Search PubMed⌕ Search

Biomedical subjects

I Gresser

Publications and source records attributed to I Gresser.

At least 91 records · Page 5Linked to original sources
PubMed1985

Interferon alters the composition and metabolism of lipids in the liver of suckling mice.

Daily injection of suckling Swiss, C3H, and C57BL/6 mice with potent preparations of mouse interferon (IFN) alpha/beta resulted in a decrease in phospholipids and a decrease in the phospholipid-to-protein ratio in the liver. This decrease in polar lipids was accompanied by a marked accumulation of triglycerides without a pronounced change in free cholesterol. In contrast, a similar IFN treatment of adult mice did not change the content of liver phospholipids, although there was an increase in liver triglycerides. In suckling mice, after 10 days of IFN administration there was a marked decrease in the incorporation of 1(3)-[3H]glycerol into liver phospholipids, which was not observed in IFN-treated adult mice. Our findings suggest that IFN treatment results in the inhibition of some component of the system of phospholipid biosynthesis during the maturation of hepatocytes in suckling mice.

Age Factors↗
PubMed1985

Role of sex and early interferon production in the susceptibility of mice to encephalomyocarditis virus.

Adult female Swiss mice showed a greater resistance to intraperitoneal (i.p.) infection with encephalomyocarditis virus (EMCV) than male mice. This difference was not observed in weanling mice, in castrated adult mice or in adult mice injected intracerebrally. Administration of antibody to mouse interferon alpha/beta enhanced the virulence of EMCV for both sexes and no difference was then observed in susceptibility between male and female mice. Six h after EMCV infection, serum interferon titres were higher in adult female mice than in male mice. There was a close correlation between the early serum interferon titre (at 6 h) and survival of EMCV-infected mice. No differences in serum interferon titres were observed between male or female weanling mice or castrated adult mice. Potent preparations of exogenous interferon provided the same degree of protection against EMCV infection in male and female mice. We conclude that the more marked early interferon response of female mice to i.p. EMCV infection is one of the important factors underlying the differential susceptibility to EMCV. It is possible that the interferon system is also involved in the reported greater prevalence of picornavirus infections of men compared with women.

Age Factors↗
PubMed1985

Injection of mice with antibody to mouse interferon alpha/beta decreases the level of 2'-5' oligoadenylate synthetase in peritoneal macrophages.

Injection of conventional or axenic weanling mice with potent sheep or goat antibody to mouse interferon alpha/beta resulted in a decrease in the basal level of 2-5A synthetase in resting peritoneal macrophages and rendered these cells permissive for vesicular stomatitis virus. There was a good inverse correlation between the level of 2-5A synthetase in peritoneal macrophages and the permissivity of these cells for vesicular stomatitis virus. The peritoneal macrophages of 1- and 2-week-old mice had low levels of 2-5A synthetase and were permissive for vesicular stomatitis virus, whereas at 3 weeks (and after) there was a marked increase in the level of 2-5A synthetase in peritoneal macrophages, and these cells were no longer permissive for vesicular stomatitis virus. We suggest that low levels of interferon alpha or beta or both are produced in normal mice, and that this interferon contributes to host defense by inducing and maintaining an antiviral state in some cells.

2',5'-Oligoadenylate Synthetase↗
PubMed1984

Biologic and biochemical differences between in vitro and in vivo passaged Friend erythroleukemia cells. I. Tumorigenicity and capacity to metastasize.

Cloned interferon-sensitive (745) and interferon-resistant (3Cl-8) Friend erythroleukemia cells (FLC) passaged in vitro, are not very tumorigenic when first injected intraperitoneally (i.p.) into syngeneic DBA/2 mice although they do form solid tumors when injected subcutaneously (s.c.). By serially passaging FLC (either 745 or 3Cl-8 cells) i.p. in DBA/2 mice, we obtained two different FLC lines capable of growing i.p. and inducing tumor ascites. The s.c. injection of DBA/2 mice with these in vivo passaged FLC resulted in tumor metastases in the liver and spleen, whereas metastases were not observed in mice inoculated s.c. with in vitro passaged FLC. The capacity of in vivo passaged FLC to metastasize was acquired after several i.p. passages. This highly malignant behavior was a stable characteristic of these cells. All the clones derived from in vivo passaged FLC and passaged more than 14 times in vitro induced hemorrhagic ascites when injected i.p., and metastasized to the liver and spleen when injected s.c. The phenotype of sensitivity or resistance to the inhibitory effect of alpha/beta mouse interferon on virus replication and cell multiplication was conserved during serial i.p. passages and maintained in the clones derived from in vivo passaged cells. These FLC showed a decreased capacity to differentiate in vitro upon treatment with dimethylsulfoxide (DMSO) and a reduced production of Friend leukemia virus with respect to the original clones passaged in vitro.

Animals↗
PubMed1984

Biologic and biochemical differences between in vitro and in vivo passaged Friend erythroleukemia cells. II. Changes in cell surface glycoproteins associated with a highly malignant phenotype.

