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P Bongioanni

Publications and source records attributed to P Bongioanni.

32 records · Page 2Linked to original sources
PubMed1997

T lymphocyte benzodiazepine binding is reduced in demented patients.

Blood cells, especially platelets and lymphocytes, are used in neuropsychiatric research as tools for investigating systemic derangements in neuropsychiatric disorders, and as peripheral models for studying central nervous system biochemistry. In the present work, we determined T lymphocyte peripheral-type benzodiazepine binding: a significant reduction of Bmax values was observed in demented patients as compared with healthy controls, whereas Kd values were similar in the two subjects' groups. A significant negative correlation was found between Bmax values and illness severity. These data, which seem to be related to an impairment of immune response and cell energy metabolism in demented patients, may represent a state-dependent marker in monitoring disease course and treatment efficacy.

Aged↗
PubMed1997

T-cell tumor necrosis factor-alpha receptor binding in patients with multiple sclerosis.

MS is a T-cell-mediated demyelinating disease of the CNS, in which the cytokine network may be deranged, leading to an altered immunoregulation. Tumor necrosis factor alpha (TNF-alpha) is a cytokine with several effects on the neuroimmune system. There are specific TNF-alpha receptors on human lymphocytes and other cell types, even in the CNS. We assayed TNF-alpha binding on peripheral blood T cells from MS patients compared with healthy subjects. T cells from MS patients have significantly more TNF-alpha receptors than those from control subjects (Bmax, 955 +/- 31 versus 126 +/- 3 [mean +/- SEM] receptors per cell). Such TNF-alpha binding sites are of the same type in patients and healthy subjects (Kd, 68.7 +/- 4.8 versus 70.2 +/- 4.1 [mean +/- SEM]pM). We discuss these results in terms of MS immunopathogenesis, because activated T cells have increased amounts of TNF-alpha receptors.

Adult↗
PubMed1996

Monoamine oxidase molecular activity in platelets of parkinsonian and demented patients.

Platelet monoamine oxidase activity levels have been evaluated in several neuropsychiatric disorders, to identify biochemical markers for pathological brain functioning. In the present work, we assayed both total and molecular monoamine oxidase activity in platelets of parkinsonian and demented patients: both showed significantly higher enzyme activity values than healthy controls. Thus, high platelet monoamine oxidase activity levels seem to be related to an increased intrinsic activity of single enzyme molecules. A significant positive correlation was found between platelet monoamine oxidase activity and severity of illness in both disorders: monoamine oxidase activity, therefore, may be considered as a state-dependent marker for neuro-degeneration. Such findings are discussed with reference to central nervous system biochemical abnormalities in parkinsonian and demented subjects; it might be that in both Parkinson's Disease and in dementia of Alzheimer type some central biochemical changes are reflected in certain peripheral tissues (thrombocytes, for instance), or that a systemic derangement accompanies the cerebral involvement.

Aged↗
PubMed1996

T-lymphocyte immunointerferon receptors in patients with multiple sclerosis.

Multiple sclerosis (MS) is a T-cell-mediated autoimmune demyelinating disease of the central nervous system (CNS), associated with an altered immunoregulation. Interferon (IFN)-gamma, also known as immune IFN, is a cytokine with several effects on the immune system. Specific IFN-gamma receptors have been found on human lymphocytes, as well as on other cell types (e.g. gliocytes), even in the CNS. The aim of the present study was to evaluate IFN-gamma binding on peripheral blood T-lymphocytes from MS patients, compared with those from healthy subjects. Thirty-two patients were selected according to the classical criteria for definite MS; as controls, 21 healthy subjects were studied. We have found that T-lymphocytes from MS patients bear a significantly smaller amount of IFN-gamma receptors than those from controls [Bmax: 568, 18 vs 708, 14 (mean, SE) receptors/ cell]. Such IFN-gamma binding sites are of the same type in patients and healthy subjects [Kd: 1.0, 0.05 vs 0.9, 0.02 (mean, SE) nM]. These findings are discussed in terms of immunopathogenesis of MS, since it has been reported that activated T-lymphocytes have decreased amounts of IFN-gamma receptors.

