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At least 505 records · Page 28Linked to original sources
PubMed1991

Human alpha-fetoprotein (AFP) causes a selective down regulation of monocyte MHC class II molecules without altering other induced or noninduced monocyte markers or functions in monocytoid cell lines.

Human alpha-fetoprotein (AFP) purified from human amniotic fluid was investigated for its effect on human monocytoid cell lines, including U 937 cells with established subclones. The impact of AFP on the expression of surface markers (MHC class I and II, CD4, CD18, CD45, Fc receptors for IgG) was analyzed using known inducers of monocyte-macrophage differentiation such as phorbol esters and IFN-gamma. Furthermore we investigated the effect of AFP on the induction of macrophage antibody-dependent cell-mediated cytolytic activity (ADCC). AFP did selectively induce a rapid down regulation of surface MHC class II expression. No evidence of alterations was found in the endogenous or differentiation-induced expression of other markers on the surface on monocytes, nor did AFP affect the functional maturation of surface Fc receptors or the ability to express ADCC.

Antigens, CD↗
PubMed1990

Quantitative measurement of Fc receptor activity on human peripheral blood monocytes and the monocyte-like cell line, U937, by laser flow cytometry.

The expression of high affinity Fc receptors for IgG (FcRI) on the cell line U937 has been measured by flow cytometry, using fluorescein isothiocyanate-conjugated human IgG (FITC-IgG) calibrated spectrofluorimetrically against lasergrade fluorescein (Fl). A standard curve is presented, relating the effective fluorescence in terms of fluorescein equivalents per IgG molecule, to the degree of conjugation of FITC-IgG. The flow cytometer was calibrated with commercially available fluorescein-coupled latex beads. The quantitation of FcRI, in terms of sites per cell and affinity constants, was compared with a radioligand assay performed concurrently on the same cell population. Good agreement between the two assays was observed. The Fc receptors on peripheral blood monocytes were measured in unpurified lysed blood by gating on forward/side scatter. Monomer IgG binding to monocyte FcRII or FcRIII cannot be measured in direct IgG radioligand analyses because of the low affinity of these receptors and their low numbers per cell. However, flow cytometry may be employed for measuring both high and low affinity ligand-FcR interactions, using monomer FITC-IgG.

Antigens, Differentiation↗
PubMed1994

Induction of proto-oncogene and cytokine expression in human peripheral blood monocytes and the monocytic cell line THP-1 after stimulation with mycoplasma-derived material MDHM.

Mycoplasma fermentans-derived high-molecular-weight material (MDHM) was originally described to induce differentiation of murine thymocytes to cytolytic effector T-cells by stimulating IL-6 release from adherent cells. This study shows that human peripheral blood monocytes (PBMo) also respond to MDHM with increases in IL-1 beta, IL-6 and TNF alpha expression, both at the mRNA and protein level. The induced expression of IL-1 beta and TNF alpha mRNA in the monocytic THP-1 cell line increased as quickly as in primary cells. In contrast to PBMo, THP-1 and 14 other monocytic/myeloid leukemia-derived cell lines did not secrete measurable amounts of the cytokines upon treatment with MDHM. IL-1 beta and IL-6 genes contain AP-1 binding sites as regulatory elements, the AP-1 protein being composed of c-jun and c-fos gene products. In THP-1 cells c-jun mRNA expression increased after incubation with MDHM while positive c-fos expression remained unaffected. Although these data suggest AP-1 regulated cytokine mRNA expression, results from PBMo are not in accordance with this notion. In the primary cells MDHM-induced elevation of cytokine mRNA levels was preceded by a downregulation of c-fos expression while positive c-jun expression was not modulated. c-myc mRNA expression, constitutively high in THP-1 cells, was induced in MDHM-stimulated PBMo. In conclusion, MDHM-stimulated induction of cytokine mRNA expression was accompanied by different proto-oncogene responses in PBMo and THP-1 cells. These differences may represent different regulatory pathways of the two cell systems. Alternatively, these data support the notion that neither AP-1 nor the c-myc protein are involved in the MDHM-induced increase in IL-1 beta, IL-6 or TNF alpha mRNA levels. Furthermore, the present results demonstrate clearly that mycoplasma products can have a profound impact on the activation status of eukaryotic cells.

