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Biomedical subjects

C Favalli

Publications and source records attributed to C Favalli.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1980

[In vitro and in vivo antibacterial activity of cephapirin-dicloxacillin combination in the ratio 1:1].

Studies were carried out on the combination, 1:1 ratio, of two antibiotics: cephapirin and dicloxacillin. After the analysis of the activity spectrum "in vitro" of each antibiotics, the synergism of this combination against the Gram-negative bacteria strains was clearly demonstrated. This combination demonstrated a particular activity against the beta-lactamases producing strains "in vitro" as well in protection tests "in vivo" in experimental infections in mice.

Animals↗
PubMed1980

The effect of PGA1 on the immune response in B-16 melanoma-bearing mice.

This study evaluated the effects of PGA1 on B-16 melanoma-bearing mice. Intraperitoneal injection of PGA1 (10 microgram/day) significantly inhibited the rate of melanoma growth measured both as delay in the rate of appearance and decrease in the tumor volume. In contrast to the diluent control-treated mice, by 17 days, less than half of the PGA1-treated animals developed measurable (greater than 2 mm) subcutaneous tumors. In addition to its effect on tumor size, PGA1 was also effective in stimulating both the humoral and cellular components of the immune response. B-16 tumor-bearing mice were shown to be immunosuppressed, in that they had decreased anti-sRBC hemagglutinin titers, decreased splenic plaque-forming cells, suppressed delayed hypersensitivity responses, and delayed rejection of skin allografts from BALB/c mice. Although, PGA1 had relatively little effect on normal mice, this prostaglandin substantially improved all these immunologic parameters in tumor-bearing animals.

Animals↗
PubMed1980

Influence of PGE on the immune response in melanoma-bearing mice.

This study was performed to correlate the role of exogenous and endogenous prostaglandins on humoral and cellular immune responses to and rate of growth of B-16 melanoma in vivo. B-16 melanomas synthesized 7 times as much PGE as did adjacent normal tissues, an effect that was abolished by indomethacin. In C57BL/6J mice bearing B-16 melanomas splenic plaque-forming cells, hemagglutinin titers, and delayed hypersensitivity (all to SRBC) were profoundly suppressed; these responses were significantly augmented by treating the mice with di-M-PGE2 (16, 16-dimethyl-PGE2-methyl ester), a long acting analogue of PGE2, and either further suppressed or unaffected by indomethacin, a potent inhibitor of endogenous PGE biosynthesis. Compared to control experiments, indomethacin hastened the rate of development of palpable subcutaneous B-16 tumors and facilitated the proliferation of these cells in solid tumors as well as in ascites. Pretreatment of mice with di-M-PGE2 (before inoculation with tumor cells) resulted in delay in the rate of appearance of tumors, decline in the growth rate, and increased survival. These data suggest that prostaglandins are involved in the control of in vivo tumor cell growth largely by virtue of their effects on the immune response.

Agglutinins↗