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Biomedical subjects

A Dolei

Publications and source records attributed to A Dolei.

At least 37 records · Page 2Linked to original sources
PubMed1994

Mutual interactions between HIV-1 and cytokines in adherent cells during acute infection.

The production of cytokines by HIV-infected cells from adherent tissues as well as their effects on HIV replication in the same cells were investigated. CD4-transfected HeLa-T4-6c epithelial cells, CD4-positive normal lung fibroblasts and CD4-negative RD rhabdomyosarcoma cells were infected with HIV-1. All cultures were permissive for virus replication, which was completed within 48-72 h by Hela-T4-6c and RD cells and 2-3 weeks in normal fibroblasts. During the course of HIV replication, a series of cytokines (particularly IL-6 and TNF alpha) was produced and released in parallel to the peak of virus growth, in amounts varying with the cell system studied. Treatment of cultures with recombinant cytokines given at concentrations in the range of those induced by HIV-1 indicated that IL-6 and TNF alpha caused an increase of: i) CD4 expression, ii) HIV absorption to uninfected cells, and iii) release of infectious virions by infected cells. The fact that HIV-1 absorption and spread can be mediated by HIV-induced cytokines may be relevant in the pathogenesis of the in vivo disease, as it may constitute a possible self-enhancing model of HIV infection also in the solid tissues.

CD4 Antigens↗
PubMed1994

Infectious virus with reduced cytopathogenicity resulting from persistent infection of normal lung fibroblasts by HIV type 1 strains.

We asked whether HIV-1 had the capacity to establish a persistent infection of cultured human diploid fibroblasts. Human strains of normal diploid embryo lung fibroblasts were infected with HIV-1 of the HTLV-IIIB and HIV-1P1 strains. Infection was followed over time, to analyze HIV expression. Virus production (intra- and extracellular virus) was evaluated as follows: ability to form syncytia in the C8166 T cell line, production of p24 and other viral antigens (ELISA and indirect immunofluorescence), search for a gag sequence in cell DNA by the polymerase chain reaction followed by hybridization to an HIV-1-specific probe (SK19). Cell-free culture supernatant was used as a virus source to infect de novo fibroblasts and C8166 T cells. Infection of cultured fibroblasts with either the HTLV-IIIB or HIV-1P1 strain led regularly to the establishment of persistently infected cultures. Fibroblast cells were capable of continuous virus production for at least 10 months. The released virus was capable of reinfecting cultured fibroblasts and of producing cytopathic effects in the C8166 T cell line. However, when compared to wild-type strains, the infectious virus derived from fibroblasts showed a prolonged replication cycle and a decreased ability to form syncytia in the T cell line. Therefore, HIV-1 can establish a persistent and productive infection in normal lung fibroblasts. The data are consistent with the hypothesis that in vivo, at least in the lung, fibroblasts may represent a virus reservoir and that infection of these cells may lead to the production of attenuated variants of HIV.

Cell Line↗
PubMed1993

Ferritin downregulation in HIV-infected cells.

Levels of serum ferritin are increased in AIDS patients in relation to the progression of the disease. To establish whether or not this in vivo increase could be due to a direct effect of the virus on the infected cells, three HIV-permissive cell lines, the CD4-positive HeLa-T4-6c and C8166 cells and the CD4-negative RD cells, were infected with HIV-1 strains. The expression of ferritin was followed during the course of acute infection, in parallel to other cellular components. Unexpectedly, all three cell lines showed a phase of decrease in their ferritin content after infection by HIV-1, not justified by the modest and late increase of ferritin in the fluids, due to disruption of infected cells. Since ferritin is involved in the control of cell growth and DNA synthesis, its downregulation may be implied both in cell toxicity and DNA abnormalities due to HIV infection.

CD4 Antigens↗
PubMed1992

Interferon-alpha/beta in virus-induced mouse mammary carcinogenesis: effects on the spontaneous process and on the progression of transplanted pre-neoplastic lesions.