Bacterial Proteins↗
PubMed1991

Monocytic origin of fibroblasts: spontaneous transformation of blood monocytes into neo-fibroblastic structures in osteomyelosclerosis and Engelmann's disease.

We describe here two pathological situations, osteomyelosclerosis and Engelmann's disease, in which HLA-DR blood monocytes modulate to the fibroblastic class, in long-term culture. Monocytes/macrophages were identified by immunofluorescence, using monoclonal antibodies against surface markers (Leu M3, CD 68, and HLA-DR) and the neo-fibroblasts by electron microscopy and immunofluorescence using monoclonal antibodies against a cytoplasmic enzyme specifically involved in the synthesis of collagen (5B5). Macrophages makers were found on the neo-fibroblasts, whereas HLA-DR macrophages expressed the cytoplasmic marker 5B5. Since osteoblasts are classically derived from fibroblasts, the significance of the in vitro differentiation of monocytes/macrophages into fibroblasts to the in vivo mechanism leading to excessive osteoblastic proliferation in both osteomyelosclerosis and Engelmann's disease, is discussed. The possible involvement of this pathway leading from monocytes to fibroblasts and osteoblasts in the normal process of bone modeling and remodeling in questioned.

Camurati-Engelmann Syndrome↗
PubMed1994

Monocytic origin of fibrosis. In vitro transformation of HLA-DR monocytes into neo-fibroblasts: inhibitory effect of all-trans retinoic acid on this process.

We report here the spontaneous in vitro transformation of blood monocytes into fibroblasts in a patient who developed pulmonary fibrosis following ciclosporin-mediated immunosuppression, necessitated by heart transplantation. The blood monocytes with this capacity expressed HLA-DR specificity. Monocytes/macrophages were identified by immunofluorescence using monoclonal antibodies against a specific monocyte/macrophage antigen, while the neo-fibroblasts were identified by electron microscopy and immunofluorescence using monoclonal antibodies against a cytoplasmic enzyme specifically involved in the synthesis of collagen. The secretion of collagen was demonstrated using antibodies against collagen. Both the monocytes/macrophages and the neo-fibroblasts express macrophage and fibroblast markers and are able to synthesize collagen. The all-trans retinoic acid derivative (all-trans RA) inhibits this in vitro transformation of HLA-DR monocytes/macrophages into neo-fibroblasts. Therefore, the possible therapeutic role of all-trans RA in controlling the development of fibrosis remains open to investigation. Until now, no efficient therapy is known for fibrotic diseases which are often lethal when affecting the lungs.

Aged↗
PubMed1993

Phagocytosis of P. falciparum malarial pigment hemozoin by human monocytes inactivates monocyte protein kinase C.

Hemozoin (malarial pigment) is a ferriprotoporphyrin IX-rich hemoglobin degradation product present in parasitized RBC. Avidly phagocytosed hemozoin abolishes phagocyte TPA-induced oxidative burst. Membrane-associated PKC increased transiently in hemozoin-fed monocytes by 50% after 30 min and decreased irreversibly to 20% of initial value within 5 h after phagocytosis. Control RBC-fed monocytes showed transient decay of membrane-associated PKC followed by complete recovery 12 h after phagocytosis. Cytosolic PKC was not impaired within 12 h and diminished drastically 24 h after phagocytosis of hemozoin. Results are compatible with increased degradation of membrane-translocated PKC, possibly by iron/H2O2-mediated damage of cysteine-rich regulatory domains of PKC.

Animals↗
PubMed1999

Microsatellite polymorphisms in the gene promoter of monocyte chemotactic protein-3 and analysis of the association between monocyte chemotactic protein-3 alleles and multiple sclerosis development.