Friend erythroleukemia cells (FLC), serially passaged in vitro or by intraperitoneal injection in DBA/2 mice, exhibit markedly different tumorigenicity and capacity to metastasize. We have attempted to determine whether the differences in tumorigenicity between these two lines of FLC were correlated with any biochemical changes in their cell membranes. Although consistent modifications of FLC membrane gangliosides were detected after FLC multiplied in the peritoneum, the pattern of FLC gangliosides was not a stable characteristic and did not correlate with tumorigenicity. In contrast, analysis of FLC membrane glycoproteins by cell surface labelling techniques (i.e., galactose-oxidase-borohydride techniques and polyacrylamide gel electrophoresis-fluorography) or by metabolic labelling of glycoproteins with 3H-galactose, revealed consistent differences in the high MW region of the gels between parental in vitro passaged FLC (either 745 or 3Cl-8 cells) and clones derived from in vivo passaged cells. No significant differences in the membrane proteins were detected between in vitro and in vivo passaged FLC when lactoperoxidase-catalyzed iodination and polyacrylamide gel electrophoresis-autoradiography were used. It is seen that repeated in vivo passages of FLC resulted in the appearance of different patterns of membrane glycoproteins and that these changes appeared to be associated consistently with the capacity of these cells to grow as tumor ascites and to metastasize to the liver and spleen.

Animals↗
PubMed1984

Reversibility of the transformed and neoplastic phenotype. IV. Effects of long-term interferon treatment of C3H/10T1/2 cells transformed by methylcholanthrene and SV40 virus.

The effects of long-term treatment with mouse interferon on the phenotype of untransformed C3H/10T1/2 cells and cloned derivatives transformed by methylcholanthrene (MCA) and Simian virus 40 (SV40) were investigated. Continuous presence of interferon induced morphologic reversion, with the development of thick, submembranous filaments in MCA-transformed cells, whereas no morphological effects were detected in SV40-transformed cells. Interferon inhibited the proliferation of all three cell lines and maintained low saturation densities. However, prolonged treatment of MCA-transformed cells with interferon rendered them tolerant toward the anti-proliferative and antiviral activities of interferon although 2-A synthetase activity was induced. Interferon treatment reduced the capacity of both MCA and SV40-transformed cells to form colonies in agar and decreased the tumorigenicity of MCA-transformed but not SV40-transformed cells in mice. These results indicate that the same cell type transformed by different means has different sensitivities to a number of interferon-induced changes in the cell phenotype.

Animals↗
PubMed1984

Injection of mice with antibody to interferon renders peritoneal macrophages permissive for vesicular stomatitis virus and encephalomyocarditis virus.

Vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV) multiply in only a small percentage of peritoneal macrophages freshly explanted from 4- to 6-week-old male or female DBA/2, BALB/c, C3H, C57BL/6, or Swiss mice. However, when these mice were injected intraperitoneally with potent sheep (or goat) anti-mouse interferon alpha/beta globulin 4 days prior to harvesting peritoneal macrophages, the viruses multiplied to high titers and most of the cells were infected, as determined by total virus yield (VSV and EMCV), percentage of VSV antigen-positive cells (immunofluorescence), and determination of VSV infectious centers. This effect was not observed when mice were inoculated with other sheep hyperimmune or normal serum globulins. Anti-interferon globulin appeared to act in vivo because incubation of this globulin with peritoneal macrophages during the period of cell attachment or during the 18 hr after virus absorption did not render these cells permissive for VSV. Injection of mice with anti-interferon globulin did not affect the binding and uptake of labeled VSV by peritoneal macrophages. Although the underlying mechanism of this phenomenon is unknown, the results suggest that there may be low levels of endogenous interferon that contribute to host defense by maintaining some cells in an antiviral state.

Age Factors↗
PubMed1984

Interferon induces pulmonary cysts in A2G mice.

Suckling A2G mice were treated for the first week of life with either partially purified or electrophoretically pure mouse alpha/beta interferon. All mice subsequently developed multiple large pulmonary cysts. The lesions were never found in interferon-treated Swiss mice and only very infrequently in interferon-treated BALB/c or F1 Swiss/A2G mice. These observations show that a brief exposure of suckling A2G mice to alpha/beta interferon can result in a severe disease that is determined by the mouse genotype.

Animals↗
PubMed1984

Inhibitory effect of mouse interferon on the growth of an embryonal carcinoma in mice.

Embryonal carcinoma cells (F9) were resistant to the inhibitory effects of interferon (IFN) on viral multiplication and cell division in vitro. Nevertheless, daily administration of IFN resulted in a marked inhibition of the growth of this carcinoma injected intraperitoneally (ip) and increased mouse survival time. An incidental finding was that daily IFN treatment increased the serum level of alpha-fetoprotein in normal 129 mice.

Animals↗
PubMed1984

Characteristics of autoantibodies to human interferon in a patient with varicella-zoster disease.

A patient with varicella-zoster disease was found to have antibodies to human interferon. These antibodies included all IgG subclasses, showed a high combined affinity (average dissociation constant, 10(-11)M), and were present in serum at a concentration of 10(-9)M. The antibodies neutralized the activity of a series of human alpha-interferons prepared from recombinant DNA as well as that of naturally occurring mixtures of alpha-type interferon prepared by viral stimulation of human cells. Examination of the patient's lymphoid cells revealed normal production of interferon and normal expression of interferon receptors. Interferon from the patient's cells was neutralized by her serum. The neutralizing capacity of this serum was analyzed with regard to levels of interferon previously detected in patients with varicella-zoster infections.

