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PubMed1994

Differences in altered expression of L-selectin and Mac-1 in monocytes and neutrophils.

We have measured the altered expression of the adhesion-promoting glucoproteins L-selectin and Mac-1 on monocytes and neutrophils after incubation with different concentrations of the chemotactic factor FMLP. We found a time- and dose-related down-regulation of L-selectin on both monocytes and neutrophils, which was more pronounced on neutrophils as compared to monocytes at both low (10(-12) M) and high (10(-7) M) concentrations of the chemotactic factor FMLP. Presence of human albumin reduced the down-regulation of L-selectin on both monocytes and neutrophils but to a greater extent on monocytes. Mac-1 expression increased in a time and dose-dependent manner on both monocytes and neutrophils when they were incubated with both low (10(-12) M) and high (10(-7) M) concentrations of FMLP, but the expression was more pronounced on neutrophils. The up-regulation of Mac-1 was equally reduced by albumin on monocytes and neutrophils. Presence of EDTA in RPMI medium reduced the FMLP-induced down-regulation of L-selectin on both monocytes and neutrophils, indicating that the down-regulation of L-selectin is partly divalent cation dependent. Differences in the altered expression of L-selectin and Mac-1 in monocytes and neutrophils with sustained expression of L-selectin on monocytes can contribute to the sequential recruitment of these cells into an inflammatory site.

Adolescent↗
PubMed1996

Retinal pigment epithelial cell proliferation: potentiation by monocytes and serum.

BACKGROUND: The development of proliferative vitreoretinopathy (PVR) results often from a breakdown of the blood-retina barrier and the intraocular accumulation of serum proteins and leukocytes, particularly monocytes, that then come into contact with retinal pigment epithelial (RPE) cells. To examine the effect of these two factors on RPE proliferation, which is characteristic of PVR, we used a coculture system of blood monocytes and human RPE cells. METHODS: RPE cells were incubated with a variable number of monocytes at different serum concentrations and assayed for proliferation by [3H]-thymidine incorporation and cell counting. To assess cell-cell communication. RPE cells were labeled with 2', 7' -bis(carboxyethyl)-5(and 6) carboxyfluorescein acetoxy-methyl ester, and the dye transfer to monocytes was analyzed using an UV microscope. RESULTS: Monocytes (P < 0.0004) and serum (P < 0.0001), each on its own, significantly stimulated RPE cell growth, and these two variables were interrelated (P < 0.0001), showing a potentiating synergism. In serum-free medium, monocytes increased proliferation to just above control levels, whereas the same number of monocytes in 5% serum increased the [3H]-thymidine incorporation 3.8 times. This effect was greatly reduced by prevention of direct cell contact by means of placement of a well insert, which also lessened the monocyte-induced proliferation in both serum-free and serum-containing medium. Furthermore, the transfer of the intracellular dye from RPE cells to cocultured monocytes indicates that RPE cells transferred parts of their cytoplasm to monocytes. CONCLUSION: These observations underline the importance of protein leakage through a damaged blood-ocular barrier and of direct contact of monocytes/macrophages with RPE cells, as well as their reciprocal potentiating effect on RPE cell proliferation. Thus, early stabilization of the blood-ocular barrier, which would preclude or reduce protein leakage and invasion of inflammatory cells into the eye, could be a target for pharmacologic prevention of PVR.

Blood Physiological Phenomena↗
PubMed1998

T-lymphocytes and monocytes in atherogenesis.

