which should always precede treatment of target cells. Potent stimulators mobilizing the majority of immune competent cells can be injected only once since repetition results in adverse effects on the response. Thus, to circumvent this difficulty, we propose the amplification, after a single shot of Corynebacterium parvum extract, of the immune response by cimetidine. Indeed, it has been reported that cimetidine inhibits suppressor T cell functions. The second phase acting on the target employs interferon and arginine butyrate since they reconvert a number of transformed target cells to normal phenotype. Important antitumor effects can be obtained in the present model even if the treatment is initiated relatively late after tumor graft. All the drugs employed are harmless on normal cells and are used at relatively low concentrations.

Adjuvants, Immunologic↗
PubMed1984

Antitumor therapy based on the use of an immune modulator, arginine butyrate and interferon.

The analysis of the likely physiological role of interferon during pregnancy and antitumor protection can be employed in developing a new strategy in antitumor therapy. Indeed, pretreatment of the patients with a potent immune stimulation compensates to some extent interferon's immune repressive effects. Through the modulation of the cytoskeleton, interferon enhances macrophage activity. Moreover, butyrate by its own effect on the malignant phenotype increases interferon sensitivity in a number of malignant cells. All of these substances should be used at the lowest possible concentration delivered as closely as possible to the target area.

Amniotic Fluid↗
PubMed1983

Effect of coordinated therapeutic assays using C. parvum, interferon and arginine butyrate on spontaneous disease and survival of AKR mice.

AKR mice, known to develop spontaneous leukemia in almost 100% of cases, were studied throughout their life-span. Different treatments combining a potent immune stimulator, Corynebacterium parvum (CP), with interferon (IFN) and arginine butyrate were initiated at the 15th week of life. In a preliminary series of experiments, CP (200 micrograms), IFN (20,000 units) and butyrate 50 mM) were employed in a well-defined chronological order. In controls, the mean survival time (MST) was 35.17 +/- 1.67 weeks and the final survival rates was 0/50 mice for all experiments. Only CP associated with arginine butyrate significantly augmented the MST (42.5 +/- 3.66 weeks) and final survival rate (9/35 mice). In an adjusted set of experiments, reducing the IFN concentration to 10,000 and 5,000 units and that of butyrate to 6 mM greatly improved the results. The MST was substantially increased with the combinations of CP + IFN + butyrate (41.4 +/- 1.86 weeks), CP + IFN (42.73 +/- 3.29 weeks) and butyrate + IFN (41 +/- 2.34 weeks), as well as the final survival rates (8/15, 10/15 and 6/15 mice respectively). An important finding was that when CP and IFN were used separately, they were ineffective.

Animals↗
PubMed1983

Coordinated therapeutic effects of immune modulators and interferon.

Immune modulators injected 24 h before encephalomyocarditis virus significantly increase antiviral resistance in mice when interferon is administered 1 h after the virus. These immune modulators can be crude bacterial extracts or synthetic drugs. In some cases, the responses are additive; in others, they are clearly cooperative. To protect the mice against the development of 180 TG Crocker sarcomas, the association of bacterial extracts and interferon is highly effective under the condition that the drug concentrations and chronological order and number of injections are well defined. In contrast, the conjunction of interferon and synthetic immune modulators, in particular cimetidine, result in delayed tumor development with no significant change in the final survival rate in the experimental model described here.

Adjuvants, Immunologic↗
PubMed1982

Antitumor effect of arginine butyrate in conjunction with Corynebacterium parvum and interferon.

The antitumor effect of arginine butyrate, used alone or in conjunction with interferon (IFN), was studied using randomly selected Swiss mice inoculated i.p. with 10(6) 180 TG Crocker tumor cells. The results of these different therapeutic regimens were estimated by tumor incidence at 10 days, by the time necessary to protect 50% of the animals, and by the final survival rate. Combined treatment by IFN and arginine butyrate was effective; but in order to compensate for IFN's immune repressive effects, a single injection of Corynebacterium parvum was administered in some experiments prior to IFN and/or arginine butyrate. After this immune potentiation, both IFN and arginine butyrate used separately significantly protected the animals. However, optimal results were obtained when a single C. parvum injection was followed by nine daily alternating shots of arginine butyrate and IFN.