Adult↗
PubMed1996

Platelet phenolsulphotransferase activity, monoamine oxidase activity and peripheral-type benzodiazepine binding in demented patients.

Blood platelet phenolsulphotransferase and monoamine oxidase activities, as well as platelet peripheral-type benzodiazepine binding have been studied in several neuropsychiatric disorders, in order to identify biochemical markers for altered brain functioning. In the present work, we determined platelet phenolsulphotransferase and monoamine oxidase activities in demented patients: they showed significantly higher phenolsulphotransferase and monoamine oxidase activities than controls. A significant positive correlation was found between enzyme activities and severity of illness. In the same subjects, we evaluated platelet peripheral-type benzodiazepine binding: a significant reduction of Bmax values was observed in demented patients, whereas Kd values did not substantially differ between the two subject groups. These findings are discussed with reference to central nervous system biochemical abnormalities of demented subjects: it may be that in Dementia of Alzheimer type either some central biochemical changes are reflected in certain peripheral tissues (such as platelets), or a systemic derangement occurs together with a cerebral involvement.

Aged↗
PubMed1996

Lymphocyte subsets in multiple sclerosis. A study with two-colour fluorescence analysis.

Multiple sclerosis (MS) is postulated to be an immunopathologically mediated disease. This concept is supported by the finding of abnormally distributed peripheral blood T-cell subsets and a decreased T-suppressor function. Thirty-seven MS patients have been selected according to the criteria for definite MS. Fluorescein- or phycoerythrin-conjugated monoclonal antibodies have been used to define different lymphocyte subsets: CD4+, CD5+, CD8+, CD19+, CD38+, CD45RA+, CD4+CD45RA+, CD19+CD5+, CD8+CD38+. In relapsing-remitting (RR)-MS patients a significantly decreased percentage of CD19+ cells and in progressive MS patients a significantly increased percentage of CD19+CD5+ cells have been found. During a relapse in RR-MS, a significantly decreased percentage of CD4+CD45RA+ cells and a significantly increased percentage of CD8+CD38+ cells have been observed. Moreover, in RR-MS patients a significantly increased percentage of CD38+ cells and significantly high IgM amounts have been found. The increased percentage of CD19+CD5+ and CD38+ cells (together with high IgM levels) and the reduced percentage of CD4+CD45RA+ lymphocytes could be related to an activation of both cellular and humoral immune response in acute MS.

Adolescent↗
PubMed1993

The human-severe combined immunodeficiency myasthenic mouse model: a new approach for the study of myasthenia gravis.

We have established a new chimeric human-mouse model of myasthenia gravis in severe combined immunodeficiency mice, using human peripheral blood lymphocytes that survive in the mouse and produce specific antibodies that mediate pathological changes typical of human myasthenia gravis. Mice given peripheral blood lymphocytes from both anti-acetylcholine receptor (AChR) antibody-positive and -negative patients with myasthenia gravis showed circulating anti-acetylcholine receptor antibodies, deposition of human IgG at muscle end-plates, and simplification of the postsynaptic membrane, findings characteristic of human myasthenia gravis. Mice given human peripheral blood lymphocytes from healthy donors and simultaneously immunized with Torpedo acetylcholine receptor showed the same changes. This chimeric model, utilizing human cells to reproduce the immunopathological findings of human myasthenia gravis in a nonhuman environment, offers new opportunities to study immune regulation in autoimmunity.

Adult↗
PubMed1991

Human blood platelet as research tool in neuropsychopharmacology.

The use of blood platelets as a nerve terminal model for serotonin is well documented. However, it is clear that the use of platelets as a model can be justified only for those parameters where it may be shown that blood platelets and neural cells share almost identical features. The excellent similarity between the serotonin transport mechanisms in platelets and in nerve terminals, and the existence of various receptors for biogenic amines, peptides and substances with neuronal activity on platelet membrane offer a really unique opportunity to utilize blood platelets as a system for drug evaluation. In our work platelet benzodiazepine binding sites and their modulation by different benzodiazepines in normals and in demented patients are examined.

Adult↗
PubMedDate not supplied

Platelet monoaminooxidase activity and behavioural characteristics in humans.

