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C Favalli

Publications and source records attributed to C Favalli.

At least 37 records · Page 2Linked to original sources
PubMed1988

Secreted proteins induced by epidermal growth factor and transforming growth factor beta in EL2 rat fibroblasts. Role in the mitogenic response.

Most growth active hormones and peptides are mitogenic only in the presence of other growth factors [e.g., Platelet Derived Growth Factor (PDGF) and Epidermal Growth Factor (EGF) in "competence-progression" fibroblast model]. We have previously described that EGF alone is able to induce the signals which appear necessary for the mitogenic stimulation of EL2 rat embryo fibroblast line. Recently, we have demonstrated that Transforming Growth Factor beta (TGF beta) slightly stimulates the mitogenic response in EL2 cells. Here, we show that in EGF-treated EL2 cells the induction of at least four inducible-secreted proteins (ISPs, range from 29,000 to 68,000 Mr) is accompanied by a marked increase in DNA synthesis. In contrast, TGF beta or different concentrations of EGF induce a slow increase of the ISPs proportional to slow induction in DNA synthesis. Our results suggest that the mitogenic response in EL2 cell line may be connected with the qualitative and quantitative induction of these secreted proteins.

Animals↗
PubMed1987

Effect of in vivo administration of prostaglandins and interferon on natural killer activity and on B-16 melanoma growth in mice.

We investigated the effect on in vivo administration of 16,16-dimethyl-prostaglandin E2 (di-M-PGE2) alone and in combined treatment with alpha-beta interferon (IFN) on NK activity in normal, cyclophosphamide (CY)-treated, tumor bearing or irradiated and bone marrow reconstituted mice and on B-16 melanoma growth. Normal mice inoculated with IFN (30,000 U/mouse, 24 hr before testing) showed a significant increase in NK activity, while those treated with di-M-PGE2 (10 micrograms/mouse daily X 4 days) showed a suppressed NK response. No difference was observed between mice treated with di-M-PGE2 alone and those treated with di-M-PGE2 associated with IFN. In immunosuppressed animals single treatments were slightly (di-M-PGE2) or not (IFN) effective, while the combined administration of di-M-PGE2 and IFN caused a marked increase in NK activity. Moreover, di-M-PGE2 was able to accelerate the recovery rate of NK activity in bone marrow-reconstituted murine chimeras, suggesting that the synergistic effect of prostaglandins and IFN could derive from the action of di-M-PGE2 on progenitor pre-NK cells and of IFN on effector cells. Finally, we observed a good correlation between the enhancement of the NK activity and the tumor growth inhibition.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Modulation of natural killer activity by thymosin alpha 1 and interferon.

A single injection of alpha beta-interferon (alpha beta-IFN) (30000 units/mouse), a major biological modifier of natural killer (NK) cytolytic activity, strongly stimulated NK activity in normal mice, as expected, while the same treatment did not statistically alter the NK response in cyclophosphamide (CY)-suppressed animals. We investigated the possibility of thymosin alpha 1 cooperating with alpha beta-IFN in boosting NK activity in CY-suppressed animals. The results show that treatment with thymosin alpha 1 (200 micrograms/kg) for 4 days, followed by a single injection of alpha beta-IFN 24 h before testing, strongly restored NK activity in CY-suppressed mice. Thymosin alpha 1 was, moreover, able to accelerate the recovery rate of NK activity in bone marrow reconstituted murine chimeras. Taken together the data support the concept that the synergic effect between thymosin alpha 1 and alpha beta-IFN could be the result of effects on differentiation of the NK lineage at different levels.

Animals↗
PubMed1983

[Relation between thymosin fraction 5, prostaglandin release and Thy-1 antigen appearance in mice lymphocytes].

Incubation with Thymosin Fraction 5 induces a dose-dependent release of PGE2 by lymphocytes obtained from adult thymectomized mice; Indomethacin inhibits this effect. The same result was not observed in lymphocytes obtained from normal mice. PGE2 release is correlated with Thy-1 appearance on Thy-1 negative lymphocytes, after incubation with Thymosin, valutated with Bach's rosette inhibition test.

Animals↗
PubMed1983

[Effects of an antiserum for epithelial-reticular cells of the thymus on T-dependent immune response].

Relations between thymic factors and Prostaglandins (PG) were studied. We investigated on the effects of different incubation times with Thymosin Fraction 5 and Indomethacin on the release by spleen cells from normal or adult thymectomized mice. Prostaglandins were measured by radioimmunoassay. Thymosin induces an increase in PGE2 release on spleen cells obtained from thymectomized mice; the same effect was not observed on spleen cells obtained from normal mice.