Animals↗
PubMed1981

Isoprinosine delays the early appearance of autoimmunity in NZB/NZW F1 mice treated with interferon.

NZB/NZW F1 hybrid mice treated for long periods with type beta interferon developed early symptoms of autoimmune disease. In these animals the level of anti-dsDNA antibody begins to increase at 4-6 months while untreated NZB/NZW mice do not display similar levels until 12 months. The concomitant administration of isoprinosine and interferon delays the early appearance of autoimmune disorders. In interferon-treated NZB/NZW mice the cytotoxic activity of natural killer lymphocytes is maintained at high levels until the age of 5 months. Nevertheless, the natural killer activity is even stronger and detected until at least 7 months in NZB/NZW mice receiving a single dose of interferon 16 hr prior to the test. Lymphoblastoid ascitic tumours appeared early (2-3 months) during interferon treatment in all groups of NZB/NZW mice. However, in the presence of isoprinosine only a few animals developed tumours. Thus, isoprinosine seems to protect NZB/NZW mice both from early autoimmune disorders due to interferon and from early tumour development.

Animals↗
PubMed1979

Isoprinosine increases the antitumor action of interferon.

The association of relatively low doses of interferon with an immunostimulant, isoprinosine, enhanced the antitumor effect of interferon. Each mouse was inoculated with 10(6) Crocker Tumor 180/TG cells. The best results were obtained when both interferon and isoprinosine were injected three times a week for 1 month. Under these conditions, the mean survival time increased from 26 days in the controls to 45 days in the interferon-treated group to 64 days when both agents were used. Isoprinosine alone had no effect. The final survival rate increased from 1 mouse out of 50 mice in the control group to 10 mice out of 50 in the interferon-treated groups and to 25 mice out of 50 with the combined treatment.

Animals↗
PubMed1979

Adverse effects of interferon treatment on the life span of NZB mice.

NZB mice treated with interferon from birth and for over a year, display early some characteristics of the autoimmune disease. In these animals, mortality is clearly higher than in controls. Their death occurs 3 to 6 months before that of mice injected with a "mock" preparation.

Animals↗
PubMed1979

Enhancement of interferon antitumor action by sodium butyrate.

Sodium butyrate together with interferon enhances the antitumor effect of interferon in vivo. When Sarcoma 180 TG cells are inoculated in mice, the mean survival time and final survival rate are greatly increased compared to those for treatment with interferon alone. Similarly, a significant delay in the mean survival time is observed when mice inoculated with L1210 cells are treated with sodium butyrate and interferon. This effect could be due at least in part to a potentiation of interferon action on the tumor cells.

Animals↗
PubMed1978

[Inhibitory effect of the tissue antagonism of interferon on the development of 180/TG Crocker tumor: recognition of a new murine lectin].

Crude and purified murine lectin preparations are extracted from costal cartilage (TAI). They inhibit the antiviral state induced by interferon. They also agglutinate the Crocker 180/TG tumor cells. After IP inoculation in mice, the purified lectin preparation significantly decreases tumor incidence and increases the animal's life span.

Agglutination Tests↗
PubMed1978

Isoprinosine increases the antitumor action of interferon.

The association of relatively low doses of interferon with an immunostimulant (isoprinosine) enhances the antitumor effect of interferon. After combined treatment, the mean survival time, tumor incidence, and final survival rate are significantly increased in mice inoculated with 10(6) Crocker tumor 180/TG cells when compared to mice treated with interferon alone.

Animals↗
PubMed1977

[Potentiating effect of cycloheximide on viral interference].

The degradation of the antiviral state can be delayed in vitro by antimetabolites, when added between 5-7 hours after interferon. We explore in this chronological order whether antiviral resistance induced by Newcastle disease virus (N.D.V.) in vivo could be modified by an antimetabolite. Cycloheximide was selected for this study because of its reversible biological effect and lack of toxicity in our experimental conditions. The model system employed was Syrian Hamsters, using N.D.V. as an interferon inducer and encephalomyocarditis virus (E.M.C.) as a challenge virus. A constant and significant increase in survival of animals treated with N.D.V.+cycloheximide is probably related to a delay in the degradation of the antiviral state and not to interferon superinduction.

Animals↗