Monocyte chemotactic protein 3 (MCP-3) is a chemokine that attracts mononuclear cells, including monocytes and lymphocytes, the inflammatory cell types that predominate in multiple sclerosis lesions. We studied the possible association between the presence of a CA/GA microsatellite repeat polymorphism in the promoter/enhancer region of the MCP-3 gene and the occurrence of multiple sclerosis. DNA samples from 192 Swedish multiple sclerosis (MS) patients and 129 healthy controls were analysed by an automated fluorescent technique. In the whole sample population, five MCP-3 allele variants (MCP-3*A1 to MCP-3*A5) were detected with an allele frequency ranging between 0.3% and 46%. The individual MCP-3 allele frequencies did not differ significantly between MS patients and control individuals. The relative MS risk, attributable to HLA-DRB1*15 was 3.05 (chi2 = 22.25, p < 0.0001). The phenotype frequency (PF) of none of the MCP-3 alleles was significantly altered in the population of controls versus unselected MS patients. When MS patients and control subjects were stratified according to positivity for HLA-DRB1*15, the MCP-3*A4-associated risk for developing MS decreased to 0.36 (p = 0.011). In the stratified groups of patients who were negative for both HLA-DRB1*15 and HLA-DRB1*03, and hence possessed a lower risk to develop MS, the MCP-3*A2-associated risk for MS development decreased significantly (p = 0.018). We conclude that the MCP-3*A4 allele might protect against MS development on the background of the increased risk in HLA-DRB1*15+ individuals and the MCP-3*A2 allele seems protective in low-risk individuals, who are both negative for DRB1*03 and DRB1*15.

Alleles↗
PubMed2003

Alteration in the production of IL-10 and IL-12 and aberrant expression of CD23, CD83 and CD86 by monocytes or monocyte-derived dendritic cells from atopic dermatitis patients.

Atopic dermatitis (AD) is characterized by the presence of Th2-type cells in the skin infiltration as well as in the peripheral blood, although a predominant infiltration of interferon-gamma (IFN-gamma)-producing cells is also reported in the chronic skin lesions of AD. Recently it has become clear that the development of Th1 or Th2 is strongly influenced by factors produced by the antigen presenting cells (APCs). To clarify whether APCs from AD patients play a favorable role in the differentiation of Th2 cells, we compared the production of cytokines and the expression of co-stimulatory molecules by monocytes (MOs) and monocyte-derived DCs (MoDCs) after stimulations with various reagents between 13 AD patients and 13 age-matched healthy controls. We examined their production of IL-1 beta, IL-10, IL-12p40, and IL-12p70, and their expression of CD23, CD40, CD54, CD80, CD83, CD86 and HLA-DR. We stimulated them with superantigens, lipopolysaccharide (LPS), agonistic anti-CD40 antibody, phytohemagglutinins (PHA), IL-1beta/TNF-alpha, IL-4, or IFN-gamma. The following results were obtained (1): IL-10 production was significantly enhanced in AD MOs after LPS stimulation. In contrast, IL-12p40 production was significantly lower in AD MOs than in HC MOs after a variety of stimulations (2). IL-12p40 was also significantly lower in AD MoDCs after LPS stimulation (3). The induction of CD23 with IL-4 was significantly higher in AD MOs. and finally (4), AD MoDCs augmented the expression of CD83, CD86, and HLA-DR less significantly than HC MoDCs after anti-CD40 Ab stimulation. These data indicate that AD APCs show some responses different from those observed in HC APCs after several stimulations, such as LPS, IL-1 beta/TNF-alpha, IL-4, or anti-CD40 Ab, and that these responses might play a role in the polarizing process of helper T cells into Th2 cells as recognized in AD patients.

Adolescent↗
PubMed1998

A functional defect in hereditary haemochromatosis monocytes and monocyte-derived macrophages.

