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PubMed1995

The role of various biomedical polymers concentration on the adhesion rate and viability of monocyte and monocyte derived macrophages.

The relationship between various polymers used in surgical implantation and cellular response at that particular site has not been fully elucidated. The objective of this study was to investigate the effect of various biomedical polymers on the adherence and viability of monocyte and monocyte derived macrophages. The monocytes were isolated from human peripheral blood, biotin labeled and seeded at a density of 5 x 10(5) cells/well according to standard laboratory procedures. Cells were considered macrophages after remaining in culture for 24 hours. Cells were then plated in each microtiter well pretreated with various concentrations of (0.01, 0.1 and 1%) poly-1-valine (P-Val), Poly-L-Alanine (P-Ala), poly-glycine (P-Gly), poly-L-tryptophan (P-Trp), Poly-L-Asparagine (P-Asn) and buffered control. At the end of 3 hours, 2 and 7 days the viability and cell number of monocyte or monocyte derived macrophages were determined using an established assay (biotin-labeled-macrophages). Cell number was determined in control wells with known amounts of cell number, a standard curve was generated by plotting absorbance units versus cell number. The data from this experiment suggest that: (I) cell number and viability of monocytes and macrophages can be measured concurrently, for the first time, by the use of Alamar Blue methodology, and (II) monocytes and macrophages are capable of surviving on all concentrations (0.01, 0.1 and 1%) of polymers tested over a 7 day period. Information obtained from this study provided new insights on the interrelationship between commercially available polymers, dose effect, incubation time and the possible cell response during chronic inflammation at the site of implantation.

Adult↗
PubMed1995

Leukemia inhibitory factor induces interleukin-8 and monocyte chemotactic and activating factor in human monocytes: differential regulation by interferon-gamma.

Leukemia inhibitory factor (LIF) is a cytokine released at the site of injuries where there is a recruitment of monocytes and polymorphonuclear cells. We analyzed the effect of LIF on human monocytes, which are a major source of chemotactic factors. We showed that supernatants of monocytes treated with LIF (50 ng/mL) for 18 hours had chemotactic activity for neutrophils and monocytes that was neutralized by anti-interleukin-8 (anti-IL-8) and anti-monocyte chemotactic and activating factor (anti-MCAF) neutralizing antibodies. Northern blot analysis showed induction of IL-8 and MCAF RNA in monocytes treated with LIF. Both IL-8 and MCAF mRNA were induced within 3 hours of stimulation. IL-8 and MCAF mRNAs expression peaked at 6 hours and 18 hours, respectively. Interferon-gamma (IFN-gamma), a potent monocyte activator, inhibited IL-8 induction by LIF. On the contrary, IFN-gamma by itself induced MCAF and did not affect the LIF-induced MCAF. These results indicate that LIF released at the site of injury by inducing IL-8 and MCAF can play an important role in recruiting leukocytes and that IFN-gamma can differentially regulate this recruitment.

Blotting, Northern↗
PubMed1993

[The roles of monocytes and the interaction between monocyte and T cell in human immune suppression induced by trichosanthin].

This paper deals with the roles of monocytes and the interaction between T cell and monocyte in Trichosanthin-induced human immune suppression. The data strongly argue that (a) monocytes could mediate the immune suppression of Trichosanthin, but T cells alone could not; (b) T cells acquire the ability to mediate the suppression effect if they were pulsed with Trichosanthin together with monocytes; (c) Antipain, a blocking agent against antigen processing and presentation, could diminish the suppressive activity of the Trichosanthin-pulsed monocytes. The results suggested the dependence of Trichosanthin on monocyte in immune down-regulation. One of the mechanisms might be that Trichosanthin induces an inhibitory network through antigen processing and presentation by monocytes.

Antipain↗
PubMed1998

The usefulness of CD64, other monocyte-associated antigens, and CD45 gating in the subclassification of acute myeloid leukemias with monocytic differentiation.

