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PubMed1994

Receptors and transduction pathways for monocyte chemotactic protein-2 and monocyte chemotactic protein-3. Similarities and differences with MCP-1.

MCP-2 and MCP-3 are recently identified members of the Cys-Cys chemokine family with high sequence similarity with MCP-1 (62% and 71%, respectively). The present study was aimed at defining receptor usage and signal transduction pathways of MCP-2 and MCP-3 in human monocytes in comparison with MCP-1. MCP-2 and MCP-3 induced migration of monocytes with a typical bell-shaped curve and maximal response at 10 and 50 ng/ml, respectively. The maximal response elicited by MCP-2 and MCP-3 was lower (approximately 60%) than that of MCP-1. Pertussis toxin (PTox) inhibited the chemotactic activity of MCP-3 and MCP-1 (IC50 = 6.2 and 4.4 ng/ml, respectively), whereas cholera toxin (CTox) had little effect on these two chemokines (IC50 > 1000 ng/ml). In contrast, MCP-2-induced chemotaxis was blocked by CTox (IC50 = 75 ng/ml) and relatively unaffected by PTox. MCP-3 and MCP-1 induced a rapid increase in intracellular Ca2+ concentration, whereas MCP-2, in the range of concentrations active on chemotaxis, did not. MCP-1-, MCP-2-, and MCP-3-induced chemotactic responses were blocked by C-I, a serine/threonine kinase inhibitor, and by genistein, a tyrosine kinase inhibitor, with the MCP-2 response being more sensitive than those induced by MCP-1 and MCP-3. MCP-1 and MCP-3 rapidly induced arachidonic acid release whereas MCP-2 was ineffective. MCP-1 and MCP-3 cross-desensitized with each other in terms of Ca2+ transients and displaced with a comparable efficiency labeled MCP-1 from human monocytes. On the other hand, MCP-2 did not cross-desensitize with MCP-1 and MCP-3 and only partially (20%) displaced labeled MCP-1. Thus, in spite of high sequence similarity, MCP-2 differed considerably from MCP-1 and MCP-3 in terms of sensitivity to CTox and PTox, arachidonate and calcium mobilization, and capacity to compete for labeled MCP-1.

Arachidonic Acid↗
PubMed1999

Chemotaxis and activation of particle-challenged human monocytes in response to monocyte migration inhibitory factor and C-C chemokines.

Cytokines that regulate monocyte migration were found in membrane tissue surrounding loosened prosthetic implants. Monocyte migration inhibition factor (MIF) is able to inhibit macrophage migration. Monocyte chemoattractant protein (MCP) and macrophage inflammatory protein (MIP) are potent macrophage chemoattractants. These cytokines may be expressed as part of the foreign body response to prosthetic particulate debris. Chemotaxis analysis and macrophage activation experiments were performed to determine the effects of MIF, MCP-1, and MIP-1alpha on macrophage migration and activation in vitro. We demonstrated that MIF had its maximal migration inhibitory effect for unchallenged and particle challenged macrophages at 1 ng/mL. MCP-1 and MIP-1alpha stimulated macrophage chemotaxis maximally at 1 to 10 ng/mL. Dose-response studies with MIF, MCP-1, and MIP-1alpha demonstrated that these cytokines did not modulate activation of unchallenged or particle challenged macrophages as evaluated by IL-6 and TNF-alpha release. However, these cytokines do not appear to affect macrophage release of proinflammatory mediators in vitro.

Biocompatible Materials↗
PubMed1997

Localization of endothelial-monocyte-activating polypeptide II (EMAP II), a novel proinflammatory cytokine, to lesions of experimental autoimmune encephalomyelitis, neuritis and uveitis: expression by monocytes and activated microglial cells.

Endothelial-Monocyte-Activating Polypeptide II (EMAP II) is a proinflammatory cytokine and chemoattractant of macrophages. In order to investigate the role of EMAP II in autoimmune lesions of the rat nervous system, we have used a synthetic gene to express EMAP II in E. coli and have produced monoclonal antibodies against EMAP II. Monoclonal antibodies are suited to demonstrate EMAP II in ELISAs, Western blots, and paraffin-embedded tissue sections. EMAP II was localized to monocytes/macrophages with rather selective staining of a minor rat monocyte subpopulation of lymphoid tissues such as spleen, lymph nodes or follicles of the gut. In the normal brain, cells of the perivascular but not parenchymal microglia were stained. We then investigated expression of EMAP II during experimental autoimmune encephalomyelitis (EAE), neuritis (EAN), and uveitis (EAU). Within the local inflammatory lesions infiltrating macrophages are prominently stained. In the diseased brain, EMAP II-positive microglial cells are not only found in the direct vicinity of the inflammatory infiltrate, but widespread activation is seen in the parenchyma. This is the first demonstration that EMAP II is present in autoimmune lesions. Immunostaining of microglial cells is noteworthy, as these cells are strategically placed regulatory elements of CNS immunosurveillance. EMAP II might be a factor regulating monocyte chemoattraction, endothelial cell activation and a regulator of microglial cell reactivity in autoimmune inflammation of the central nervous system.