BACKGROUND: Hereditary haemochromatosis (HH) is a disease of the metabolism of iron characterized by increased iron absorption and heavy parenchymal iron deposition, but with the presence of little iron in the mononuclear phagocytic system (MPS). METHODS: To investigate the role of the MPS, the phagocytic ability of HH monocytes (MNs) and in vitro monocyte-derived macrophages (MDMs) was studied. HH patients with different degrees of iron accumulation were chosen. RESULTS: We observed that HH patients' MNs and MDMs have a significantly decreased ability to phagocytose rabbit red blood cells (RRBCs) and that HH MNs possess a significantly decreased capacity to phagocytose Staphylococcus aureus (S. aureus). The decrease in the ability to phagocytose S. aureus, however, was kinetic in nature, explaining the absence of increased prevalence of bacterial infections among HH patients. Both RRBCs and S. aureus were preopsonized with heat-inactivated serum. No alteration in the complement-dependent phagocytosis of Cryptococcus neoformans was demonstrated when normal human serum was used. The phagocytosis defect was observed in 100% of HH patients and was independent of the magnitude of iron overload, age or liver damage, and affected the antibody-mediated uptake of bacteria and (R)RBCs.

Adult↗
PubMed1999

Cyclooxygenase metabolites mediate glomerular monocyte chemoattractant protein-1 formation and monocyte recruitment in experimental glomerulonephritis.

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) has been shown to play a significant role in the recruitment of monocytes/macrophages in experimental glomerulonephritis. Whereas a number of inflammatory mediators have been characterized that are involved in the expression of MCP-1 in renal disease, little is known about repressors of chemokine formation in vivo. We hypothesized that cyclooxygenase (COX) products influence the formation of MCP-1 and affect inflammatory cell recruitment in glomerulonephritis. METHODS: The effect of COX inhibitors was evaluated in the antithymocyte antibody model and an anti-glomerular basement membrane model of glomerulonephritis. Rats were treated with the COX-1/COX-2 inhibitor indomethacin and the selective COX-2 inhibitors meloxicam and SC 58125. Animals were studied at 1 hour, 24 hours, and 5 days after induction of the disease. RESULTS: Indomethacin, to a lesser degree the selective COX-2 inhibitors, enhanced glomerular MCP-1 and RANTES mRNA levels. Indomethacin enhanced glomerular monocyte chemoattractant activity an the infiltration of monocytes/macrophages at 24 hours and 5 days. CONCLUSIONS: Our studies demonstrate that COX products may serve as endogenous repressors of MCP-1 formation in experimental glomerulonephritis. The data suggest that COX-1 and COX-2 products mediate these effects differently because the selective COX-2 inhibitors had less influence on chemokine expression.

Animals↗
PubMed1982

Isolation of the receptor for IgG from a human monocyte cell line (U937) and from human peripheral blood monocytes.

The Fc receptors for IgG from a human monocyte line (U937) and from highly purified human peripheral blood monocytes were solubilized, purified, and partially characterized. Both sources of cells gave indistinguishable results. Two molecules (or sets of molecules), one of about 72,000 mol wt and the other of 40,000-43,000 mol wt were discerned on autoradiograms of sodium dodecyl sulfate (SDS)-polyacrylamide gels analyzing acid eluates from Sepharose-IgG columns over which detergent lysates of radioiodinated cells had been passed. The larger of the two molecules, p72, accounted for greater than or equal to 90% of the radioactivity. This component was noted to be heterodisperse both by size on SDS gels and by charge on isoelectric focusing gels. The charge heterogeneity, being virtually eliminated by neuraminidase and tunicamycin, was probably due to variable glycosylation. Several lines of evidence indicated that p72 is probably all or part of the Fc receptor: (a) radiolabeling of this molecule using chloroglycouril was blocked by IgG of the Fc receptor; (b) in soluble form this molecule expressed ligand specificity identical to the in situ receptor; (c) the molecule was not recovered from affinity adsorbants bearing proteins that do not bind to the Fc receptors, nor (d) from a human T cell line that does not bear Fc receptors. The smaller of the two molecules isolated, p40-43, is at least in part actin. Its relationship to p72 is not understood.

Autoradiography↗
PubMed2003

Suppression by Candida albicans beta-glucan of cytokine release from activated human monocytes and from T cells in the presence of monocytes.

The effect of a soluble beta-glucan from Candida albicans (CSBG) on cytokine production by cultured human peripheral blood mononuclear cells (PBMC) was assessed. CSBG induced a slight increase in the spontaneous release of proinflammatory cytokines, such as interleukin (IL)-6, but significantly suppressed endotoxin-induced IL-6 production in cultures of PBMC and monocytes isolated from PBMC. CSBG also suppressed the release of type 1 cytokines, IL-2, and interferon-gamma. These findings suggest that CSBG suppresses monocyte functions directly and thus suppresses T cell function indirectly. CSBG may play a role in the development of candidiasis.