Atherosclerosis is characterized as a chronic inflammatory-fibroproliferative disease of the vessel wall. The attachment of monocytes and T-lymphocytes to the injured endothelium followed by their migration into the intima is one of the first and most crucial steps in lesion development. The co-localization of CD4+ T-cells and macrophages in the lesion, the abundant expression of HLA Class II molecules and the co-stimulatory molecule CD40 and its ligand (CD40L) indicate a contribution of cell-mediated immunity to atherogenesis. Transgenic mouse models revealed that dependent on the model T- and B-cells may promote lesion progression, monocytes and macrophages are in contrast essential for the development of atherosclerotic lesions. Apart from the local process in the vessel wall, systemic signs of an inflammatory reaction are also associated with lesion development. Thus plasma levels of C-reactive protein and fibrinogen and the white blood cell count are positively correlated to the risk of cardiovascular disease. Recently, an inflammatory phenotype of circulating peripheral blood monocytes could be demonstrated as a specific cellular correlate to lipid and lipoprotein risk factors. Thus the pool size of LPS receptor (CD14)dim and Fc gamma IIIa receptor (CD16a)+ monocytes positively correlates to plasma cholesterol levels, to triglycerides levels and to the apolipoprotein E4 (apo E4) phenotype in contrast to a negative correlation to the high density lipoprotein (HDL) cholesterol concentration. This CD14dim CD16a+ monocytes are further characterized by a high expression of beta 1- and beta 2-integrins, suggesting a higher capacity for attachment at sites of inflammation. A proinflammatory cytokine pattern and an expansion of these cells in other inflammatory diseases are indicating that these cells promote the inflammatory process during atherogenesis. Surface expression of the activation antigen CD45RA on monocytes in correlation to plasma LDL cholesterol and Lp(a) levels further indicates an inflammatory reaction. Regarding the potential mechanisms of the phenotypic changes of peripheral blood monocytes, in a serum free in vitro differentiation model supplemented with M-CSF monocytes from probands which are homozygous for apo E4 showed a significantly higher increase of CD16a expression compared to apo E3/E3 cells indicating that a genetic polymorphism of a single apolipoprotein gene locus may affect monocyte differentiation. The further characterization of the cellular immunology of monocytes and T-lymphocytes in lesion development will provide new specific diagnostic and therapeutic targets in atherogenesis.

Animals↗
PubMed2004

NADPH oxidase is not required for spontaneous and Staphylococcus aureus-induced apoptosis of monocytes.

Reactive oxygen intermediates (ROI) generated in the respiratory burst reaction are crucial for the killing of bacteria and fungi in phagocytes. The key enzyme for the respiratory burst reaction is the NADPH oxidase. Reactive oxygen intermediates have additionally been proposed to be of general importance for the expression of FAS and soluble FAS ligand (sFASL) and the subsequent induction of apoptosis. This conclusion has been drawn from the observation that neutrophils with an inborn lack of the NADPH oxidase as well as cell lines and monocytes with artificially blocked NADPH oxidase exhibit impaired apoptosis. Being one of the few centers caring for patients with chronic granulomatous disease (CGD) who exhibit an inborn lack of NADPH oxidase, we had the unique opportunity to determine the role of the NADPH oxidase for apoptosis in monocytes with otherwise unmanipulated cells of these patients (CGD monocytes). We compared the expression of FAS on monocytes and the concentration of sFASL in the supernatant between CGD monocytes and healthy donors undergoing spontaneous apoptosis. Neither the expression of FAS nor the concentration of sFASL was decreased in CGD monocytes. We further compared spontaneous apoptosis and apoptosis occurring after the phagocytosis of Staphylococcus aureus in CGD monocytes to monocytes of healthy controls. In these experiments we could not determine any significant impairment of apoptosis in CGD monocytes. Our data indicate for the first time that in an unmanipulated human model a functional NADPH oxidase is not crucial for the apoptosis of monocytes and disprove a general role of ROI for the induction of apoptosis in phagocytes.

Apoptosis↗
PubMed2005

Viable head and neck tumor spheroids stimulate in vitro autologous monocyte MCP-1 secretion through soluble substances and CD14/lectin-like receptors.

Biopsies from carcinoma tissue and benign control mucosa from head and neck squamous cell carcinoma (HNSCC) patients were used to establish fragment (F)-spheroids in vitro. We have previously shown that autologous monocytes co-cultured with F-spheroids in vitro augment their secretion of monocyte chemotactic protein-1 (MCP-1). Presently, the aims of the present work were to study whether the metabolic activity, secreted products and/or specific receptor/ligand on the surface of the F-spheroids and monocytes are necessary for stimulation of the monocyte MCP-1 secretion upon F-spheroid co-culture. Actinomycin D (1 mug/ml for 24 h) pre-treatment of the F-spheroids abolished the monocyte MCP-1 co-culture response. Co-culture of monocytes and F-spheroids separated by a semi-permeable membrane showed a decreased, but still present, monocyte MCP-1 co-culture response. Conditioned medium from F-spheroids stimulated allogenous monocytes to secrete MCP-1. The addition of glucose or galactose, but not mannose, to co-cultures partially inhibited the monocyte MCP-1 co-culture response. The addition of anti-CD14 antibody diminished the MCP-1 co-culture response. In conclusion, the monocyte MCP-1 co-culture response is dependent on metabolically active spheroids, secreted stimuli, and is augmented by direct contact with F-spheroids, possibly via lectin-like receptors and the CD14 receptor.