Animals↗
PubMed1983

Is thymosin action mediated by prostaglandin release?

Treatment of spleen cells derived from adult thymectomized mice with thymosin fraction 5 resulted in a rapid and dose-dependent stimulation of the release of immunoreactive prostaglandin E2. The release of prostaglandin E2 was associated with induction of theta antigen and was totally inhibited by indomethacin. In contrast, prostaglandin E2 release from spleen cells from intact donors was inhibited by treatment with fraction 5. The data support the concept that prostaglandin E2 mediates the effects of thymosin fraction 5 on lymphocytes.

Animals↗
PubMed1983

Modulation of endogenous prostaglandins by thymosin-alpha 1 in lymphocytes.

The effects of thymosin-alpha 1 on the stimulation of specific release of prostaglandin E2 (PGE2) from splenic lymphocytes and thymocytes were studied. Experiments were also performed to study in parallel the absolute levels of thymosin-alpha 1 in the blood and the induction of serum FTS activity and of azathioprine sensitivity of spleen cells from adult thymectomized (ATx) mice. A significant difference in the release of PGE2 between normal splenocytes and splenocytes from ATx mice was observed. Thymosin-alpha 1 at certain concentrations was able to stimulate PGE2 release from lymphocytes of ATx mice while inhibiting release in lymphocytes of normal mice. Also, thymocytes were stimulated to release PGE2 after incubation with alpha 1 in a manner similar to that seen in spleen cells of ATx mice. Approximately the same concentrations of alpha 1 was found to also correct the low azathioprine sensitivity of splenocytes from ATx mice. Determinations of FTS-like activity in the blood and the pharmacokinetics of alpha 1 after administration of this synthetic molecule show a clear dissociation. A maximum peak of alpha 1 activity was obtained after 1 hr, while maximal FTS-like activity was observed after 24 hr. The inhibition of the induction by alpha 1 of FTS-like activity and of Thy 1.2 antigen by indomethacin suggests that the action of alpha 1 requires prostaglandin biosynthesis.

Animals↗
PubMed1983

Comparison between natural reactivity (NR) against Candida albicans and natural killer (NK) activity against YAC-1 tumour cells.

Cytotoxic activity against Candida albicans was measured in vitro in a 4-h 51Cr-release assay. The levels of reactivity correlated well with the number of polymorphonuclear cells in the effector population, being augmented by the enrichment of polymorphonuclear granulocytes. To exclude the possible role of contaminating natural killer cells, natural killer activity against tumour cells was compared with natural reactivity against Candida albicans in vitro. The findings indicate that there are many differences between these reactivities including organ and strain distribution, age dependency, adherence to nylon, and susceptibility to modulation by immuno-adjuvants and to treatment with anti-Thy 1.2 antiserum plus complement. These data further define in vitro polymorphonucleate-mediated cytotoxicity against Candida albicans on the basis of the above-mentioned criteria and clearly demonstrate that this in vitro reactivity could not be due to the presence of contaminating natural killer cells in the effector cell population.

Age Factors↗
PubMed1982

PGE restores the immune response in chemotherapy-treated, tumor-bearing mice.

Two hundred seventy-one B-16 melanoma-bearing mice were randomized and treated for 4 days with either control diluent, 10 micrograms of 16,16-dimethyl-PGE2-methyl-ester (di-M-PGE2), chemotherapy, or chemotherapy plus di-M-PGE2. The chemotherapeutic regimens included adriamycin (7.5 mg/kg), 5-fluorouracil (250 mg/kg), nitrogen mustard (5 mg/kg), and vincristine (0.5 mg/kg). The number of plaque-forming cells and hemagglutinin titers in response to sheep erythrocytes were used as measures of humoral immunity while cellular immunity was assessed by evaluation of delayed hypersensitivity. As we previously reported, the presence of subcutaneous B-16 tumors induced substantial immunosuppression and this suppression was reversed by treatment with di-M-PGE2. Treatment with all four chemotherapeutic agents induced profound immunosuppression. Similarly, the addition of di-M-PGE2 to the chemotherapy protocols resulted in significant augmentation of cellular and humoral immunity.

16,16-Dimethylprostaglandin E2↗
PubMed1980

[Effects of PGA 1 on immune response in mice with melanoma B 16].

This study evaluated the effects of PGA1 on B 16 melanoma bearing mice. PGA1 was observed to inhibit the rate of melanoma growth, both as delay in the rate of appearance and decrease in tumor volume. Furthermore PGA1 stimulated humoral but not cellular immune response in melanoma bearing mice, while it was ineffective in normal mice.

Animals↗