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Biomedical subjects

F Chiappelli

Publications and source records attributed to F Chiappelli.

53 records · Page 3Linked to original sources
PubMed1989

Social confrontation "stress" in aggressive fish is associated with an endogenous opioid-mediated suppression of proliferative response to mitogens and nonspecific cytotoxicity.

We have previously shown that social confrontation between aggressive fish (e.g., Tilapia) produces a suppression of several immunological parameters--nonspecific cytotoxicity and mitogen-stimulated proliferation in pronephric leukocytes--in the subordinate fish. By using the opioid antagonist, naltrexone, we now demonstrate indirectly that this immunosuppression is in part mediated by the endogenous opioid system. Evidence is presented that naltrexone-mediated reversal of immunosuppression may be limited to the populations of the cytotoxic and T-cell lineages. The proliferation response to lipopolysaccharide is unaffected by naltrexone. Our data also demonstrate that serum from subordinate (immunosuppressed) fish is immunosuppressive in normal fish--an effect that can be reversed by naltrexone. These results support a link between the neuroendocrine and immune systems in fish, the lowest vertebrate.

Animals↗
PubMed1989

Differential regulation of oligodendrocyte markers by glucocorticoids: post-transcriptional regulation of both proteolipid protein and myelin basic protein and transcriptional regulation of glycerol phosphate dehydrogenase.

During neonatal development glucocorticoids potentiate oligodendrocyte differentiation and myelinogenesis by regulating the expression of myelin basic protein, proteolipid protein, and glycerol phosphate dehydrogenase (sn-glycerol-3-phosphate: NAD+ 2-oxidoreductase, EC 1.1.1.8). The actual locus at which hydrocortisone exerts its developmental influence on glial physiology is, however, not well understood. Glycerol phosphate dehydrogenase is glucocorticoid-inducible in oligodendrocytes at all stages of development both in vivo and in vitro. In newborn rat cerebral cultures, between 9 and 15 days in vitro, a 2- to 3-fold increase in myelin basic protein and proteolipid protein mRNA levels occurs in oligodendrocytes within 12 hr of hydrocortisone treatment. Immunostaining demonstrates that this increase in mRNAs is followed by a 2- to 3-fold increase in the protein levels within 24 hr. In vitro transcription assays performed with oligodendrocyte nuclei show an 11-fold increase in the transcriptional activity of glycerol phosphate dehydrogenase in response to hydrocortisone but no increase in transcription of myelin basic protein or proteolipid protein. These results indicate that during early myelinogenesis, glucocorticoids influence the expression of key oligodendroglial markers by different processes: The expression of glycerol phosphate dehydrogenase is regulated at the transcriptional level, whereas the expression of myelin basic protein and proteolipid protein is modulated via a different, yet uncharacterized, mechanism involving post-transcriptional regulation.

Animals↗
PubMed1988

Expression of glial fibrillary acidic protein by differentiated astrocytes is regulated by serum antagonistic factors.

We report here that, in culture, the expression of glial fibrillary acidic protein (GFAP) by astrocytes, as well as their shape (flat-polygonal vs. stellate) can be regulated by 4 serum antagonistic factors. Three of these factors are stimulatory, while the fourth exerts an inhibitory effect upon these astrocytic properties. As suggested by temperature and trypsin treatments, the inhibitory factor is a polypeptide or a protein of 15-35 kDa. The stimulatory factors are smaller: two of them have a mol. wt. between 0.2 and 5 kDa; the third is smaller than 0.2 kDa. Treatments with chloroform/methanol, ammonium sulfate, neuraminidase, and papain, indicate that at least one glycolipid and one glycoprotein are involved. We speculate that, during development, cells from the astrocytic line could be susceptible selectively to one or another of these factors, which would explain their great plasticity.

Animals↗
PubMed1988

Serum contains inducers and repressors of oligodendrocyte differentiation.

An important stage in oligodendrocyte development is the expression of galactocerebroside (GC), the major glycolipid in myelin. Although oligodendrocyte cell lineage and differentiation in vitro have been the object of many studies, to date there is sparse information on the regulation of GC expression in oligodendrocytes already committed to be positive for GC. We report here that GC expression in these cells is controlled by three serum factors. Two of these, possibly a lipoprotein and a mucoprotein, increase GC levels, whereas the third, probably a glycoprotein, exerts an inhibitory effect. The developmental increase of GC in postnatal rat brain cerebral cultures and its induction by serum factors are reversible phenomena. The isolation of the GC-regulatory factors would allow experimental manipulation of impaired GC expression by differentiated oligodendrocytes.

Animals↗
PubMed1988

The "stress analogy" in the context of psychoneuroimmunology.

The "stress analogy" is examined from the perspective of psychoneuroimmunology. Arguments are presented that do not support a linear and mathematical conception of psychosocial stress, as defended by the "stress analogy" concept. Implications for the study of schizophrenia are discussed.