Autoantibodies↗
PubMed1980

Correlation between phagocytic and membrane surface properties reflected by partitioning of human peripheral blood monocytes in two-polymer aqueous phases.

Human peripheral blood monocyte-enriched fractions (identified by staining for peroxidase and by sizing) were obtained by velocity sedimentation at unit gravity of peripheral blood mononuclear cells. They were then fractionated by countercurrent distribution (a multiple-extraction procedure) in a charged Dextran/poly(ethylene glycol) aqueous phase system. The monocytes remained viable after the separation (order of 90%). Cells obtained from different cavities along the extraction train were tested for their ability to phagocytize latex particles. With increasing partition coefficient (presumably higher charge-associated membrane properties) the ratio of monocytes that phagocytized to monocytes that did not phagocytize increased appreciably. When, however, monocytes were permitted to phagocytize particles prior to countercurrent distribution, an increase in partition coefficient was associated with an appreciable decrease in the above-specified ratio. Control experiments indicate that the observed change in partitioning behavior cannot be ascribed to an alteration in size and/or density of the monocytes as a function of phagocytosis. It may be due to the internalization of charged surface groups during phagocytosis. We conclude that there is a correlation between the surface properties of monocytes (as reflected by partitiartitioning behavior cannot be ascribed to an alteration in size and/or density of the monocytes as a function of phagocytosis. It may be due to the internalization of charged surface groups during phagocytosis. We conclude that there is a correlation between the surface properties of monocytes (as reflected by partitioning) and their ability to ingest particles. Furthermore, an alteration in the surface charge-associated properties of monocytes as a consequence of phagocytosis is indicated by the cells' reduced partition coefficient.

Cell Membrane↗
PubMed1996

Gangliosides block antigen presentation by human monocytes.

Gangliosides, immunosuppressive molecules shed by tumor cells, are potent inhibitors of monocyte accessory cell function. However, the specific monocyte cellular defect caused by gangliosides is unknown. Here we sought to delineate whether this abnormality is in the induction of suppressor cells, in intracellular antigen processing, or in intercellular antigen presentation. Three sets of studies of the tetanus toxoid (TT)-induced lymphoproliferative response, which is dependent upon monocyte accessory function, address this issue: (1) Antigen (TT)-primed human monocytes incubated with 50-100 microM human brain gangliosides for 24-48 h, washed, and then combined with T-cells, were inhibited in triggering T-cell proliferation, showing that the effect was occurring after antigen processing was complete. (2) T-cell responses to immobilized anti-CD3 or to antigen-primed control monocytes in the presence of ganglioside-exposed monocytes were unaffected, showing that ganglioside-exposed monocytes did not act as suppressor cells. (3) Stimulation by TT peptide fragment 830-843, which does not require processing, was completely inhibited by exposure of monocytes to gangliosides. These findings identify ganglioside interference with monocyte accessory cell function at the level of antigen presentation. We conclude that tumor gangliosides may inhibit host anti-tumor cellular immune responses by preventing the effective cellular interactions of the antigen-primed monocyte with the responding T-lymphocyte.

Antigen Presentation↗
PubMed1986

Population kinetic study on the origin of guinea pig monocyte heterogeneity.

Population kinetic studies were performed on guinea pig peripheral blood monocyte fractions isolated by counter-flow centrifugation elutriation following a single in vivo pulse of tritiated thymidine. Labeled large monocytes (volume 317 micron3; relative distribution 49%; circulating half-life 5.7 hr; and production rate 17,000 cells/ml blood/hr) accumulated in the circulation more rapidly, had a faster turnover time, and were produced in greater numbers than small monocytes (volume 283 micron3; relative distribution 34%; circulating half-life 10.8 hr; and production rate of 6100 cells/ml blood/hr). The kinetic data do not support a maturational sequence of small into large monocytes. Intermediate monocytes (volume 300 micron3; relative distribution 11%; circulating half-life 18.2 hr) and very large monocytes (volume 354 micron3; relative distribution 6%; circulating half-life 36.5 hr) had production rates, respectively, of only 1200 and 320 cells/ml blood/hr. Maxima in the labeling index curve for small and large monocytes suggested a generation time of 24 hr while grain count analysis revealed that these two cell fractions were derived from a precursor population with similar numbers of reductive divisions. Grain count analysis of intermediate and very large monocytes revealed that these cells differed from both small and large monocytes. Our data support the concept that monocyte subsets exist in guinea pig peripheral blood with different kinetics of production and survival.