Low levels of anti-viral activity, mainly interferon alpha/beta (IFN-alpha/beta), are regularly found in lymphoid tissues of BALB/c mice infected with the C3H strain of mammary tumor virus. At the time of tumor development, significant amounts of anti-viral activity were detected in homogenates of spleen and mammary tumors, but not in blood and normal mammary glands. This activity is pH2-resistant and neutralized by antibody to IFN/alpha-beta. The pathogenetic role of IFN in mammary carcinogenesis was investigated in 2 ways: (a) by treating virus-infected newborn mice with antibody to IFN-alpha/beta, and (b) by giving either the latter antibody or IFN-alpha/beta to virus-free animals transplanted with pre-neoplastic lesions. Mice were treated only for 2 months, starting either 1 week after birth or immediately after tumor transplant. In case (a), treatment with antibody to IFN-alpha/beta shortened the incubation period of mammary carcinomas and decreased the mean survival time. In case (b), anti-IFN antibody did not significantly affect the development of mammary tumors. However, exogenous IFN-alpha/beta markedly reduced both tumor incidence and mortality rate. These results indicate that endogenous IFN-alpha/beta plays a crucial role in the in vivo restriction of the early infectious phase of spontaneous carcinogenesis and that relatively high doses of IFN-alpha/beta may inhibit the progression of pre-neoplastic lesions.

Aging↗
PubMed1992

Regulation of surface-differentiation molecules by epidermal growth factor, transforming growth factor alpha, and hydrocortisone in human mammary epithelial cells transformed by an activated c-Ha-ras proto-oncogene.

Spontaneously immortalized human mammary epithelial cells MCF-10A were transfected with an activated c-Ha-ras oncogene. Transfected cells (MCF-10T) acquire a malignant phenotype, as already reported. Studies of 125I-2'-deoxyuridine incorporation in cultures given graded doses of hydrocortisone (HC), cholera toxin (CT), epidermal growth factor (EGF), and transforming growth factor alpha (TGF-alpha) showed that though MCF-10T had become almost independent on exogenous EGF and TGF-alpha, they continued to respond to the synergistic effect of HC and CT plus EGF. Both lines were phenotypically characterized with an immunoradiometric assay in live cells. Expression of MHC class-I molecules, human milk-fat-globule-I antigen, and EGF receptor was reduced in ras-transfected cells, although other differentiation markers were unchanged. Exogenous EGF down-regulated the expression of functional EGF-R, selectively in transformed cells. TGF-alpha failed to modulate EGF-R. In contrast, HC strongly stimulated the expression of EGF-R while depressing MHC class-I molecules. Thus, it appears that in vivo HC may co-operate with TGF-alpha and EGF in promoting the growth of transformed mammary cells. This hormone might also favor the escape from immune surveillance by reducing the expression of surface differentiation markers.

Antigens, Differentiation↗
PubMed1988

Induction and regulation of cytotoxic T cells by microbial antigens and recombinant interleukin 2.

The proliferation and development of cytotoxic T cells was investigated in human peripheral blood mononuclear cell (PBMC) cultures stimulated with an antigenic extract from Candida albicans (MPPS), or with the purified protein derivative from Mycobacterium tuberculosis (PPD), or with human recombinant interleukin 2 (rIL-2). Microbial antigen- and rIL-2-induced cytotoxic T cells were able to lyse both natural killer (NK) sensitive and resistant targets. No correlation was observed between the development of T cell cytotoxicity and interferon (IFN) production in vitro. The addition of anti-class II monoclonal antibodies at the beginning of MPPS/PPD-stimulated cultures inhibited the cell proliferation, IFN production and T cell cytotoxicity, while all these cellular activities were not inhibited by anti-class II antibodies in rIL-2-stimulated cultures. Finally, antibodies to class I determinants inhibit T cell cytotoxicity, suggesting a role of such determinants in the development of the non-adaptive immunity to microbial infections.

