[Knee joint hematomas not due to accidents].
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Bone and Bones↗
Biomedical subjects
R Andreesen
Publications and source records attributed to R Andreesen.
[Is the healing of malacia of the semilunar bone possible?].
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Adult↗
[Proposal for simplification of occupational disease no. 42].
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Disability Evaluation↗
Defective monocyte to macrophage maturation in human immunodeficiency virus infection.
To look for possible defects in cells of the monocyte/macrophage system, blood monocytes from patients infected with human immunodeficiency virus (HIV) were cultured on hydrophobic Teflon for 7 days and their ability to differentiate into mature macrophages in the presence of serum was followed. The following parameters were studied as indicative of successful terminal maturation: (1) the expression of maturation-associated antigens (transferrin receptor, surface transferrin, the BA-2 antigen, MAX antigens), (2) the disappearance of the MOP15 antigen, and (3) a more than 20-fold increase in intracellular ferritin concentration. It was found that the patients' blood monocytes did not differentiate in vitro but rather remained immature precursor cells. If the same holds true in vivo, the results could indicate that the pathophysiology of the acquired immunodeficiency syndrome (AIDS) may be, to a large extent, linked with the functional consequences of this impaired monocyte-to-macrophage maturation.
AIDS-Related Complex↗
Infection of monocytes/macrophages by HIV in vitro.
Because of the very important role of the mononuclear phagocyte system in the immunopathogenesis of HIV infection, a culture system for in vitro studies of infection of monocytes/macrophages with HIV was developed. A method is described for the infection of human monocytes/macrophages cultured on hydrophobic membranes (Teflon) with different strains of HIV. The HIV isolates can be characterized according to their replication potential on monocytes/macrophages cultures. The biological properties of some HIV1 and HIV2 isolates are compared in lymphocyte and monocyte/macrophage cultures.
Acquired Immunodeficiency Syndrome↗
The polysulphated polyxylan Hoe/Bay-946 inhibits HIV replication on human monocytes/macrophages.
Due to the important role of monocytes/macrophages in the pathogenesis of AIDS, potential drugs with anti-HIV activity in lymphocytes must also be effective in monocytes/macrophages. For testing the efficacy of antiviral substances, monocytes/macrophages from peripheral blood were infected, respectively, with highly replicating HIV1 and HIV2 strains, thereby providing an extremely sensitive system of testing. Azidothymidine was found to inhibit both HIV types at 0.04 microgram/ml. The polysulphated polyxylan, Hoe/Bay-946 (MW 6,000 Daltons), which acts through a different mechanism and is being tested in clinical pilot studies in Germany, was also found to be effective against HIV1 and HIV2 in macrophages at concentrations of 10-50 micrograms/ml.
Acquired Immunodeficiency Syndrome↗
Effect of cytokines and lipopolysaccharides on HIV infection of human macrophages.
Human blood-borne monocytes (MO) differentiating into mature macrophages (MAC) were cultured on hydrophobic Teflon membranes. The cells were infected with two different monocytotropic HIV isolates: HIV1D117III obtained from a perinatally infected child, and HIV2D194 obtained from an AIDS patient who suffered exclusively from neurological symptoms. Virus production monitored by reverse transcriptase activity and HIV-antigen ELISA in cell-free supernatant was of a high level and continued for several weeks. To investigate possible modulatory pathways interfering with HIV infection in MAC we tested various recombinant cytokines as well as bacterial lipopolysaccharides (LPS) in our culture system. Whereas interleukin-1 (IL1) accelerated and increased HIV replication in MO/MAC, the interferons (IFN) alpha, beta and gamma effectively suppressed or delayed infection depending on the concentration used. Suppression was seen at concentrations as low as 0.3 U/ml and was most effective when the IFN were given prior to infection. No effect was observed with IL6 up to 2,000 U/ml. LPS affected virus infection in a complex manner: at 1-100 ng/ml virus replication was inhibited, but it was enhanced at subnanogram concentrations (25-100 pg/ml).
Cytokines↗
Differential effects of cell adherence on LPS-stimulated cytokine production by human monocytes and macrophages.
It is well known that adherence of monocytes (MO) to extracellular matrix substrates or tissue culture plastic activates these cells and induces the expression of a multitude of genes. Especially, it was described, that MO are primed by cell adhesion to produce higher amounts of some cytokines, e.g. interleukin (IL)-8 and tumor necrosis factor alpha (TNF-alpha). In order to investigate adherence-induced effects upon cytokine production, we seeded MO into tissue cultures and stimulated cells by lipopolysaccharide (LPS) simultaneously or at later time points. An increasing time-lag between cell adhesion and LPS-stimulation led to differential effects upon cytokine production: whereas TNF was upregulated (in accordance with reports by others), granulocyte colony-stimulating factor (G-CSF) was considerably down-regulated. In contrast, G-CSF production did not change, when cells were kept under non-adherent conditions in whole blood. In adherent cultures down-regulation of G-CSF could already be observed after two hours with a maximum after 24 h and was paralleled by a much lower abundance of G-CSF mRNA. Adhesion induced a significant suppression of G-CSF comparable to MO, if mature macrophages derived from MO in vitro were examined. Furthermore, two other cytokines, granulocyte-macrophage (GM)-CSF and IL-6, were also down-regulated following adhesion. In conclusion, activation of mononuclear phagocytes by adhesion can lead to "priming" for the production of some cytokines and at the same time to "silencing" for the production of others.