Animals↗
PubMed1988

Glucocorticosteroid-induced immunoglobulin production requires intimate contact between B cells and monocytes.

Glucocorticosteroid (GCS)-induced immunoglobulin (Ig) production in vitro is dependent on the functions of T cells and monocytes. T cells produce a replacing factor (TRF-S) which, with monocytes and a broad spectrum of concentrations (both above and below the physiologic range) of GCS, stimulates B cells to synthesize Ig. TRF-S is produced by T cells in cultures of mononuclear cells in the absence of stimulation over the initial 72 hr in culture. T cells, however, require the presence of monocytes or small quantities of interleukin 1 in order for the synthesis of TRF-S to occur. In addition to their role in stimulating TRF-S production, monocytes are also required in cultures of B cells responding to GCS and the cytokine. These experiments demonstrate that this monocyte function cannot be replaced by IL-1 or crude supernatants of monocyte cultures. Furthermore, exposure of TRF-S containing supernatants to oxidizing conditions does not alter the dependence of the cytokine on monocytes or GCS. Coculture of B cells and monocytes separated by a permeable membrane demonstrated that the influence of monocytes on GCS-induced Ig production is unlikely to be mediated by stable soluble factors. Thus, GCS-induced Ig production requires intimate contact between monocytes and B cells in the form of surface contact or unstable soluble mediators.

Adult↗
PubMed1989

Lysis of mycobacteria-infected monocytes by IL-2-activated killer cells: role of LFA-1.

Mycobacterium avium-intracellulare (MAI) is a ubiquitous soil contaminant that rarely causes disseminated disease in adults regardless of immunological status. In AIDS patients, however, this organism invades virtually every tissue and organ, and most conventional chemotherapeutic agents are usually ineffective against MAI. We report here that monocytes, in which MAI has established an intracellular parasitic stage, are under the control of natural killer (NK) cells. Autologous large granular lymphocytes (LGL), purified from human peripheral blood leukocytes, were capable of efficiently lysing autologous MAI-infected monocytes in a 5-hr 51Cr release assay. More importantly, interleukin 2 (IL-2) was able to activate the LGL to a higher degree of lysis of infected monocytes. LGL cultured in medium alone could not kill normal monocytes, but showed some degree of lysis of MAI-infected cells. IL-2 activated killer (LAK) cells, on the other hand, lysed normal monocytes to a moderate degree and this activity was makedly enhanced if the monocytes were infected with MAI. The sensitivity of monocytes was directly proportional to the inoculating number of bacteria, indicating that increased bacterial burden would enhance susceptibility to LAK-mediated lysis. Finally, the addition of monoclonal antibodies to LFA-1 (both alpha and beta chains), but not LFA-2 or LFA-3, blocked lysis of both infected and uninfected monocytes when added directly to the cytotoxicity assays, indicating that this adhesion protein is involved in the lysis of autologous, infected monocytes. Thus, NK/LAK cells may be important in containment of infection by lysis of infected monocytes before the bacteria can multiply and spread to other sites.

Antigens, Differentiation↗
PubMed1989

beta-VLDL and acetylated-LDL binding to pigeon monocyte macrophages.