Adaptation, Psychological↗
PubMed1987

Interleukin-2 inhibition of oligodendrocyte progenitor cell proliferation depends on expression of the TAC receptor.

Interleukin-2 (IL-2) has been shown to inhibit oligodendrocyte progenitor cell proliferation. Within the immune system, IL-2 biological action is dependent strictly on the expression of the IL-2 receptor. The antibody TAC, which specifically binds the lymphocyte IL-2 receptor, has been shown to also bind oligodendrocyte progenitor cells cultured in a serumless, chemically defined medium. The expression of the TAC antigen was found necessary for IL-2 inhibition of oligodendrocyte progenitor cell proliferation. After IL-2 induced down-regulation of the TAC antigen, the progenitor cell was unresponsive to IL-2, even 72 hr after IL-2 withdrawal. During this unresponsive period, the oligodendrocyte progenitor cell was immunocytochemically negative for the TAC antigen. Thus, in contrast to IL-2 receptors on T-cells, IL-2 does not up-regulate its receptor on oligodendrocyte progenitor cells. However, upon interleukin 1 (IL-1) addition both IL-2 responsiveness and TAC immunocytochemical staining reappeared. These data suggest that IL-2 inhibition of progenitor cell proliferation depends on the expression of the TAC antigen, which can be regulated by IL-1.

Animals↗
PubMed1986

Synthesis of a myelin-like membrane by oligodendrocytes in culture.

We have prepared highly purified cultures of rat oligodendrocytes by a modification of the procedure of McCarthy and de Vellis [1980]. By utilizing a substratum derived from lysed glia and a calf serum-containing medium with a high concentration of transferrin, the oligodendrocyte cultures display a high degree of purity, the ability to survive several months of culture, and a striking ability to produce a myelin-like membrane. We have examined the production of this myelin-like membrane using immunocytochemical and biochemical probes as well as an extensive morphological examination at the electron microscopic level. The membrane appears to be produced in a similar developmental pattern to that observed in vivo and it has the structural characteristics of loosely packed central nervous system myelin.

Animals↗
PubMed1986

Regulation of myelin basic protein in oligodendrocytes by a soluble neuronal factor.

Myelin basic protein (MBP) is one of the most important myelin components. Based on our previous studies, we hypothesized that neurons might have regulatory effects on the production of MBP by oligodendrocytes, and we conducted studies designed to verify this hypothesis. Oligodendroglia-rich cultures from total brain of neonatal rats or mice and pure cultures of embryonic rats or chicks were prepared. Cultures of mouse fibroblasts and astrocytes were prepared as well. We show here that MBP production by oligodendrocytes was greatly enhanced by treatment with either pure neurons, rat neuronal conditioned medium, or chick neuronal conditioned medium, while chemically defined, hormonally supplemented medium or medium conditioned by astrocytes and fibroblasts had no effect on MBP expression. We conclude that the production of MBP by oligodendrocytes is regulated by a nonspecies specific soluble neuronal factor. The conservation of this phenomenon from avian to rodent species implies its critical role in myelination and suggests its potential application as a treatment in demyelination.

Animals↗
PubMed1985

Binding and internalization of lysosomal enzymes by primary cultures of rat glia.

Highly purified cultures of rat astrocytes and oligodendrocytes were examined for their ability to bind and internalize lysosomal enzymes. Astrocytes displayed a saturable uptake of beta-glucosidase and beta-galactosidase. The uptake was specifically inhibited by mannose-6-phosphate but not by several other sugars or sugar phosphates, indicating that the process was mediated by mannose-6-phosphate receptors. When cells were allowed to take up 125I-beta-glucosidase for 1 hr at 37 degrees C and subcellular organelles were isolated, the enzyme was shown to comigrate with a lysosomal organelle marker enzyme, suggesting that the enzyme was targeted to lysosomes. Astrocyte receptors were probed directly by binding of 125I labeled beta-glucosidase to astrocyte membranes at 4 degrees C. Binding was saturable and competitively inhibited by mannose-6-phosphate. In contrast to the astrocytes, cultured oligodendrocytes showed no specific binding or uptake of the lysosomal enzymes. Immunocytochemical staining of mixed glial cultures supported the biochemical data; only the astrocytes stained positive with anti-mannose-6-phosphate receptor antibodies.

Animals↗
PubMed1983

Regulation by glucocorticoids of rat-liver phenylalanine hydroxylase in vivo.