Aged↗
PubMed1983

Injection of mice with antibody to interferon enhances the growth of transplantable murine tumors.

Injection of DBA/2, C57Bl/6, or BALB/c mice with antibody to mouse interferon alpha/beta enhanced the i.p. transplantability of six different murine tumors, as manifested by an increase in the percentage of tumor-bearing mice and a decrease in survival time. The effect was observed in mice injected with antibody to interferon raised in three sheep, a goat, and a rabbit, but not with sheep antibody to "impurities" present in the mouse interferon preparations or with normal sheep or goat globulins. The enhancement in transplantability was most marked when tumor cells had been previously passaged in vitro and were of low tumorigenicity. Analysis of some of the experimental conditions using interferon-sensitive and interferon-resistant lines of Friend erythroleukemia cells (FLC) showed that the enhancing effect was observed over a wide range of tumor cell inocula, was directly related to the amount of antibody to interferon injected and was most pronounced when antibody was administered at the time of tumor cell injection. Enhancement was also observed when FLC were injected subcutaneously (s.c.). Antibody did not act directly on the tumor cells in vitro. Although we were unable to demonstrate any biologically active interferon in mice before or after tumor cell inoculation, the results suggest that endogenous interferon is present and plays a role in inhibiting the transplantability of some murine tumors in immunocompetent mice.

Animals↗
PubMed1983

Antitumor effects of interferon in mice injected with interferon-sensitive and interferon-resistant Friend leukemia cells. III. Inhibition of growth and necrosis of tumors implanted subcutaneously.

Administration of highly purified interferon to DBA/2 mice inhibited the growth of interferon-sensitive or interferon-resistant Friend erythroleukemia cells implanted subcutaneously. Injection of interferon at the site of tumor inoculation was more effective than injection of interferon intraperitoneally. Histologic examination of tumors in interferon-treated mice showed extensive areas of tumor-cell necrosis in the absence of an obvious host-cell infiltrate. Interferon inhibited the growth of established subcutaneous tumors and induced complete tumor regression in some mice. Interferon treatment also resulted in an inhibition of tumor metastases in the liver and spleen.

Animals↗
PubMed1983

2-5A synthetase activity does not increase in interferon-resistant Friend leukemia cell variants treated with alpha/beta interferon despite the presence of high-affinity interferon receptor sites.

The presence of interferon (IFN) receptors on mouse Friend leukemia cells (FLC) has been investigated in binding experiments with highly purified 125I-labeled mouse alpha/beta IFN. Both IFN-resistant clones and wild-type IFN-sensitive FLC showed a specific saturable binding site for mouse IFN with a similar affinity constant. In contrast to IFN-sensitive FLC, IFN-resistant FLC variants were not inducible by IFN for double-stranded RNA-dependent 2-5A synthetase activity.

2',5'-Oligoadenylate Synthetase↗
PubMed1983

Interferon as a defence mechanism in mouse cytomegalovirus infection.

Mouse cytomegalovirus (MCMV) grew to higher titres in spleen, liver, kidney and salivary gland of mice, and caused more sickness and death in susceptible (CD1) mice following treatment with anti-interferon globulin (AIG). In the resistant (C3H) strain of mice, organ titres were higher following AIG treatment but there was no sickness or mortality. Spleen necrosis was more severe in AIG-treated mice, indicating that this necrosis was not caused by interferon-mediated activation of natural killer (NK) cells. CD1 mice developed a high level of NK activity during MCMV infection and this was greatly reduced by AIG treatment. AIG was equally effective in increasing virus titres in NK-deficient beige (bg/bg) C57 B1.6 mice which showed a low level of NK activity even after MCMV infection, suggesting that interferon protects against MCMV by its direct antiviral effect on cells rather than by activating NK cells.

Animals↗
PubMed1983

Lethal role of interferon in lymphocytic choriomeningitis virus-induced encephalitis.

After intracerebral inoculation of adult C3H mice, the 'docile' strain of lymphocytic choriomeningitis (LCM) virus multiplied to high titre in several visceral organs. Although the virus content of lung, liver, spleen and brain was high, these mice did not die but became long-term carriers of the virus. Injection of mice with the same dose of the 'aggressive' strain of LCM virus resulted in much lower virus titres in these organs; nevertheless, 100% of the mice died within 7 to 9 days. The results presented here show that mice infected with the 'aggressive' virus do not die if treated with anti-interferon globulin. Under these conditions the titres of 'aggressive' virus were as high in the different organs as in mice injected with the 'docile' virus. These results are consistent with the hypothesis that inhibition of LCM virus multiplication in various organs by interferon results in a lethal disease. The possible mechanisms underlying this seemingly paradoxical phenomenon are discussed.

Animals↗
PubMed1983

[Interferon].

Explore the source record for details and available documents.

Animals↗