Blood-derived monocytes are an important source of foam cells in atherosclerotic lesions of White Carneau pigeons. Based upon studies with cultured blood monocytes (monocyte macrophages) and peritoneal macrophages from a variety of mammalian species, it has been proposed that these cells become loaded with cholesteryl esters through the uptake of lipoproteins including beta-migrating very low density lipoproteins (beta-VLDL) and low density lipoproteins that have been chemically modified in a manner analogous to experimental acetylation (Ac-LDL). The purpose of this study was to determine whether similar mechanisms functioned in pigeon monocyte macrophages. Radioiodinated pigeon beta-VLDL and Ac-LDL were incubated with White Carneau pigeon monocyte macrophages that had been maintained in culture for 7 days. Scatchard analysis of the specific binding data revealed the presence of specific and saturable receptors for both beta-VLDL and Ac-LDL. beta-VLDL receptors had both low and high affinity binding components, whereas Ac-LDL receptors displayed a single class of high affinity binding sites. beta-VLDL binding remained relatively constant from 3 to 10 days in culture while Ac-LDL binding increased with time in culture. Competition studies demonstrated a high degree of binding specificity for 125I-Ac-LDL, but less for 125I-beta-VLDL. Binding of 125I-beta-VLDL was not competed for by Ac-LDL, but was by beta-VLDL and by low density lipoproteins from both normal and hypercholesterolemic pigeons. Following binding of beta-VLDL and Ac-LDL, the lipoproteins were rapidly internalized and degraded. Although the majority of degradation was secondary to internalization by the monocyte macrophages, approx. 5% of the degradation resulted from enzymatic activity in the culture medium, presumably due to secretion of proteolytic enzymes by the cells. As measured by esterification of [14C]oleate to cholesterol, it was shown that the cholesterol liberated from the degradation of both beta-VLDL and Ac-LDL stimulated cholesteryl ester synthesis in pigeon monocyte macrophages. These studies confirm the existence of specific beta-VLDL and Ac-LDL receptors on the surface of pigeon monocyte macrophages which facilitate both internalization of the lipoproteins and subsequent stimulation of cholesteryl ester synthesis. This is the first demonstration of beta-VLDL and Ac-LDL receptors on monocyte macrophages from an avian species, and the findings support the potential role for the receptor-mediated uptake of a variety of abnormal lipoproteins in the formation of monocyte-derived foam cells in the arterial wall of White Carneau pigeons during the development of atherosclerosis.

Animals↗
PubMed1993

Heterogeneity of cellular cholesteryl ester accumulation by human monocyte-derived macrophages.

We have studied cholesteryl ester accumulation in human monocyte-derived macrophages, which together with smooth muscle cells, represent the major cell types that accumulate cholesterol in atherosclerotic lesions. Monocyte-derived macrophages were incubated with either acetylated low density lipoprotein (AcLDL) or non-lipoprotein cholesterol and the question as to whether all of the cells, or specific cell subpopulations could accumulate cholesteryl ester was examined. We stained cholesteryl ester in monocyte-macrophages with the fluorescent probe filipin. Cholesteryl ester accumulated as lipid droplets that were widely dispersed in the cell cytoplasm. Interestingly, no more than 65% of monocyte-macrophages accumulated cholesteryl ester during the 1st day of incubation with non-lipoprotein cholesterol. By 2 days of incubation, greater than 90% of cells displayed cholesteryl ester deposition. The cholesteryl ester which accumulated during the 2nd day of incubation was derived from unesterified cholesterol that had accumulated during the 1st day of incubation. This finding was substantiated by the following: (1) chemical measurements showed that the total cholesterol content of monocyte-macrophages did not increase further after the 1st day of incubation, and (2) all monocyte-macrophages had accumulated fluorescent tagged cholesterol during the 1st day of incubation. In contrast to the results obtained with non-lipoprotein cholesterol, more than 90% of monocyte-macrophages incubated with AcLDL for 1 day accumulated cholesteryl ester in two experiments. However, less than 62% of monocyte-macrophages accumulated cholesteryl ester in two other experiments, thereby resembling results obtained with non-lipoprotein cholesterol. Again, the lack of cholesteryl ester accumulation with AcLDL was not due to a lack of uptake of AcLDL, as greater than 90% of monocyte-macrophages accumulated fluorescent tagged AcLDL. The observed heterogeneity in cholesterol esterification among human monocyte-macrophages suggests that functional subpopulations of these cells may exist with respect to cholesterol processing. However, heterogeneity in cholesteryl ester accumulation did not seem to correlate with expression of HLA-DR antigen, a marker of immunological activation of macrophages. Other sources of heterogeneity most likely result from inter-cellular variation at one or more levels of regulation of the cholesterol trafficking and esterification process.

Acetylation↗
PubMed1984

Deficient DR antigen expression on human cord blood monocytes: reversal with lymphokines.

