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Biomedical subjects

G B Rossi

Publications and source records attributed to G B Rossi.

At least 91 records · Page 5Linked to original sources
PubMed1984

Natural resistance against hematopoietic cells in lethally-irradiated mice infected with Friend leukemia virus.

The influence of in vivo infection with the polycythemic substrain of Friend leukemia virus on noninducible ('natural') resistance against allogeneic normal or malignant grafts was studied in lethally irradiated mice. Parallel studies were performed on the NK system in the same experimental conditions. The results indicate that FLV-P infection of mice with full (DBA/2) vs partial (BALB/c and CD2F1) susceptibility did not suppress their in vivo natural resistance against bone marrow or El-4 leukemia cells. On the other hand, a decline in NK activity paralleled the progression of leukemic disease in the more susceptible DBA/2 hosts.

Animals↗
PubMed1983

Modulation of natural killer (nk) cell activity during FLV-P virus infection of mice.

We analyzed the effects of a polycythemic substrain of Friend leukemia virus, i.e. the FLV-P virus, on splenic NK activity of DBA/2 susceptible mice. One day after virus injection a significant increase of NK activity was found, which persisted until day 10. On the other hand, 14-21 days after virus injection a marked and significant depression of activity was measured. This depression was associated with the appearance of suppressor cells able to inhibit the lytic activity of untreated splenocytes when mixed in vitro in the 4 h 51Cr-release assay. The suppressor cell population was insensitive to treatment with anti-Thy 1.2 plus complement, was adherent to Sephadex G-10 and nylon, but did not adhere to plastic, suggesting it is neither a T-cell nor a typical macrophage. The possible relevance of NK activity modulation in relation to the induction of leukemia is discussed.

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

Growth and differentiation of Friend erythroleukemia cells in serum-free culture.

A synthetic medium allowing indefinite optimal growth of Friend erythroleukemia cells (FLC) is described. It consists of Iscove's modified Dulbecco's medium supplemented with bovine serum albumin, transferrin, and a lipid mixture. Transferrin and lipids are essential for Friend cells growth. Under these conditions, FLC erythroid differentiation, promoted by a number of inducers, is less efficient than in cultures with serum-rich medium, suggesting that unknown serum factors may play an additional role in this phenomenon. Conversely, the enhancement of erythroid differentiation induced by low doses of Interferon is superimposable in both types of cultures.

Animals↗
PubMed1983

Renal metabolism of homologous serum interferon.

The metabolic behaviour of homologous native and desialylated serum and urinary interferons has been investigated by using an isolated and perfused rabbit kidney, the performance of which is comparable to that in vivo. Serum native and urinary interferons disappear from the plasma perfusate with a fractional turnover rate of 1.8 and 2% and half-lives of 3 and 35 min, respectively. Serum desialylated interferon disappears much more rapidly in keeping with the finding that the glomerular sieve poses less steric hindrance and electrophysical repulsion to the passage of less anionic proteins. These results confirm and extend our previous findings, which indicated that the kidneys have a predominant catabolic role and can explain to some extent the rapid disappearance of interferon from plasma.

Animals↗
PubMed1983

Modulation of hemoglobin synthesis in K-562(S) cells treated with interferons.

Treatment of K-562(S) cells with human interferons (HulFN) alpha, beta, or gamma results in a modulation of hemoglobin (Hb) production. When K-562(S) cells, "induced" with butyric acid or hemin, are given low dosages of all three types of IFN, the percent benzidine-positive cells doubles. Treatment with low doses of IFN causes the acceleration and increased production of those Hb types (as shown by Cellogel analysis) that are already synthesized either in untreated or in "induced" cultures. These results were confirmed by using pure HulFN-beta, and were abrogated, for HulFN-alpha, in presence of its specific antiserum. In contrast, cultures of K-562 cells treated with either inducer and given more than 10(4) IU/ml of alpha- or beta-IFN show a dose-dependent decrease of hemoglobinization in the absence of cell death. The inhibitory effect was reversible upon removal of IFN and culture reseeding in IFN- and inducer-free medium. The significance of both sets of data is strengthened by the pronounced heterogeneity of K-562S cells with respect to their sensitivity to IFN treatment as evaluated by the establishment of the antiviral state. Apparently, one cell out of two is sensitive to IFN, which suggests that the magnitude of IFN effects described here may be larger than it appears to be from the data taken at face value.

Animals↗
PubMed1983

Effects of in vivo Friend leukemia virus infection on levels of serum thymic factors and on selected T-cell functions in mice.