Immunophenotyping by flow cytometry is widely used in the diagnosis and subclassification of acute myeloid leukemia (AML). CD14 is the monocyte-associated antigen most widely used to identify AML with monocytic differentiation (French-American-British classes M4 and M5); however, we observed that CD14 expression is frequently diminished or absent in such cases. To identify monocyte-associated antigens that might improve recognition of AML M4 and M5, we used 3-color flow cytometry and a panel of antibodies reported to distinguish cells of monocytic lineage in 44 cases of AML. In addition, CD45 vs logarithmic side scatter plots were analyzed in all cases. As expected, CD14 was highly specific but was only moderately sensitive for monocytic differentiation. CD64 had the best-combined sensitivity and specificity for AML M4 and M5. CD45 vs logarithmic side scatter analysis showed a higher percentage of monocytes in AML M4 and M5 compared with nonmonocytic AML. CD64 was expressed in 5 of 5 cases of acute promyelocytic leukemia (AML M3), but the intensity of staining was significantly less in AML M3 than in AML M4 and M5. Our findings show that addition of CD64 and CD45 vs logarithmic side scatter analysis to CD14 greatly improves flow cytometric detection of AML with monocytic differentiation and that CD64, also expressed in AML M3, may help distinguish AML M3 from other subtypes.

Flow Cytometry↗
PubMed1988

Human granulocyte-monocyte colony-stimulating factor and interleukin 3 stimulate monocyte cytotoxicity through a tumor necrosis factor-dependent mechanism.

Human colony-stimulating factors (CSF) exert multiple effects on the proliferation, differentiation, and function of myeloid lineage cells. In this study, the effects of three recombinant human CSFs (granulocyte-monocyte CSF [GM-CSF], interleukin 3 [IL-3], and granulocyte CSF [G-CSF]) on antibody-independent monocyte tumoricidal activity were investigated by using WEHI 164 fibrosarcoma cells as monocyte-sensitive targets. None of the CSFs directly induced monocyte cytotoxicity, although both GM-CSF and IL-3 were found to significantly enhance monocyte killing in response to a second stimulatory event (endotoxin). No effect was seen with G-CSF. Antitumor necrosis factor antibody completely abolished CSF-enhanced monocyte cytotoxicity, which suggests that this effect was mediated through increased release of tumor necrosis factor (TNF). As previously shown for GM-CSF, IL-3 was found to induce cytoplasmic accumulation of TNF messenger RNA (mRNA) after 18 hours of exposure. These results suggest that GM-CSF and IL-3 may stimulate monocyte killing indirectly by enhancing expression of TNF mRNA, thereby leading to augmented TNF protein secretion in response to a second activation signal.

Biomechanical Phenomena↗
PubMed1981

Electron microscopy of E-rosette-forming leukemic monocytes in a child with acute monocytic leukemia.

A 7-year-old boy with acute monocytic leukemia (AMoL) had leukemic monocytes that formed spontaneous rosettes with sheep red blood cells (E-rosette). The E-rosette formation was observed in 75% of leukemic monocytes at 4 C and in 37% at 37 C. Cytochemical and ultrastructural studies confirmed that the rosette-forming cells were leukemic monocytes. The leukemic monocytes attached to the red blood cells at a portion of their surface and did not show any phagocytic processes at the electron microscopic level. The data from this patient seem to indicate that in a rare case of AMoL, abnormal myeloid lymphoid stem cells can differentiate to monocytes while retaining lymphoid properties.

Child↗
PubMed1993

Studies of binding and internalization of human recombinant monocyte chemotactic and activating factor (MCAF) by monocytic cells.

Recombinant human monocyte chemotactic and activating factor (MCAF) was iodinated and specific binding sites for this cytokine were detected on human peripheral blood monocytes, the monocytic leukemia cell line THP-1, and on PMA-differentiated HL60 and U937 cell lines. The binding sites were specific for MCAF since other polypeptide cytokines and the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMLP) failed to compete for 125I-rhMCAF binding. Steady-state binding experiments at 4 degrees C revealed the presence of 13,000 and 18,000 receptor sites/cell on monocytes and THP-1 cells with Kd values of 22.5 nM and 25.7 nM, respectively. Compared to a human natural MCAF, rhMCAF was less potent in inducing maximal monocyte migration. Human natural MCAF similarly competed more efficiently for 125I-rhMCAF binding than unlabelled rhMCAF. The ligand-receptor association was highly temperature-dependent, with maximal ligand uptake at 37 degrees C accompanied by internalization of the ligand-receptor complexes. The internalized 125I-MCAF was progressively degraded and released into the culture medium starting at 30 min. Lysosomotropic ammonium chloride could inhibit the degradation of this ligand suggesting the involvement of lysosomal enzymes in the proteolytic digestion. Incubation with cycloheximide did not block the rapid reappearance of MCAF receptors within 20 min on the cell surface indicative of receptor recycling rather than new protein synthesis. These data indicate that monocytic cells express specific receptors for rhMCAF which can be dynamically regulated by MCAF.