Expression of DR antigen on cord blood (neonatal) human monocytes using complement-mediated cytotoxicity with anti-DR alloantisera and fluorescent-activated cell sorting (FACS) utilizing a battery of anti-DR mouse monoclonal antibodies was assessed. Forty preparations of neonatal cord blood monocytes were purified by adherence and elution from plastic petri dishes: lymphocyte contamination was less than 5% as indicated by esterase and peroxidase stains and cell sizing. By cytotoxicity tests 22 +/- 5.5% (SD) of neonatal monocytes expressed DR compared to its expression on 78.6 +/- 3.1% of adult monocytes. By FACS analysis, the frequency of DR expression on neonatal monocytes was 19-33% compared to 71-82% for adult monocytes. Incubation of neonatal monocytes with concanavalin A (Con A) or phytohemagglutinin (PHA)-stimulated human peripheral blood mononuclear cell culture supernatants (lymphokine) or recombinant interferon-alpha (IFN-alpha) increased the expression of DR antigens in a dose- and time-dependent manner. A Con A-supplemented culture supernatant of unstimulated peripheral blood mononuclear cells had no effect on DR expression. Neonatal monocytes that were pretreated with anti-DR and complement in order to remove DR-positive cells were induced to express DR antigen after 2 days in culture with lymphokine. Thus DR-negative neonatal monocytes can be induced to express DR antigen. These results suggest a correctable maturational deficiency of neonatal monocytes. The inducibility of DR antigen expression by lymphokines and recombinant IFN-alpha suggests that they play an important role in the regulation of immune responses.

Concanavalin A↗
PubMed1986

Cultured bovine monocytes exhibit decreased release of superoxide anion and increased levels of lysosomal enzymes but do not secrete detectable lysozyme activity.

In this study we determined the effects of in vitro maturation on the phagocytic activity, lysosomal enzyme content and oxidative response of bovine monocytes. Intracellular levels of the lysosomal enzymes acid phosphatase, beta glucuronidase, and beta glucosaminidase increased as bovine monocytes matured in vitro. However, in marked contrast to the mononuclear phagocytes of other mammalian species, lysozyme activity was undetectable in the culture supernatants and cell lysates of adherent bovine blood monocytes cultured for one to fifteen days. In vitro maturation of bovine monocytes also increased their phagocytic activity as determined by the ingestion of opsonized yeast. A greater percentage of monocyte-derived macrophages that were stimulated with opsonized yeast and phorbol myristic acetate (PMA) reduced nitroblue tetrazolium than did similarly treated monocytes. Monocyte-derived macrophages stimulated with PMA released significantly less superoxide anion than did PMA-stimulated monocytes. Bovine monocytes and macrophages also failed to bind the monoclonal antibody Mac-1, which binds to human and mouse macrophages. Bovine monocytes demonstrated both similarities and differences with other mammalian mononuclear phagocytes, thus making them a useful model for further study of the comparative and developmental biology of mononuclear phagocytes.

Acid Phosphatase↗
PubMed1995

Physical interaction with monocytes rescues human mature CD4+ T-cell lines from anti-CD3-induced apoptosis.

Crosslinking of the TcR-CD3 complex with immobilized anti-CD3 antibodies without sufficient co-stimulation induced cell death in human mature CD4+ T-cell lines. In these T cells, DNA fragmentation and morphological characteristics of apoptosis were seen. The anti-CD3-induced apoptosis was inhibited by co-culture with monocytes. The rescue signal provided by monocytes does not need to be present simultaneously with signals mediated by anti-CD3. When T cells were precultured with monocytes for 24 h before anti-CD3 stimulation and then the monocytes were removed from the culture, anti-CD3-induced T-cell apoptosis was also inhibited. To determine whether the monocyte-derived rescue signals were transduced by soluble factors or by direct cell-to-cell interaction with monocytes, we precultured T cells with monocytes separated by a micropore membrane which prevented T cell-monocyte physical interaction but not the diffusion of secreted molecules. In this system, rescue signals could not reach the T cells. To further assess the importance of physical interaction, we precultured T cells with fixed monocytes. T cells could not be rescued from apoptosis under these experimental conditions, either. The results considered collectively suggest that sufficient physical interaction with viable monocytes is important for the rescue of anti-CD3-induced apoptosis of CD4+ T cells.

Antibodies, Monoclonal↗
PubMed1992

In vivo activation of circulating monocytes by exogenous growth hormone in man.