Candida albicans↗
PubMed2000

Stimulation of Fc gamma R receptors induces monocyte chemoattractant protein-1 in the human monocytic cell line THP-1 by a mechanism involving I kappa B-alpha degradation and formation of p50/p65 NF-kappa B/Rel complexes.

THP-1 monocytic/macrophage cells were stimulated via their FcgammaR receptors with insoluble aggregates of human IgG and the production of the C-C chemokine monocyte chemoattractant protein (MCP)-1 assayed. A dose- and time-dependent production of MCP-1 comparable to that produced by the most potent agonists could be detected in the culture medium by a sensitive ELISA assay. This was accompanied by a parallel activation of the transcription factor NF-kappaB as judged from both the appearance of kappaB-binding activity containing p50/p65 NF-kappaB/Rel complexes in the nuclear extract and the disappearance of the NF-kappaB inhibitor IkappaB-alpha in the cell lysate. In contrast, IkappaB-beta and IkappaB-epsilon expression was not modified, thus pointing to the occurrence of a selective degradation of IkappaB-alpha under those conditions. Attempts to modulate MCP-1 production with compounds that display inhibitory effects on the activation of NF-kappaB such as the proteasome inhibitor N-acetyl-leucinyl-leucinyl-norleucinal, the antioxidant pyrrolidine dithiocarbamate and the salicylate derivative 2-hydroxy-4-trifluoromethylbenzoic acid showed a parallel effect on both MCP-1 production and NF-kappaB activation, thus pointing to the involvement of kappaB-binding sites on the transcriptional regulation of MCP-1 production. Our findings suggest the existence in monocytic cells of a signaling mechanism initiated by cross-linking of low-affinity FcgammaR, most likely of the FcgammaRII family since THP-1 cells do not express FcgammaRIII receptors, that involves activation of NF-kappaB associated to the proteolytic degradation of IkappaB-alpha and leads to the transcriptional up-regulation of MCP-1.

Cell Line↗
PubMed1997

Human monocytes activate porcine endothelial cells, resulting in increased E-selectin, interleukin-8, monocyte chemotactic protein-1, and plasminogen activator inhibitor-type-1 expression.

Monocytes (Mo) are thought to be important effector cells in early xenograft rejection. Effects of Mo-endothelial cell (EC) interactions on EC activation in vitro were studied by coculturing human Mo or human monocytoid cell lines, U937 and THP-1, with porcine EC. Without preactivation, U937 cells and Mo induced mRNA for the EC-specific adhesion receptor, E-selectin, expressed only on activated cells, after 2 hr. Surface protein was maximal when equal numbers of EC and Mo were cocultured. Increased mRNA expression of the chemokines, interleukin-8 and monocyte chemotactic protein-1, and the antifibrinolytic protein plasminogen activator inhibitor type-1, confirmed EC activation. Like E-selectin, plasminogen activator inhibitor type-1 mRNA was rapidly induced and returned to baseline after 24 hr, whereas chemokine gene expression was slower and more prolonged. Interleukin-1 receptor antagonist failed to modulate induction of E-selectin. Soluble tumor necrosis factor (TNF) alpha receptor inhibited E-selectin induced by TNF alpha, but not by U937 cells, and mRNA and protein on EC in Mo-EC mixtures cocultured at 1:1 ratios were not significantly reduced. The TNF alpha inhibitor did reduce E-selectin expression (30-40%), as well as induced chemokine gene expression (80%), at higher Mo-EC ratios. Despite this, minimal TNF alpha was detectable in supernatants. These results, along with the transwell experiments that confirmed a requirement for Mo-EC contact, suggest that membrane-bound TNF alpha may be involved. Thus, Mo-EC interactions in the porcine to human combination activated several EC functions, suggesting that initial Mo contact with the vessel wall of a xenogeneic graft may promote leukocyte recruitment, inflammation, and maintenance of thrombus, resulting in eventual organ destruction.