Biological Transport↗
PubMed1992

Pokeweed mitogen induces p55 interleukin-2 receptor expression on human monocytes and its effect on interleukin-2 activated monocyte cytotoxicity.

Activation of human peripheral blood monocytes by pokeweed mitogen (PWM) results in the expression of interleukin 2 receptor(IL-2R) p55 chains, which are absent on resting monocytes. By dual-fluorescence flow cytometry, we found PWM induced detectable numbers of IL-2R+ cell which were further identified as LeuM3+ monocytes (22.91% of the LeuM3+ cells were IL-2R+ within 24h, and 32.17% in 48h). In addition, LPS can also induce IL-2R on 15.39% of LeuM3+ cells. On the contrary, other mitogens such as PHA or Con A, and cytokines as IFN-gamma, IL-2, M-CSF, TNF-alpha and IL-1 beta showed no influence on the IL-2R expression on monocytes. It was also noticed that PWM itself had no direct effect on HLA-DR antigen expression on LeuM3+ cells. The addition of IL-2 to PWM-pretreated IL-2R positive monocytes significantly augmented their tumoricidal activity. Thus monocytes when activated underwent a series of phenotypic and functional changes including the expression of IL-2R which may provide an important immunoregulatory pathway.

Cytotoxicity, Immunologic↗
PubMed2004

17 beta-estradiol regulates cytokine release through modulation of CD16 expression in monocytes and monocyte-derived macrophages.

OBJECTIVE: Macrophages release cytokines, such as tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), and IL-6, which modulate the symptoms of rheumatoid arthritis (RA). Macrophage release of these cytokines can be modulated by estrogen. Fc gamma receptor type IIIA (CD16a) is a receptor expressed on macrophages that selectively binds IgG molecules, an important rheumatoid factor in RA. Binding of CD16 by anti-CD16 monoclonal antibodies stimulates macrophage cytokine release. We undertook this study to test the hypothesis that decreased concentrations of estrogen (17 beta-estradiol) directly cause an increase in CD16 expression, resulting in increased release of proinflammatory cytokines from monocytes and/or macrophages upon receptor binding. METHODS: THP-1 cells and female human primary monocytes and monocyte-derived macrophages were treated with no 17 beta-estradiol, physiologic levels (1 x 10(-8)M) of 17 beta-estradiol, or 1 x 10(-8)M 17 beta-estradiol followed by withdrawal of 17 beta-estradiol. Surface expression of CD16 and CD16 messenger RNA was measured using fluorescence-activated cell sorting (FACS) and semiquantitative reverse transcription-polymerase chain reaction, respectively. Cytokine release from 17 beta-estradiol-treated or untreated monocytes was then quantitated by enzyme-linked immunosorbent assay and FACS after crosslinking the receptor with anti-CD16 antibodies. RESULTS: CD16 transcript significantly increased in macrophage-like THP-1 cells and in primary, peripheral blood macrophages in the absence of 17 beta-estradiol, and the observed increase in message was dependent on transcription. CD16 receptor levels on CD14+, transforming growth factor beta-treated primary monocytes also increased in cells deprived of 17 beta-estradiol. Analysis of the cytokines released showed that CD16 crosslinking stimulated significant increases in TNF alpha, IL-1 beta, and IL-6 due to the absence of estrogen. CONCLUSION: Estrogen can modulate proinflammatory cytokine release from activated monocytes and/or macrophages, in part through modulation of CD16 expression.

Adult↗
PubMed1985

Serum-free conditions for the growth of avian granulocyte and monocyte clones and primary leukemic cells induced by AMV, and the apparent conversion of granulocytic progenitors into monocytic cells by a factor in chicken serum.