The levels of serum thymic factor(s) (STF), of Thy-1.2 positivity of splenocytes [as measured by their azathioprine (AZ) sensitivity], and of Thy-1.2-positive "spontaneous" spleen rosette-forming cells (SSRFCs), as well as the presence of infectious virus in the thymus, were assessed as a function of time after virus inoculation in susceptible DBA/2, partially resistant BALB/c, and fully resistant C57BL/6 mice given the polycythemia- or anemia-inducing strain of Friend leukemia virus (FLV-P and FLV-A, respectively). As early as Days 2 to 3, the levels of STF and of AZ sensitivity of splenocytes were profoundly decreased in DBA/2 mice, and, to a lesser extent, in BALB/c mice given FLV-P; however, SSRFCs/spleen were increased in both mouse strains. Conclusive evidence of infectious FLV-P was obtained in the thymuses of DBA/2 mice soon after infection. In mice of the same strains infected with FLV-A, STF levels were similarly decreased, but AZ sensitivity of splenocytes was unaffected, and SSRFCs were decreased. Evidence of early FLV-A infection in the thymus of DBA/2 mice was likewise obtained. In C57BL/6 mice given FLV-A, STF levels, AZ sensitivity of splenocytes, and SSRFC showed changes similar to, but of lower magnitude than, those in BALB/c mice. On the other hand, in C57BL/6 mice given FLV-P, the decrease in STF and AZ sensitivity was almost as pronounced as in susceptible DBA/2 mice in the face of complete absence of infectious virus or viral markers in the thymuses. The observed changes are ascribed to virus infection in view of the following: (a) good temporal correlation between these changes and virus infection; (b) absence of any change in mice given heat-inactivated viruses or spleen homogenate of normal DBA/2 mouse spleen; (c) overall good correlation between mouse genotype and genetic (Fv-1 and Fv-2) restrictions of virus infection on one hand and the magnitude of the observed changes on the other. In particular, the decrease in STF and SSRFC levels is ascribed to the replication-competent (Friend-murine leukemia virus) component of Friend leukemia virus complex, whereas the decrease in AZ sensitivity of splenocytes and the increase of SSRFCs are ascribed to the defective spleen focus-forming virus component of the complex. All changes described so far were transient, since they were not detectable beyond 42 days after virus inoculation in overtly leukemic animals. The observed derangements of thymus-derived immune functions may play an important cofactor role during the onset of leukemia in mice genetically permissive to Friend leukemia virus replication and transformation, but they do not seem relevant to the maintenance of leukemia.

Animals↗
PubMed1983

Suppression of Friend leukemia cell-induced tumours by cellular preparations of Candida albicans.

Inactivated cellular preparations and cell wall materials of Candida albicans (CA) were tested for their capacity to suppress the growth of Friend Leukemia Cell (FLC)-induced tumours and the infection by Friend Leukemia Virus (FLV) in histocompatible mice. Factors affecting the inhibition of tumor growth by CA cellular preparations were: i) the schedule of agent administration; ii) the method of cell inactivation; iii) the FLC load. In particular, mice given 10(7) yeast cells, inactivated by cold alkali, on days -14 and +1 with respect to 10(4) FLC challenge on day 0 did not develop tumors. A crude cell wall fraction derived from cells extracted with hot alkali was still effective in reducing (but not suppressing) tumour growth whereas a purified, particulate glucan fraction (glucan "ghosts", essentially consisting of beta 1,3-1,6 glucan) was ineffective. No cellular preparation or cell wall fraction exerted anti-FLV effects (as shown by splenomegaly measurements) nor did any CA material induce interferon-like activity in the serum of animals injected with either FLC or FLV. Therefore, the observed antitumor activity by CA was not mediated by antiviral effects but possibly due to an "adjuvant-type", nonspecific, immunopotentiation of host antitumor response, as documented in other animal tumor models.

Animals↗
PubMed1982

A human amniotic cell line yielding high titres of human fibroblast interferon.

A line of human amniotic cells (UAC) was found to yield large amounts of fibroblast interferon (IFN-beta; 100 to 150 IU/10(3) cells) upon induction with Newcastle disease virus (NDV). UAC cells have a doubling time of about 24 h, and do not require foetal calf serum for growth or optimal IFN yield. The IFN produced was shown to be HuIFN-beta by assaying it on homologous and heterologous cells, and by neutralization tests with specific antisera. It could be purified to a specific activity of 0 . 6 X 10(7) IU/mg protein by chromatography on Blue Sepharose. Addition of 8 micrograms poly(A+) RNA from NDV-induced UAC in 100 microliter of reticulocyte lysate resulted in the production of 510 +/- 340 IU/ml of an IFN that was neutralized only by anti-HuIFN-beta serum.

Amnion↗