Animals↗
PubMed1981

Herpes simplex virus infection in human monocyte cultures: dose-dependent inhibition of monocyte differentiation resulting in abortive infection.

Monocyte-enriched cultures of human blood leukocytes were exposed to herpes simplex virus (HSV) at different multiplicities of infection (m.o.i., from about 10 to 0.001 p.f.u./cell). Highest maximum progeny virus titres were invariably obtained with low initial m.o.i., i.e. those between 0.01 and 0.0001 p.f.u./cell, while little if any infectious progeny was produced in cultures inoculated with the highest virus concentrations. By the time of maximum virus production, i.e. 5 to 7 days after inoculation, monocytes in the uninfected cultures had mostly differentiated to macrophages. This differentiation was partially inhibited in cultures initially exposed to the higher concentrations of HSV. Synthesis of HSV antigens was detected by indirect immunofluorescence both in the high m.o.i. cultures and in the productively infected cultures. By this criterion, a maximum of 10 to 15% of all adherent cells became infected in both culture types. It is suggested that the higher doses of HSV, by inhibiting cellular maturation, also prevent the subsequent completion of its own infectious cycle.

Cell Differentiation↗
PubMed1988

Monocyte-derived macrophages as helper cells in monocyte-mediated cytolysis.

Human peripheral blood monocytes (M), incubated with opsonized zymosan particles (OPZ), lysed human erythrocyte (RBC) targets, as detected by a 51Cr release method. Conversely, cells derived in vitro from M (monocyte-derived macrophages, MDM) were ineffective. When added to the M-RBC system, MDM enhanced the lysis. The lysis by M and M plus MDM was prevented by catalase, azide and amino acids (alanine, taurine), consistent with the requirement for hypochlorous acid (HOCl). Moreover, MDM per se incapable of generating HOCl augmented the HOCl recovery from the M-RBC system. The results provide evidence for a previously unrecognized form of interaction between two distinct populations of mononuclear phagocytes.

Amino Acids↗
PubMed1985

Dendritic cells and monocytes as accessory cells in T-cell responses in man. I. Phenotypic analysis of dendritic cells and monocytes.

A method is described for simple and rapid preparation of human dendritic cells (DC) and monocytes (Mo) from peripheral blood. The phenotype of enriched DC and Mo was determined and compared by means of a panel of monoclonal antibodies (Mab's). The distribution and quantitative expression of HLA class II molecules encoded by the subloci DP, DQ, and DR were the same on the two cell types. During in vitro culture a rapid decrease of class II antigens on Mo was observed, whereas the expression of class II antigens on DC was relatively stable. The absence of monocyte markers on DC may indicate that this cell type does not belong to the monocyte/macrophage cell lineage. The phenotypic analysis shows that peripheral blood DC also lack differentiation antigens expressed by epidermal Langerhans cells (OKT6) and lymph node follicular dendritic reticulum cells (DRC-1). The relationship between peripheral blood DC and tissue-localized DC thus remains unsolved. With relatively high numbers of DC now available, production of DC lineage-specific Mab's may be approached.

Antibodies, Monoclonal↗
PubMed1980

Impaired monocyte cyclic AMP responses and monocyte cytotoxicity in atopic dermatitis.

Purified monocytes from 21 patients with mild and severe atopic dermatitis (AD) were compared with 22 healthy controls with respect to antibody-dependent cell-mediated cytotoxicity (ADCC) and cyclic adenosine 3',5'-monophosphate (cAMP) responses to stimulatory agents. ADCC was depressed in both severe and mild atopic dermatitis. The patients showed decreased cAMP responses to isoproterenol and histamine, the decrement being more distinct in severe atopic dermatitis. Formation of cAMP was diminished with PGE1 only in patients with severe AD. ADCC is inhibited by the agents that increase cAMP. In the severe dermatitis group reduced inhibition induced by isoproterenol, histamine, but not PGE1, was obtained. It is suggested that a general suppression of membrane activation may explain the reduced cAMP responses to various stimulatory agents and the impaired monocyte cytotoxicity.

Adolescent↗