Biomedical subjects
F Capsoni
Publications and source records attributed to F Capsoni.
Inhibition of polymorphonuclear leukocyte-mediated cytotoxicity by hydrocortisone "in vitro".
The effect of hydrocortisone (HC) on in vitro human polymorphonuclear leukocyte cytotoxicity was studied. HC was able to inhibit reversibly and in a dose-dependent way the antibody-dependent cellular cytotoxicity (ADCC) and the phytohemagglutinin-dependent cellular cytotoxicity (PDCC). The killing defect was partially overcome by increasing the antibody or the phytohemagglutinin (PHA) concentrations on the target cells. HC inhibited the PDCC more efficiently than ADCC; in fact the inhibition was present even at 10-5 M HC levels. Higher concentrations caused a progressive reduction in both tests. Inhibition of these PMN-mediated cytotoxicities may explain, in part, bot the anti-inflammatory actions of steroids and their deleterious effects on host defenses.
[Granulocyte function in patients in the acute phase of severe diseases].
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The role of superoxide anion generation in antibody-dependent polymorphonuclear leukocyte-mediated cytotoxicity.
Human polymorphonuclear leukocytes (PMNs) can act as killer cells in an antibody-dependent cellular cytotoxicity (ADCC) system. Cytolysis is rapid and detectable at low effector/target cell ratios. PMNs from a patient affected by chronic granulomatous disease (CGD) exhibit an absolute defect in ADCC. In order to investigate the role of the toxic oxygen derivatives (H2O2 and superoxide anions) lacking in CGD, experiments in presence of specific inhibitors were carried out. Superoxide dismutase, an O-2 scavenger, displayed a significant inhibition activity in a dose dependent way. On the other hand neither catalase, which degrades H2O2, nor sodium azide, a myeloperoxidae inhibitor, affect the cytotoxic activity. Our results suggest that the importance of the intact oxidative metabolism in PMN-mediated ADCC against chicken red blood cells could be referred to the correlated production of O-2 anions.
Cytotoxic mechanism in white blood cells.
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[Deficits of granulocytic function in pathology of adult and pediatric ages. (Personal observations and review of the literature)].
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IgG and C3 receptors on polymorphonuclear leukocytes in phagocytosis. Role of C3-receptors in the attachment and ingestion phases.
The role of IgG and complement (C3) receptors in the adhesion and ingestion phases of immune complexes by normal human polymorphonuclear leukocytes (PMN) were examined. The immune complexes were sheep red cells (E) sensitized with IgG (EA) or IgM antibodies plus complement (EAC'). Both types of receptor sites are involved in the adhesion phase. Moreover IgG receptors are primarily involved in the ingestion phase. Nevertheless even C3-receptors may be sufficient for complete phagocytosis. Even if EAC' adhesion was still high, C3-receptor specific phagocytosis decreased parallel with the amount of the complement used for EA19S sensibilization. The role of receptor sites on human PMN in adhesion and ingestion phases is discussed.
[Demonstration of a granulocyte defect in aged persons correlated with the presence of autoantibodies].
Assessment of PMN leukocyte function and search for autoantibodies were performed in 36 aged human subjects (more than 60 years of age) and in 15 younger controls (40 to 60 years of age). Autoantibodies were found in 15 of the 36 aged subjects, and in none of the controls. Leukocyte function defects were therefore correlated to old age and to markers of autoimmunity. Phagocytosis of bacteria was significantly impaired in both groups of old-aged subjects, irrespective to the presence or absence of autoimmunity. Intracellular killing of bacteria was shown to be normal in all the examined subjects. Nitroblue tetrazolium reduction by resting and latex-stimulated leukocytes was significantly impaired only in the group of old-aged subjects with autoimmunity. These leukocyte function defects are similar to those already described in human autoimmune diseases -- particularly S.I.E. -- and confirm the possible association between P.M.N. dysfunction and autoimmunity.
Letter: Phagocyte function in systemic lupus erythematosus.
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Leucocyte function after antenatal betamethasone given to prevent respiratory distress.
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Recurrent proximal white subungual onychomycosis associated with a defect of the polymorphonuclear chemotaxis.
Proximal white subungual onychomycosis (PWSO) is a rare form of nail infection that occurs almost exclusively in immunocompromised patients. Initially, in several reports, PWSO was described in ARC and AIDS patients. Later this pattern of onychomycosis was observed in patients with renal transplants, who received immunosuppressive therapy, and recently in a woman with active systemic lupus erythematosus (SLE) treated with systemic steroid therapy. We report a case of recurrent PWSO in a woman affected by a defect of polymorphonuclear chemotaxis. The association between PWSO and a defect of neutrophil chemotaxis, not yet described in the literature, suggests a point of discussion about the role of polymorphonuclear leucocyte functions in the defense mechanisms of the host affected by dermatophytosis. In this report the close association between PWSO and an immunocompromised condition is once again described. For this reason the authors emphasize the importance of investigating the common and uncommon causes of immunodeficiency in all patients affected by PWSO.
