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Biomedical subjects

F De Benedetti

Publications and source records attributed to F De Benedetti.

At least 55 records · Page 3Linked to original sources
PubMed1991

Synergistic inhibition of phorbol ester-induced transformation of JB6 cells by transforming growth factor-beta and retinoic acid.

Transforming growth factor-beta (TGF-beta) plays a complex role as a regulator of proliferation and differentiation of many cell types, including cells of epithelial origin. In this study, we examined whether TGF-beta, alone or in combination with retinoic acid, was able to inhibit the transformation of the murine epidermal cell line JB6. When treated with phorbol myristate acetate (PMA) and other tumor promoters, the nontumorigenic and anchorage-dependent JB6 cells acquired a tumor phenotype, as shown by the acquisition of tumorigenicity and anchorage independence. We found that TGB-beta inhibited the PMA-induced transformation of a subclone of JB6 cells. The effect of TGF-beta was due to an anti-transformation promoting activity, rather than to generalized growth inhibition, since TGF-beta neither inhibited the growth of monolayer cultures of JB6 cells, nor affected the colony-forming efficiency in agar of the JB6-derived permanently transformed RT101 cell line. TGF-beta was synergistic with retinoic acid, a known anti-tumor promoter, in inhibiting the PMA-induced transformation of JB6 cells. Examination of TGF-beta receptor expression on JB6 cells, by both binding and affinity labeling, showed that treatment with PMA significantly decreased TGF-beta receptor expression while retinoic acid counteracted this effect of PMA, thus suggesting that the synergy between retinoic acid and TGF-beta may be due, at least in part, to modulation of TGF-beta receptor expression. TGF-beta, therefore, appears to function as an incomplete antipromoter whose action can be permitted and/or complemented by retinoic acid. Our data demonstrating that TGF-beta has anti-transformation promoting activity suggest that TGF-beta plays a role in maintaining homeostasis of epithelial cells, not only by regulating cell proliferation and differentiation, but also by counteracting events that lead to malignant transformation.

Animals↗
PubMed1990

Synergy between transforming growth factor-beta and tumor necrosis factor-alpha in the induction of monocytic differentiation of human leukemic cell lines.

We examined the effect of transforming growth factor-beta (TGF-beta) alone and in combinations with other factors on the growth and differentiation of the human promyelocytic cell line HL60 and the human monoblastic cell line U937. Treatment with TGF-beta alone did not significantly affect growth or differentiation of HL60 cells, while it significantly inhibited proliferation and induced monocytic differentiation of a small percentage of U937 cells. Combinations of TGF-beta and tumor necrosis factor-alpha (TNF-alpha) acted in synergy to inhibit cell proliferation and to induce monocytic differentiation of both HL60 and U937 cells. In contrast, no synergy was observed when HL60 cells were treated with TGF-beta in various combinations with interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma), and retinoic acid. Examination of TNF-alpha receptor expression on HL60 and U937 cells showed that these cell lines expressed comparable levels of high-affinity TNF-alpha binding sites. Treatment of HL60 and U937 cells with TGF-beta did not induce significant changes in TNF-alpha receptor expression in either cell line. In contrast, HL60 cells expressed much lower levels of TGF-beta receptors than did U937 cells. Treatment of both HL60 and U937 cells with TNF-alpha induced a dose-dependent increase in expression of TGF-beta receptors, suggesting that the synergy between TNF-alpha and TGF-beta may result, at least in part, from upregulation of TGF-beta receptor expression by TNF-alpha.

Cell Differentiation↗
PubMed1990

Decreased fibrinolytic activity in juvenile chronic arthritis.

The basal fibrinolytic activity in 17 children with active juvenile chronic arthritis (JCA) was investigated. It was found that patients with JCA, and particularly those with the systemic form, show decreased plasma fibrinolytic activity and a marked increase in plasminogen activator inhibitor. Additionally, it was found that patients with systemic JCA, but not those with the polyarticular or pauciarticular form, have increased circulating levels of tissue-type plasminogen activator, and endothelial cell protein, suggesting possible endothelial cell participation in systemic JCA.