Cell Adhesion↗
Expression of macrophage products after in vitro infection of human monocytes/macrophages with HIV.
We studied the response of monocytes/macrophages (MO/MAC) to lipopolysaccharide (LPS) and interferon-gamma (IFN gamma) stimulation with respect to the expression of macrophage-specific products, i.e. macrophage-colony-stimulating factor (M-CSF), c-fms, c-sis, tissue factors, transforming growth factor-beta (TGF beta) and interleukin-8 (IL8) after in vitro infection with HIV. The expression of IL8 was strongly elevated in HIV-infected cells, peaking at 4 h after stimulation with LPS. At that time, the uninfected control showed only weak expression of IL8. Other products, e.g. tissue factor, c-fms, M-CSF and TGF beta were not modulated after stimulation. In contrast to IL8, the expression of c-cis was significantly lower in infected cells after stimulation with IFN gamma compared to uninfected control cells.
Base Sequence↗
Cytokine expression of HIV-infected monocytes/macrophages at the single-cell level.
Monocytes of healthy donors were infected with HIV1 in vitro: 14-21 days after infection 50-70% of the cells produced p24 HIV1 antigen as detected with anti-p24 immunostaining; infected cultures showed enhanced secretion of interleukin-6 (IL6), interleukin-8 (IL8) and tumour necrosis factor alpha (TNF-alpha). The expression of cytokines on the single-cell level was further analysed by in situ hybridization using nonradioactive digoxigenin for detection. HIV1 (p24+) -producing cells were compared with non-HIV (p24-) -producing cells. All morphological subtypes of macrophages showed HIV production; no difference in cytokine expression was observed. Immunocytochemistry of HIV-infected and uninfected cultures also showed no difference in the pattern of IL1-beta, IL6, IL8 and TNF-alpha protein expression in the cells.
Cytokines↗
Expression of heme oxygenase-1 protects endothelial cells from irradiation-induced apoptosis.
A common side effect of therapeutic use of ionizing irradiation is endothelial cell damage resulting in a variety of clinical complications. Thus, preservation of endothelial function after irradiation could potentially limit toxicity. Using the murine endothelioma cell line bEnd2 we show here that induction of heme oxygenase-1 (HO-1) by cobalt protoporphyrine IX (CoPP) inhibits irradiation-induced apoptosis. In contrast, HO-1 induction by tin protoporphyrine IX (SnPP), a HO-1 inhibitor, does not affect survival after irradiation. The protective effects of CoPP could be partially reversed by blockade of HO-1 function with SnPP after induction by CoPP. Vice versa, blockade of HO-1 function by SnPP was reversible using CoPP. Treatment with CoPP inhibited cytochrome c release induced by irradiation. These results demonstrate that HO-1 induction and activation prior to irradiation inhibits endothelial apoptosis and might be used for possible cell protection in vivo.
Animals↗
Adoptive immunotherapy of solid tumors with activated macrophages: experimental and clinical results.
Adoptive immunotherapy in cancer has been essentially restricted to the use of lymphoid effector cells (NK, TIL, LAK) stimulated with IL-2. Differentiated macrophages represent another key effector population even more important for the immune control of cancer. We have shown that activated murine macrophages reduced primary tumors and experimental metastases. Human macrophages differentiated from circulating monocytes and activated with IFN gamma (MAK) were cytotoxic in vitro for a variety of tumor cell and caused regression of human tumors implanted in nude mice. A large scale technology has been developed for the generation of antitumor macrophages. These MAK cells (10(8) to 10(9] were injected in cancer patients in pilot clinical trials and were well tolerated. MAK treatment is technically feasible, clinically safe and presents several advantages compared to other immunotherapies.
Animals↗
Studies on various parameters influencing leukemic cell destruction by alkyl-lysophospholipids.
Critical parameters of alkyl-lysophospholipid (ALP) induced destruction of freshly isolated human leukemic cells have been evaluated. The destructive activity of ALP is shown to be competitively inhibited by metabolizable lysophospholipids added to the cultures. It has also been found that destruction depends on the amount of serum present. Temperature and Ph strongly influence the cytotoxic activity of ALP. A slight decrease in temperature causes a reduction in cell death, whereas a temperature increase results in a marked potentiation. At low pH ALP cytotoxicity is inhibited. Incubation of cells with combinations of ALP and other cytotoxic drugs revealed a striking cytotoxic synergism with vinca-alkaloids, whereas corticosteroids retarded ALP induced cell destruction.
Acute Disease↗