We investigated the possible relationship between platelet MAO activity and behavioural characteristics, measured by MMPI, in a group of 19 healthy volunteers. The results showed that high MAO activity tended to be typical of subjects with inhibitory characteristics and that low MAO activity was more typical of uninhibited subjects.

Adult↗
PubMedDate not supplied

[T-cell interferon-gamma, tumor necrosis factor-alpha and interleukin-6 receptor binding in patients with multiple sclerosis. Effects of interferon-beta-1b treatment].

INTRODUCTION: Multiple sclerosis (MS) is a T-cell-mediated demyelinating disease of the central nervous system (CNS), in which the cytokine network may be deranged. Interferon (IFN)-gamma, interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha are cytokines with several effects on the neuroimmune system. Specific IFN-gamma, IL-6, and TNF-alpha receptors have been found on human lymphocytes and other cell types. PATIENTS AND METHODS: We assayed IFN-gamma, TNF-alpha, and IL-6 binding on peripheral blood T cells from MS patients, as compared with healthy subjects. T cells from MS patients have significantly less IFN-gamma receptors, and more TNF-alpha and IL-6 receptors than those from controls. Such receptors are of the same type in patients and healthy subjects. By comparing MS patients' subgroups with each other, significant differences in mean Bmax values have been found between patients in a stable phase and those in relapse, and between stable patients and those in an evolutive phase. As far as IL-6 binding is concerned, significant differences in mean Bmax values were observed only between patients in stable phase and those in relapse. RESULTS: T lymphocytes from untreated MS patients, which had significantly smaller amounts of IFN-gamma receptors than those from controls, and more TNF-alpha and IL-6 receptors than controls showed a significant increase in IFN-gamma binding, and a significant decrease in TNF-alpha and IL-6 binding after a 3-month IFN-beta 1b treatment. T-cell IFN-gamma Bmax values were even higher, and those of TNF-alpha and IL-6 were lower after 6 months. CONCLUSION: We discuss these results in terms of MS immunopathophysiology, since activated T cells have decreased IFN-gamma, and increased TNF-alpha and IL-6 receptor amounts.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Neuroimmunomodulation. The bi- and unilateral correlations between the nervous system and the immune system].

The nervous system-immune system relationships, namely the modulatory effects of the former upon the latter and vice versa, have been considered both in physiological and pathological conditions. The nervous system communicates with the immune system in two biochemical ways, by means of neurohormones and neurotransmitters, using anatomical and functional pathways related to the pituitary system (the manifold endocrine axes between hypophysis and peripheral endocrine glands) and autonomic system (especially the orthosympathetic one, and to much lesser extent the parasympathetic system). The immune system is able to modulate some nervous functions via cytokines, peptidic molecules produced by immunocytes, that can also be secreted in certain conditions by neural cells, such as astrocytes, microgliocytes and even neurons. The knowledge of physiology of the neuroimmunomodulation and related pathological changes may be very useful for understanding the pathogenesis and the pathophysiology of neuroimmunological diseases, and for their diagnosis and treatment.

Animals↗
PubMedDate not supplied

[Immunohistochemical study of the enteric glia in chronic intestinal inflammatory disease].

Enteric glial cells, strictly associated with enteric neurons to build up enteric ganglia, belong to the enteric nervous system (ENS), which coordinates many bowel functions. The ENS is spread throughout the gut in myenteric and submucosal plexuses. In our research work, we studied immunohistochemically the ENS in two typical chronic inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), by using specific antibodies against gliocyte (S-100) and neuronal (neurofilaments, NF) markers. We found high S-100 immunoreactivity within the submucosal and muscular layers in samples from CD patients, but not as such in those from UC patients; similar results were also achieved using anti-NF antibodies. Moreover, immunohistochemistry has pointed out that alterations of the ENS are associated, in CD more than in UC, with the expression of major histocompatibility complex class II antigens on components of the ENS, especially on enteroglial cells. These data suggest that histopathological differences exist between CD and UC also within the ENS, especially as far as the glial cells are concerned. Such ENS changes might significantly contribute to the immunopathogenesis and immunopathophysiology of chronic inflammatory bowel diseases.

Colitis, Ulcerative↗