Adult↗
PubMed1986

A new type of human interferon produced by peripheral blood mononuclear cells treated with inhibitors of transcription.

Peripheral blood mononuclear cells from human normal donors treated with inhibitors of transcription produce a protein with the properties of interferon (IFN) [activity against a broad range of viruses, species specificity, lack of blockade of virus attachment, capability to induce in cells durable antiviral state, establishment of antiviral state requiring ongoing protein and RNA synthesis, capability to induce 2',5'-oligoadenylate synthetase]. This IFN-like protein has a molecular weight of approximately 7000 daltons and is not neutralized by antibody to alpha-, beta-, and gamma-IFNs tested singularly or in a pooled fashion. Taken together the data suggest that this IFN-like protein may indeed be a new type of human IFN.

2',5'-Oligoadenylate Synthetase↗
PubMed1986

Direct and cell-mediated effects of interferon-alpha and -gamma on cells chronically infected with HTLV-III.

The replication of the human T lymphotropic retrovirus HTLV-III in persistently infected cells is relatively insensitive to the direct antiviral action of human interferon-alpha or -gamma (IFN-alpha or -gamma), showing only a two- to threefold reduction of HTLV-III, even though the host cells are very sensitive to IFN, as shown by vesicular stomatitis virus (VSV)-yield reduction assay (4-5 log reduction of VSV). However, IFN anticellular activity is strongly enhanced in the presence of normal peripheral blood mononuclear cells, suggesting a cell-mediated effect of IFNs.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Effects of dexamethasone on human natural killer cell cytotoxicity, interferon production, and interleukin-2 receptor expression induced by microbial antigens.

Dexamethasone inhibits the expression of the interleukin-2 receptor, the synthesis of immune interferon, and the development of natural killer cells when added to peripheral blood mononuclear cells cultured with soluble microbial antigens (purified protein derivative and a polysaccharide extract from Candida albicans [MPPS]) or human recombinant interleukin-2.

Antigens, Bacterial↗
PubMed1986

Regulation of immune interferon production during the response to soluble microbial antigens.

Human peripheral blood mononuclear cells (PBMC) stimulated in vitro with purified protein derivative (PPD) or with a Candida albicans polysaccharide extract (MPPS) released immune interferon (IFN) and interleukin 2 (IL-2). Kinetic studies showed a biphasic production of IFN with maximum levels at days 3-4 and days 5-6 of culture. In contrast, the IL-2 production is only observed at days 2-3 of culture. The relationship between IFN and IL-2, analysed both in responder and nonresponder PBMC cultures, showed that the early peak of IFN production appears to be IL-2 independent whereas the second peak seems strictly related to the presence of IL-2 culture. Furthermore, monoclonal antibodies against class I and class II products of the major histocompatibility complex (MHC) inhibited IFN production when added at the beginning of culture, whereas only anti-class I antibodies interfered with the release of IFN when added to antigen-primed lymphocytes.

Adult↗
PubMed1985

Differences in the expression and release of DR, BR, and DQ molecules in human cells treated with recombinant interferon gamma: comparison to other interferons.

This study presents a comparative analysis of the effects of different interferons (IFN) on the three recognizable subsets of human HLA class II molecules: DR, BR, and DQ. Both cellular expression and shedding of class II molecules have been determined on three different cell types. The results can be summarized as follows: class II molecules are markedly increased by IFN gamma; IFN beta has a lower enhancing effect, and IFN alpha has only a slight, if any, effect. Kinetically, the action of IFN gamma is prompter and longer lasting than that of IFN beta. DQ expression is much more enhanced by IFN gamma than either DR or BR; IFN beta has the same effect on all three subsets. Parallel changes of the cellular expression and of the shedding of these molecules are observed. A melanoma and a lymphoblastoid cell line and peripheral blood mononuclear cells show qualitatively similar modifications.

B-Lymphocytes↗