Arthritis, Juvenile↗
PubMed1990

CD5 positive B lymphocytes in seronegative juvenile arthritis.

We investigated the levels of circulating CD5+ B cells in 43 patients with seronegative, HLA-B27 negative juvenile arthritis, 7 patients with juvenile dermatomyositis (DM) and 16 children with systemic lupus erythematosus (SLE). We found that CD5+ B cell levels were high in juvenile arthritis (p less than 0.01), normal in juvenile DM and decreased in SLE (p less than 0.01) compared to 33 age matched controls. In juvenile arthritis, the increase of CD5+ B cells appeared to be independent of discuss activity and was present in all the onset types except in a subset of patient with late onset pauciarthritis.

Adolescent↗
PubMed1987

Calcinosis as the presenting sign of juvenile dermatomyositis in a 14-month-old boy.

We describe a 14-month-old child with dermatomyositis in whom calcinosis was the first sign of the disease. This case shows that calcinosis, usually a late complication of dermatomyositis, may be the presenting sign of the disease even in young children and when Gottron's sign is still absent and muscular weakness not prominent.

Calcinosis↗
PubMed1978

Morphology of the gastric mucosa, gastric secretion and serum gastrin concentration following a test meal.

In 32 subjects, the HCl secretion, the histological state of the antral and fundic mucosa and the gastrin response to a liquid meal extract were studied. Atrophy of the antrum was associated with normal gastrin concentration in the fasting state and after the test meal, in the presence of normal fundic mucosa and HCl secretion. In achlorhydria and atrophic gastritis, fasting gastrinemia was significantly elevated in subjects with a normal antrum, and only moderately increased in subjects with an atrophic antrum. The gastrin response to feeding was correlated to the fasting gastrin concentration in achlorhydric subjects with normal antral mucosa, in contrast to a uniformly reduced output in achlorhydric subjects with atrophic lesions of the antral mucosa.

Achlorhydria↗
PubMed1976

[Hemato-tissue eosinophilia in a case of ulcerative rectocolitis].

A case of ulcerous rectocolitis presenting a remarkable haematic and tissue eosinophilia, both rectal and gastric, is described. After therapy, the eosinphil complement decreased in the blood but not in the colic mucosa. It is suggested that eosinphilia is not a particular characteristic of ulcerous colitis, but the expression of an inidvidual reaction to an inflammatory stimulus.

Adult↗
PubMedDate not supplied

Activation-induced cell death and Fas-induced apoptosis in patients with systemic or pauciarticular juvenile idiopathic arthritis.

OBJECTIVE: To investigate the functionality of the Fas-induced apoptotic pathway in peripheral blood mononuclear cells (PBMC) from patients with systemic or pauciarticular juvenile idiopathic arthritis (JIA). METHODS: PBMC from 12 patients with systemic and 6 with pauciarticular JIA were activated with anti-CD3 and rhIL-2 and then incubated in the presence or absence of the anti-Fas MoAb CH11 inducing activation of the Fas apoptotic pathway. Apoptosis was evaluated by flow cytometry and fluorescence microscopy. RESULTS: The percentage of apoptotic cells following triggering of Fas did not differ between patients with systemic JIA (12.5 +/- 9.5%) or pauciarticular JIA (18.7 +/- 8.9%) and controls (16.1 +/- 6.8%). Evaluation of activation-induced cell death (AICD) in the absence of exogenous triggering of Fas showed that 44% (8/18) of the patients with JIA, compared to none of the controls (0/16), had a percentage of apoptotic cells higher than the mean + 2 SD of controls. The increased AICD was neutralized by the addition of an anti-TNF-alpha antibody. CONCLUSION: Patients with systemic or pauciarticular JIA do not show a defect in the Fas-dependent apoptotic pathway of T cells. The increased AICD present in some patients with JIA appears to be at least in part related to the inflammatory cytokine TNF-alpha.

Adolescent↗
PubMedDate not supplied

Serum interleukin-6 levels and joint involvement in polyarticular and pauciarticular juvenile chronic arthritis.