The supportive activity of chicken serum for the soft-agar growth of chicken granulocyte and monocyte clones could be replaced with defined ingredients [bovine serum albumin (BSA), conalbumin, selenium, linoleic acid and for routine work, a liquid soy lecithin preparation (59% phospholipids, 39% linoleic acid, and less than 2% of inositol and choline)]. The lecithin preparation could be replaced with L-alpha-phosphatidylcholine. The source of colony-stimulating factor was medium conditioned by fibroblasts cultured under protein-free conditions. AMV-induced leukemic cells could be cloned under identical conditions. In the presence of both chicken serum (10%) and the replacement ingredients, most of the proliferative clones produced were monocytic (84%). In the presence of serum alone, all of them were monocytic. Under serum-free conditions, all the clones produced were granulocytic when a day-3 conditioned medium (CM) was used; monocytic ones were also present when a day-6 CM was used. When the serum was serially diluted in the presence of the replacement ingredients, the number of proliferative monocytic clones progressively decreased while the number of proliferative granulocytic clones progressively increased and the kinetics of each were essentially the same, only opposite in direction. Moreover, the total number of proliferative clones did not change more than 33% at any dilution (or in the absence of serum). We postulate the existence in the chick system of a serum macrophage differentiation factor (M-DF) which converts early granulocytic progenitors (or exclusively diverts a common progenitor) into monocytic cells.

Animals↗
PubMed1992

Interactions between HIV-infected monocytes and the extracellular matrix: HIV-infected monocytes secrete neutral metalloproteases that degrade basement membrane protein matrices.

The frequency of human immunodeficiency virus (HIV)-infected monocytes that spread on a model basement membrane was about twofold greater than that of an equal number of uninfected control cells through the initial 12 to 18 h of culture. By 24 h, virtually all HIV-infected and uninfected control cells spread on the basement membrane gel. The frequency of spread cells in the uninfected control population was less than 10% of total cells by 12 days. In contrast, 30 to 40% of HIV-infected monocytes remained spread through this time interval and formed a dense interdigitated network of cell processes on and into the gel matrix. Invasion of the basement membrane matrix by HIV-infected monocytes suggested increased secretion of proteases able to digest the gel. Indeed, levels of neutral protease activity in culture fluids from HIV-infected monocytes were significantly higher than those from equal numbers of uninfected control cells. High levels of protease activity in culture fluids of HIV-infected monocytes required productive virus infection and were not observed with cells exposed to T cell-tropic HIV isolates. The predominant protease activity in these cultures was a 92-kd neutral metallogelatinase. HIV-induced changes in monocyte metalloprotease activity may be important for extravasation of infected cells to tissue or for the development of AIDS-associated neuropathology, carcinogenesis, and opportunistic infection.

Basement Membrane↗
PubMed1998

Endogenous monocyte chemoattractant protein-1 recruits monocytes in the zymosan peritonitis model.

The role of monocyte chemoattractant protein-1 (MCP-1) in the recruitment of blood-derived monocytes in a model of zymosan peritoneal inflammation was investigated. After zymosan injection (1 mg) a rapid influx of polymorphonuclear leukocytes (PMN) and monocytes into the peritoneal cavity associated with mouse MCP-1 (JE) gene activation and protein secretion in the exudates occurred. MCP-1 production (maximal at 4 h) preceded the accumulation of monocytes (F4/80-positive cells, maximally recovered between 16 and 24 h). Treatment of mice with a single injection of anti-mouse MCP-1 antibody inhibited 16-h monocyte accumulation by approximately 40%, however, a significant decrease in the number of PMN was also measured. Finally, intraperitoneal injection of murine recombinant MCP-1 (1 microg) produced a selective accumulation of monocytes (F4/80-positive cells) into the peritoneal cavity. In conclusion, we show the novel existence of a strict relationship between MCP-1 production and leukocyte accumulation in this model of acute inflammation.

Acute Disease↗
PubMed2000

Monocyte chemotactic protein 1 upregulates IL-1beta expression in human monocytes.