Animal studies have shown that administration of growth hormone improves wound healing. Monocyte activation is a prerequisite for optimal repair of damage. In vitro, human recombinant growth hormone was shown to be a potent human monocyte chemoattractant. It induced random migration and chemotaxis at picomolar concentrations of recombinant human growth hormone; combinations of growth hormone with other chemoattractants deactivated the chemotactic response. Other functions of monocytes that are activated by growth hormone include release of superoxide anion and production of cytokines. In order to test activation of human monocytes by growth hormone in vivo, we investigated the effects of recombinant human growth hormone administration on monocyte migration in nine healthy young adults. After a single dose of recombinant human growth hormone (4 IU subcutaneously injected), random migration of circulating monocytes significantly increased, whereas chemotaxis of monocytes that was maximally stimulated with f-Meth-Leu-Phe decreased (p < .05). The alterations paralleled the concomitantly measured plasma levels of growth hormone. After recombinant human growth hormone administration, no changes were seen in plasma levels of proinflammatory cytokines. These in vivo data on monocyte migration are comparable to effects of growth hormone on monocyte migration in vitro and strongly suggest that recombinant human growth hormone can activate circulating monocytes in man.

Adult↗
PubMed1994

Synergistic effects of IL-4 and either GM-CSF or IL-3 on the induction of CD23 expression by human monocytes: regulatory effects of IFN-alpha and IFN-gamma.

CD23 expression by B cells and monocytes can be regulated by cytokines including IL-4, IFN-gamma and IFN-alpha. We recently reported that GM-CSF and IL-3 are also capable of regulating CD23 expression, with GM-CSF enhancing CD23 expression by monocytes and IL-3 enhancing CD23 expression by both monocytes and B cells. In this study, we have assessed the effect of combinations of cytokines on monocyte CD23 expression. IL-4 acted in a synergistic manner with either GM-CSF or IL-3 to induce monocyte CD23 expression. Interestingly, culture of monocytes with GM-CSF, IL-3 or IL-4 resulted in two subpopulations of cells, one negative or dull for surface CD23 and the other expressing relatively high levels of CD23. In contrast, culturing monocytes in the combination of IL-4 with either GM-CSF or IL-3 resulted in a single population of cells expressing very high levels of CD23. The synergy between IL-4 and either GM-CSF or IL-3 was also reflected at the level of release of soluble CD23 and CD23 mRNA expression and was seen at both sub-optimal and optimal cytokine concentrations. GM-CSF, IL-3 and IL-4 all enhanced monocyte expression of class II MHC, though no additive or synergistic effects were seen with cytokine combinations. IFN-gamma failed to induce monocyte CD23 expression when acting alone, though it enhanced both surface and soluble CD23 when acting in the presence of GM-CSF, IL-3 or IL-4. In contrast, IFN-alpha was a potent inhibitor of monocyte CD23 expression induced by these three cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed2005

Preferential binding of platelets to monocytes over neutrophils under flow.

This study was undertaken to systematically investigate the binding kinetics of platelet recruitment by monocytes relative to neutrophils in bulk suspensions subjected to shear as well as the molecular requirements of leukocyte-platelet binding. Hydrodynamic shear-induced collisions augment the proportion of monocytes with adherent platelets more drastically than that of neutrophils with bound platelets. These heterotypic interactions are further potentiated by platelet activation with thrombin or to a lesser extent by monocyte stimulation with N-formyl-methionyl-leucyl-phenylalanine (fMLP). Monocyte-platelet heteroaggregation increases with increasing shear rate and shear exposure time. Platelet P-selectin binding to monocyte P-selectin-glycoprotein-ligand-1 is solely responsible for maximal platelet adhesion to unstimulated monocytes in shear flow. However, the enhanced platelet binding to fMLP-treated monocytes involves a sequential two-step process, wherein P-selectin-PSGL-1 interactions are stabilized by CD18-integrin involvement. Blocking platelet alpha(IIb)beta(3) or monocyte beta(1)-integrin function had no effect. This study underscores the preferential recruitment of platelets by monocytes relative to neutrophils in shear flow, and demonstrates that the shear environment of the vasculature coupled to the state of cell activation modulates the dynamics and molecular constituents mediating monocyte-platelet adhesion.

Antibodies, Monoclonal↗