Successful treatment of pure red cell aplasia in systemic lupus erythematosus with cyclosporin A.
We report a patient with longstanding systemic lupus erythematosus (SLE) who developed pure red cell aplasia (PRCA). This condition is rare in connective tissue diseases and is reported in 32 previous cases of SLE in literature. Our patient recovered, apparently in response to treatment with high dosage of corticosteroids, but relapse occurred when the prednisone dosage was tapered down to 10 mg/day. The patient was successfully treated with cyclosporin A with no recurrence of the disease in the last 2 years.
CD69 expression on neutrophils from patients with rheumatoid arthritis.
OBJECTIVE: Since the early activation antigen CD69 has been implicated in the pathogenesis of some inflammatory diseases, we evaluated the expression of the molecule on peripheral blood (PB) and synovial fluid (SF) neutrophils obtained from RA patients and its possible correlation with PB and SF cytokine concentration. METHODS: CD69 membrane expression (and CD11b as control marker) was assessed by indirect immunofluorescence and flow cytometry analysis on purified PB and SF neutrophils. Cytokine levels (GM-CSF, IFN-gamma, TNF-alpha) in plasma and SF supernatants were measured by ELISA. RESULTS: CD69 was absent on control neutrophils, while it was expressed on PB neutrophils from RA patients although no detectable GM-CSF, IFN-gamma or TNF-alpha was observed in their plasma. CD69 expression was still more evident on SF neutrophils from RA patients; 59% had detectable levels of INF-gamma in their SF while GM-CSF and TNF-alpha were detectable in SF from 95% and 33% of RA patients, respectively. However, no correlation was observed between cytokine concentrations and CD69 expression on SF neutrophils. SF but not PB neutrophils from RA patients expressed increased amounts of CD11b when compared to control PB neutrophils without any correlation with CD69 membrane expression. CONCLUSION: The activation antigen CD69 is significantly expressed on PB and SF neutrophils from RA patients. However, the mechanism(s) of induction and its possible role in the pathogenesis of RA remain to be defined.
Thyroid acropachy: an unusual rheumatic manifestation of Graves' disease.
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Successful treatment of resistant Behçet's disease with etanercept.
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Immunostimulation of neutrophil phagocytic function by RU41740 (Biostim) in elderly subjects.
On this randomized, double-blind trial we investigated the effect of RU41740, a glycoprotein extracted from Klebsiella pneumoniae, on human neutrophil function after oral administration to elderly subjects with a previously demonstrated phagocytic defect. Six subjects were given RU41740 orally at a daily dose of 2 mg for one week the first month and of 1 mg for one week the second month, while six subjects received placebo. Already after the first week of treatment with RU41740 (T1) and more evidently 3 weeks after the last administration of the first course of therapy (T2), a significant improvement of the neutrophil phagocytic capacity was observed; at the time T2, as well as at the end of the second course of therapy (T3), the phagocytic capacity was completely restored with no differences between control and aged subjects. Similar results were obtained in the chemiluminescence assays. As expected, placebo had no significant effect on neutrophil functions. No significant differences were observed between the two group of elderly subjects for total or differential leukocyte number. These results suggest that RU41740 exerts, almost in part, its clinical effect, i.e. the prevention of recurrent infections, by stimulating blood neutrophil phagocytic function.
Clinical and laboratory findings in a new case of leukocyte adhesion deficiency.
We describe a child suffering from recurrent bacterial infections whose cells exhibited laboratory findings compatible with the leukocyte adhesion deficiency (LAD) syndrome. Surface marker analysis with monoclonal antibodies (MAbs) to the individual alpha and beta chains of LFA-1/Mac-1/p150,95 antigens revealed that the patient's neutrophils did not express the common beta chain and LFA-1/p150,95 alpha subunits, but reacted weakly with four different MAbs specific for the Mac-1 alpha chain; however, no glycoprotein was immunoprecipitated from the patient's cells using the same anti-Mac-1 alpha MAbs. Functional analysis of the patient's phagocytes revealed many of the defects in adherence-dependent functions (adherence, chemotaxis and phagocytosis) described in patients with LAD. The studies performed on the phagocytes of the patient's relatives showed normal phenotypes and function, suggesting the possibility of a non heritable form of disease in this family.
Polymorphonuclear leukocyte function in burned patients: effect of isoprinosine.
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