Monocyte chemotactic protein-1 (MCP-1) chemoattracts and activates monocytes. The nature of the genes that are transcriptionally activated in the monocytes by MCP-1 is not well understood. To identify such genes, human blood monocytes were incubated with or without MCP-1 for periods of 1, 4, and 12 h and the RNA extracted from these monocytes was subjected to differential display. The differentially expressed transcripts were cloned and sequenced. Differential display showed that interleukin-1beta (IL-1beta) gene expression was upregulated by MCP-1 treatment of monocytes for 4 to 12 h. Quantitative PCR and ELISA assays showed that MCP-1 treatment caused elevation in the levels of IL-1beta transcripts and protein, respectively. Immunoblot analysis showed that most of the protein was pro-IL-1beta. Since IL-1beta is known to induce MCP-1 synthesis, the present demonstration that MCP-1 induces IL-1beta synthesis suggests that the induction of each other would amplify the biological effects of these cytokines during inflammation.

Blotting, Western↗
PubMed1998

Induction of nitric oxide in human monocytes and monocyte cell lines by Mycobacterium tuberculosis.

The induction of nitric oxide in human monocytes during mycobacterial infection has been a controversial issue. This study describes a comparative evaluation of the colorimetric and fluorometric methods for the detection of NO in response to Mycobacterium tuberculosis (MTB) infection in human peripheral blood-derived monocytes (PBM) and in U937, a human monocyte-derived cell line. MTB was grown in monocyte cultures in vitro for 7 or 10 days. RPMI 1640 medium, without antibiotics and supplemented with L-arginine, Hepes, 5% human AB serum, and tetrahydrobiopterin was used to support monocyte growth. As early as 72 h after infection, soluble nitrite was detectable in the medium using the fluorometric assay with diaminonaphthalene (DAN). Early induction of NO correlated with an increase in the levels of iNOS mRNA as quantitated by RT-PCR. NO levels increased progressively up to day 10 (PBM) or day 7 (U937), when 150-200 nM/10(6) cells of soluble nitrite accumulated in cultures, as measured by DAN. Furthermore, monocytes stained positively for human iNOS protein and peroxynitrite after infection with MTB. The induction of NO by MTB was inhibited by four different inhibitors of iNOS enzyme including N-monomethylarginine. Inhibition of NO resulted in the enhancement of the intracellular growth of two of five clinical isolates of MTB. NO released from a donor (S-nitroso-N-penicillamine) also had a direct bacteriostatic effect on the same isolates in broth cultures. MTB strains thus showed a differential susceptibility to intracellular and extracellular NO. In most of these assays, the Greiss reagent was limited by its sensitivity and remained negative for soluble nitrite throughout the 7-10 days of incubation. Thus, the colorimetric method, which is widely used, may give false-negative results in NO assays. This report also demonstrates for the first time that MTB induces mRNA for iNOS, iNOS protein, NO, and peroxynitrite in human monocyte/macrophage cultures.

Cell Line↗
PubMed1998

Generation and subcellular distribution of histamine in human blood monocytes and monocyte subsets.

OBJECTIVE AND DESIGN: This study was designed to establish the sites of formation and storage of histamine and histidine decarboxylase (HDC) in human monocytes and two of their subsets. MATERIALS AND METHODS: The experiments were carried out using monocytes from buffy coats of healthy blood donors. Histamine was quantitated by RIA, HDC activity by the formation of histamine. RESULTS: The monocyte subtype RM3/1 contained significantly more histamine than the subset 27E10 (0.041+/-0.025 vs. 0.005+/-0.004 pg/cell, p < 0.05) and also more HDC activity and HDC mRNA. After fractionation of monocyte homogenates in a discontinuous Percoll gradient or by differential centrifugation more than 80% of both, HDC activity and histamine, were recovered from the cytosolic fractions. About 50% of this histamine was found to be bound to proteins. CONCLUSIONS: In monocytes histamine and HDC are colocalized in the cytoplasm indicating a subcellular distribution different from mast cells or basophils. The data also show that histamine is synthesized by the monocytes themselves.

Cell Fractionation↗
PubMed1996

Platelet-derived growth factor-BB and monocyte chemotactic protein-1 induce human peripheral blood monocytes to express tissue factor.

