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F Mercuri

Publications and source records attributed to F Mercuri.

33 records · Page 2Linked to original sources
PubMed1995

Host cell antigenic profile acquired by HIV-1 is a marker of its cellular origin.

HIV-1 acquires cell membrane proteins during budding. The cell membrane proteins (CMP) profile of laboratory HIV-1 strains grown in different host cells was established, by using an immobilized antibody capture (IAC), to verify whether CMPs present on HIV-1 correlate with its host cell origin. HIV-1 grown in different cell lines incorporates cell markers such as CD3, CD19, CD14, CD31 and IL 2-R, according to the distinctive expression of these antigens on the host cells. Furthermore, also T-tropic and monocytotropic HIV-1 strains display host cell specific markers, supporting the hypothesis that virus associated CMPs are a marker of host cell origin.

Antigens, CD↗
PubMed1994

Interferon expression in Crohn's disease patients: increased interferon-gamma and -alpha mRNA in the intestinal lamina propria mononuclear cells.

The in vivo interferon (IFN) activation in Crohn's disease was evaluated by measuring the relative amounts of IFN-alpha and -gamma mRNA in freshly isolated human lamina propria mononuclear cells (LPMC) from patients with Crohn's disease and controls. Both IFN-gamma and IFN-alpha mRNA, as estimated by dot blot analysis, were increased in Crohn's disease (LPMC), although the relative amounts of IFN mRNA appeared to differ among patients. Appreciable amounts of IFN-gamma mRNA were found in Crohn's disease peripheral blood mononuclear cells (PBMC) extracts, whereas the same cells were negative for IFN-alpha mRNA. Only minute amounts of IFN-gamma RNA were found sporadically in control LPMC while no IFN-alpha was detected. Control PBMC were shown to be virtually negative for both IFN-alpha and IFN-gamma mRNA. These data suggest that IFN induction in the normal human gut is a well-controlled function and that in Crohn's disease tissues, both IFN-gamma and IFN-alpha production are dysregulated. The increased IFN activity may represent a major feature in the induction and perpetuation of the chronic inflammatory process in Crohn's disease.

Crohn Disease↗
PubMed1993

Coordinate induction of interferon alpha and gamma by recombinant HIV-1 glycoprotein 120.

Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-alpha and -gamma molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-gamma, the presence of IFN-gamma was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-gamma appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production. Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-alpha and -gamma observed in AIDS patients.

Cell Adhesion Molecules↗
PubMed1992

Acid lability is not an intrinsic property of interferon-alpha induced by HIV-infected cells.

Human immunodeficiency virus (HIV)-infected cells induce acid-labile interferon-alpha (al-IFN-alpha) in cultures of mononuclear cells from peripheral human blood. We have investigated the physiochemical properties of such preparations to elucidate the reasons for acid-lability of this IFN. Al-IFN-alpha is a mixture of both glycosylated and unglycosylated molecules as shown by separation on Concanavalin-A Sepharose. Acid-lability is associated only with glycosylated molecules. Upon chromatography of the glycosylated fraction on Sepharose coupled to IFN-alpha-specific antibody, the portion of the IFN that is retained and eluted with guanidine-HCl is acid-stable, whereas the excluded antiviral activity is acid-labile, and is partially neutralized by antibodies to either IFN-alpha or IFN-gamma. Also, upon further purification of the unglycosylated fraction on the same antibody column, all antiviral activity remains indistinguishable from conventional IFN-alpha. Reconstitution experiments showed that glycosylated material excluded from the anti-IFN-alpha column potentiates antiviral activity of the IFN that is specifically retained by the column. This potentiation is abolished by acid treatment. Similar results are obtained with al-IFN-alpha from the serum of acquired immunodeficiency syndrome (AIDS) patients, indicating that its acid-lability is also the consequence of an acid-labile component that is capable of enhancing the antiviral activity. The potentiation of antiviral activity obtained by combining recombinant preparations of IFN-alpha and IFN-gamma suggests that the cooperating molecule is IFN-gamma.(ABSTRACT TRUNCATED AT 250 WORDS)

Acids↗
PubMed1992

Interferon-alpha (IFN-alpha) production by human intestinal mononuclear cells. Response to virus in control subjects and in Crohn's disease.

The virus induced production of interferon alpha by human intestinal lamina propria mononuclear cells was investigated. Intestinal and autologous peripheral cells from control subjects and patients with Crohn's disease were cultured in vitro with and without stimulation with the Newcastle disease virus. Interferon alpha was measured and characterised in the culture supernatants after 12 hours and the kinetics of production was evaluated over the following four days of culture. No detectable interferon alpha was found in cultures of unstimulated intestinal and autologous peripheral mononuclear cells from controls and Crohn's disease whereas interferon alpha was released in all cultures stimulated with the virus. In all 12 hours experiments in both groups, virus stimulated intestinal mononuclear cells yielded significantly less interferon alpha than the autologous peripheral cells. The kinetics experiments showed that control intestinal mononuclear cells appeared to be poorly responsive to virus stimulation showing a release of interferon alpha significantly lower than that of the autologous peripheral cells. The interferon alpha release at day 4 by control cells (either intestinal or peripheral) did not differ from that measured after the first 12 hours. In contrast, the interferon alpha produced by Crohn's disease cells progressively increased during the culture period and the amount of interferon alpha measured at day 4 was significantly higher than that released at 12 hours. These data suggest that normal human intestinal mononuclear cells are down regulated in their capability of producing interferon alpha and that in Crohn's disease their activation for this function is enhanced. These data also suggest that in Crohn's disease intestinal mononuclear cells exhibit a transient hyporesponsiveness to in vitro stimulation possibly related to massive in vivo exposure to interferon alpha inducers.

Cells, Cultured↗
PubMedDate not supplied

Membrane interactions involved in the induction of acid labile interferon alpha.

Human normal peripheral blood mononuclear cells (PBMC) produce acid-labile interferon (IFN) alpha when stimulated in vitro with HIV-infected cells fixed with glutaraldehyde. The cells responsible for IFN production are mainly B lymphocytes. The present study was aimed to further elucidate the cellular source of this IFN and to analyze the membrane interactions involved in the induction process. To this purpose PBMC were stimulated with inducers of acid labile IFN alpha in the presence or absence of a panel of monoclonal antibodies (MoAbs) against antigens of the lymphocyte membrane, namely HLA Class I and II and CD4. The results indicate that both HLA Class II and CD4 antigens are involved in the induction process. Conversely B cell lines seem capable of producing conventional alpha IFN but they fail to produce acid labile IFN alpha even in the presence of cooperating CD4 positive T cell lines. Furthermore PBMC cultured for more than 20 hours prior to stimulation lose the ability to produce acid labile IFN alpha, while remaining fully capable of producing conventional IFN alpha and gamma. It remains to be established whether this phenomenon reflects the disappearance of some membrane structure necessary for acid labile IFN alpha induction, or whether it is due to some early appearing functional alteration of B cells.

Antibodies, Monoclonal↗