Phenylalanine hydroxylase, a liver-associated enzyme, is induced markedly by glucocorticoids in two permanent rat-hepatoma cell lines. In order to gain evidence that this phenomenon also occurs in vivo, we examined the effect of adrenalectomy and/or hormone supplementation on the levels of phenylalanine hydroxylase in the livers of adult rats: glucocorticoid administration increases, and adrenal ablation reduces, the activity of the hepatic enzyme, and the diminution occurring in the latter instance is entirely prevented by concurrent hormone replacement. These results thus corroborate earlier findings from a single experiment and are consistent with the hypothesis that adrenal corticosteroid hormones participate in modulating phenylalanine-hydroxylase levels within the diploid hepatocyte.

Adrenalectomy↗
PubMed1981

Translation of phenylalanine hydroxylase-specific mRNA in vitro: evidence for pretranslational control by glucocorticoids.

We have found that the induction of phenylalanine hydroxylase by hydrocortisone and serum in confluent cultures of H4-II-E-C3 rat hepatoma cells is accompanied by an increase in polysomal mRNA specific for phenylalanine hydroxylase, as measured by translation in a cell-free protein-synthesizing system. Thus, the induction is mediated largely, if not entirely, by a pretranslational mechanism, possibly by stimulation of the transcription of the phenylalanine hydroxylase gene.

Animals↗
PubMedDate not supplied

Cocaine blunts human CD4+ cell activation.

Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of enriched CD4+ T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections.

Antigens, CD↗
PubMedDate not supplied

Effects of intravenous and oral dexamethasone on selected lymphocyte subpopulations in normal subjects.

Our studies describe the effects of 1 mg oral (PO) and intravenous (IV) administration of dexamethasone (DEX) on certain subpopulations of circulating lymphocytes in normal subjects. We compared the outcomes of PO and IV DEX administration because of individual differences in gastro-intestinal absorption of DEX and the issue of noncompliance in patients undergoing the dexamethasone suppression test (DST). Both routes of DEX administration were equally effective in suppressing plasma cortisol levels below 5 micrograms/dl, the customary criterion level. Both routes of DEX administration also significantly decreased the percent and absolute number of CD4+ cells, the CD4+/CD8+ ratio, and the percent and absolute number of virgin, but not of memory, CD4+ cells.

Administration, Oral↗
PubMedDate not supplied

Selective effects of fetal alcohol exposure on rat thymocyte development.

The thymoproliferative response to concanavalin A (ConA) following fetal alcohol exposure (FAE) is higher than control (149%) on day 44, is lower than control (64%) by day 51, and normalizes by day 69 (88% of controls). The ontogeny of HLA-Dr and transferrin receptor (CD71) expression in response to anti-CD3 stimulation is similar among the groups, but is distinct from that of ConA proliferation. The ontogeny of glucocorticoid cytoplasmic receptor (GCCR) sites per thymocyte is also different from the ontogeny of the ConA response. The number of GCCR sites rises sharply (2.5-fold) in control rat thymocytes between days 30 and 44, and remains at that level at later time points. By contrast, the number of GCCR sites per FAE thymocytes rises nearly linearly and normalizes by day 72. Our data support the notion that prenatal alcohol exposure significantly alters thymic development and indicates that the relationship between the development of thymocyte functional responses and that of GCCR is more complex than initially hypothesized.

Animals↗
PubMedDate not supplied

Effect of acute dietary restriction on the colonization of MADB106 tumor cells in the rat.

The effects of acute food restriction (i.e. 24-72 h) on (1) the colonization of MADB106 tumor cells; (2) the response of specific T cell subsets in peripheral blood (i.e. CD4+ and CD8+ cells), and (3) natural killer cell activity (NKCA) in the spleen were studied in the Fischer 344 rat. Previous studies have demonstrated that the spread of this tumor cell is enhanced by exposure to an acute stressor within 24 h of tumor inoculation. Consistent with these reports, 72-hour food restricton after tumor inoculation enhanced colonization of tumor cells to the lungs when assessed 4 weeks after inoculation. Food restriction was found to markedly influence the percentage of T cell subsets (i.e. CD4+ and CD8+ cells) and NKCA in the early (24-72 h) postinoculation stage. At 72 h after inoculation, food restriction was associated with a significant reduction in the percentage of CD4+ cells in tumor- or saline-inoculated animals. The percentage of CD8+ cells was significantly increased at 24 and 72 h after tumor inoculation in ad libitum, but not in food-deprived animals. NKCA at 72 h was significantly reduced in saline-treated food-deprived animals compared to animals fed ad libitum. Given that glucocorticoids are typically increased during acute food deprivation and that glucocorticoids are in some instances associated with depressed NKCA, the present study investigated whether there was a relationship between plasma glucocorticoid levels (i.e. corticosterone) and NKCA; however, no significant relationship was found. In conclusion, the present findings demonstrate that 72-hour food deprivation is associated with enhancement of tumor metastasis. This outcome is mediated, at least in part, by the modulatory effect of the physiological response to acute food restriction upon the distribution of circulating T cells and NKCA in the spleen during the early (24-72 h) postinoculation phase.

Adenocarcinoma↗