Monocytes induced to express tissue factor (TF), the initiator of the clotting cascade, might play an important role in the pathogenesis of atherosclerosis. We have investigated the TF-inducing capacity of two factors thought to be involved in atherogenesis, i.e. the platelet derived growth factor-BB (PDGF-BB) and monocyte chemotactic protein-1 (MCP-1), a member of the chemokine superfamily. PDGF-BB and MCP-1 are potent chemotactic and activating factors for human blood monocytes. alpha-thrombin which is known to induce TF in endothelial cells and that recently has been shown to induce secretion of MCP-1 from endothelial cells and monocytes was also studied. PDGF-BB induced a dose-dependent expression of TF-antigen in monocytes with maximal response at 20-50 ng/mL. At higher concentrations the expression was reduced. No synergistic effect between PDGF-BB and LPS was seen. MCP-1 also induced a dose-dependent TF-expression with maximal response at 50 ng/mL. In contrast to these results thrombin did not. MCP-1 had a slight, but not significant, priming effect on LPS-induced TF expression. These data show that PDGF-BB and MCP-1 are potent inducers of TF in human peripheral blood monocytes. We suggest that this TF-induction might be an important link between hemostasis and inflammation.

Arteriosclerosis↗
PubMed2006

Serum monocyte chemoattractant protein-1 and monocyte adhesion molecules in type 1 diabetic patients with nephropathy.

BACKGROUND: Monocyte chemoattractant protein (MCP)-1 is suggested to be implicated in the pathogenesis of diabetic nephropathy by activating and recruiting monocytes to the glomerulus via regulation of adhesion molecule expressions. The aim of this study was to test potential associations between serum concentrations of MCP-1, monocyte expression of Mac-1 and LFA-1 and nephropathy in type 1 diabetes mellitus. METHODS: Serum MCP-1 levels and expression of monocyte adhesion molecules in 51 type 1 diabetic patients with and without diabetic nephropathy were compared with matched 15 healthy control subjects. Concentrations of serum MCP-1 were determined by enzyme-linked immunosorbent assays whereas monocyte expression of adhesion molecules Mac-1 and LFA-1 was measured by flow cytometry. RESULTS: Serum MCP-1 levels and expression of Mac-1, but not LFA-1, were significantly higher in diabetic patients compared with controls. The mean serum MCP-1 level was 137.2 +/- 71.4 pg/mL in control patients, whereas it was 246.2 +/- 114.9 pg/ml in diabetic patients (p = 0.002). Serum MCP-1 levels were positively correlated with HbA1c and plasma fasting glucose levels. There was no difference in serum levels of MCP-1 and expression of monocyte adhesion molecules between type 1 diabetic patients with and without diabetic nephropathy. CONCLUSIONS: In type 1 diabetic patients, the levels of circulating MCP-1 concentration and expression of Mac-1 is mostly influenced by glycemic control rather than the existence of diabetic nephropathy.

Adult↗
PubMed2004

Apoptosis of monocytes and the influence on yield of monocyte-derived dendritic cells.

Monocyte-derived dendritic cells (DC) are currently under extensive evaluation as cell vaccines for cancer treatment. The requirement for large-scale cell products demands optimized and standardized protocols. However, the yield of DCs from inoculated monocytes is reported to be always lower than 50%. In this present study we investigated whether this cell loss was caused by the properties of the starting population of inoculated monocytes. CD14 cells were enriched by immunomagnetic-bead selection and analyzed for apoptosis by an annexin V/propidium iodide assay. We found that 37.8+/-11.1% (n=8) of freshly isolated monocytes from buffy coats of healthy donors underwent programmed cell death. Further analysis of the fate of apoptotic cells during differentiation suggested phagocytosis. Monocytes were differentiated with GM-CSF and interleukin-4 into a viable, non-apoptotic population of immature dendritic cells. Addition of tumor necrosis factor-alpha and prostaglandin E2 resulted in fully matured dendritic cells, which were evaluated by phenotypic analysis and by allogeneic and MHC class-I-restricted T-cell responses. About 90.2+/-16.7% of the non-apoptotic monocyte population differentiated to viable matured dendritic cells. These results indicate that the yield of dendritic cells is mainly influenced by the percentage of apoptotic cells in the inoculum, and this has implications for DC generation in clinical applications.

Annexin A5↗