We measured serum and synovial fluid interleukin 6 (IL-6) levels in patients with polyarticular-onset and pauciarticular-onset juvenile chronic arthritis (JCA), using the hybridoma cell line B9. During active disease, but not during remission, serum IL-6 levels were significantly elevated in patients with polyarticular (p < 0.0001 vs controls) and in patients with pauciarticular JCA (p < 0.01 vs controls). In patients with active polyarticular disease (polyarticular and extended pauciarticular) serum IL-6 levels correlated with the extent and severity of joint involvement (p < 0.05), with erythrocyte sedimentation rate values (p < 0.005) and with C reactive protein concentrations (p < 0.05). In patients with persistent pauciarticular JCA, serum IL-6 levels correlated with the joint swelling score (p < 0.05). Synovial fluid IL-6 levels, measured in 5 patients with pauciarticular JCA, were markedly elevated (range 600-24,000 HGF U/ml). In conclusion, our data suggest that IL-6 is an important pathogenic mediator in polyarticular and pauciarticular JCA.

Adolescent↗
PubMedDate not supplied

Multiple inhibitors of mitogen-induced proliferation of normal lymphocytes in juvenile chronic arthritis sera.

We evaluated the effect of 47 serum samples obtained from 34 children with juvenile chronic arthritis (JCA) on mitogen-induced proliferation of normal peripheral blood lymphocytes (nPBL). We found that sera from patients with active disease, and particularly those with the systemic form, inhibited significantly PHA-induced proliferation of nPBL at all the PHA concentrations tested. This inhibitory activity was independent of the treatment and was correlated with the value of the erythrocyte sedimentation rate. Part of the JCA sera inhibitory effect could be reversed by the addition of exogenous interleukin 2 (IL-2), but not of interleukin 1 (IL-1) or interferon-gamma, moreover, JCA sera were able to partially inhibit the IL-2 dependent proliferation of CTLL. When we tested serum fractions obtained by Sephadex G-200 chromatography for their inhibitory activity, we observed that: a) two major peaks of inhibitory activity on PHA-induced proliferation were present: peak 1 with MW less than 600,000 and peak 2 with MW between 70,000 and 35,000; b) the inhibitory activity present in the high MW peak was in part IL-2 related; and c) both peaks contained elevated levels of acute phase proteins (APP) which are known to inhibit mitogen-induced lymphocyte proliferation. We conclude that sera from patients with active systemic JCA contain inhibitory activity on mitogen-induced lymphocyte proliferation. We conclude that sera from patients with active systemic JCA contain inhibitory activity on mitogen-induced lymphocyte proliferation. This activity is due to the presence of multiple inhibitors, one of which appears to be IL-2 related; at least part of the inhibitory activity may be due to elevated serum levels of APP.

Adolescent↗
PubMedDate not supplied

[Changes in the production of IgM in response to pokeweed mitogen in juvenile rheumatoid arthritis. Correlations with disease activity].

Unstimulated and pokeweed mitogen (PWM)-stimulated "in vitro" IgM synthesis by peripheral blood lymphocytes has been evaluated by an ELISA method in 33 patients with juvenile rheumatoid arthritis (JRA). Lymphocyte PWM responses were significantly reduced in patients with JRA compared with healthy controls. When patients were divided according to disease activity, a significant increase of stimulation index (ratio of IgM synthesis with over that without PWM) has been observed in patients with disease remission compared with those with active disease. These findings confirm the defect in PWM-induced IgM synthesis by peripheral blood lymphocytes of patients with JRA and suggest that these abnormalities may be related to disease activity.

Adolescent↗
PubMedDate not supplied

[Cytokines: present and future therapeutic applications].

Recent technological developments have led in the the last years to the isolation and characterization of a group of polypeptides, generally termed cytokines, which are produced by cells of the immune system, and by other cell types; these peptides regulate the immune response and the inflammatory reaction, and, in general, cellular growth and differentiation. Because of the availability of large quantities of these cytokines, produced with recombinant DNA techniques, their use in therapy is now possible; promising results have been obtained in some diseases.

Anemia↗