Amino Acid Sequence↗
PubMed1998

Effects of methotrexate on differentiation of monocytes and production of cytokine inhibitors by monocytes.

OBJECTIVE: To examine the potential of methotrexate (MTX) to act as a differentiation-stimulating factor for monocytes, which could explain the antiinflammatory properties of this agent in the treatment of rheumatoid arthritis (RA). METHODS: Fluorescence-activated cell sorter analysis was used to measure the changes in antigen expression (CD11b/c, CD16, CD64, CD14, CD68, and CD95) in response to MTX, 1,25-OH-cholecalciferol (1,25-OH-CCF), and granulocyte-macrophage colony-stimulating factor in the human monoblastic leukemia cell line U937, bone marrow mononuclear cells (BMMC), and peripheral blood mononuclear cells (PBMC). Release of interleukin-1beta (IL-1beta), IL-1 receptor antagonist (IL-1Ra), tumor necrosis factor a, and soluble tumor necrosis factor receptors (sTNFR) p55 and p75 during the differentiation in vitro was assessed by immunoassay in the culture supernatants. RESULTS: MTX alone and in combination with 1,25-OH-CCF markedly stimulated the differentiation of the monocytic U937 cells and simultaneously increased Fas-antigen expression. Differentiation was associated with enhanced IL-1Ra and sTNFR p75 release from U937 cells. MTX had fewer effects on phenotypic differentiation of human BMMC and PBMC, but did stimulate IL-1Ra release and inhibit IL-1beta synthesis in BMMC. CONCLUSION: MTX acts as a strong differentiation factor for immature and undifferentiated monocytic cells. Differentiation in vitro is associated with an increase in natural cytokine inhibitor release and a simultaneous down-regulation of IL-1beta. These findings may explain the marked clinical antiinflammatory effects of MTX when used in the treatment of RA.

Antigens, CD↗
PubMed2005

Role of granulocytes and monocytes in the polyvinyl chloride-induced synthesis of interleukin 8, monocyte chemoattractant protein 1, and leukotriene B4.

In an in vitro whole blood model of artificial surface-induced inflammation, we have studied the contribution of leukocyte populations in the synthesis of inflammatory mediators. This was done by depleting the blood of specific cell types using magnetic beads coated with monoclonal antibodies against leukocyte surface antigens. Synthesis of interleukin 8 (IL-8) was highly dependent on CD15+ cells and was reduced by 80% when these cells were removed from the blood. Correspondingly, IL-8 production showed a high correlation with the concentration of granulocytes (r = 0.77, p < 0.0001). Synthesis of monocyte chemoattractant protein 1 (MCP-1) was dependent on CD14+ cells and was reduced by 35% when these cells were removed from the blood. Correspondingly, MCP-1 production correlated with the concentration of monocytes (r = 0.39, p < 0.0001). Synthesis of leukotriene B4 (LTB4) was highly dependent on CD15+ cells and was reduced by 75% when these cells were removed from the blood. Correspondingly, LTB4 production correlated strongly with the granulocyte concentration (r = 0.54, p < 0.0001). As expected, complement activation was not affected by cell depletion and did not correlate with the concentration of any of the cell types. Thus, artificial surface-induced IL-8 and LTB4 synthesis was almost exclusively granulocyte dependent. However, MCP-1 synthesis was mainly a product of monocytes, although granulocytes and other subpopulations may partly contribute. (c) 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005.

Chemokine CCL2↗
PubMed1988

Characterization of a monocyte differentiation factor distinct from gamma-interferon, tumor necrosis factor, or G,M-colony-stimulating factor that regulates the growth and functional capabilities of the U937 monocytic cell line.

We have analyzed the characteristics and cellular sources of the T cell-derived lymphokines that affect the proliferation and the oxidative metabolic capabilities of the U937 monocytic cell line. Although gamma-interferon (gIFN) and tumor necrosis factor-alpha (TNFa) can, in high doses, inhibit the proliferation of U937 cells, the predominant antiproliferative factor produced by activated CD4+ and CD8+ T cells has a MW = 45-55 Kd, is resistant to heat treatment, and is distinct and independent from gIFN, TNFa, and GM-CSF. The inhibitory effect of this lymphokine on U937 cell growth requires an 18-24-hr induction period; thereafter, this growth arrest persists for up to 5 d, even in the absence of the factor. The lymphokine responsible for inducing oxidative metabolic capabilities in U937 cells is also a non-gIFN, heat-resistant, 45-55-Kd factor secreted by CD4+ and CD8+ cells, and we postulate that this differentiation factor is identical to the factor responsible for inhibiting U937 growth. These data demonstrate the prominent role of T cell-derived factors distinct from gIFN, TNFa, or GM-CSF in regulating the growth and functional capabilities of monocyte-lineage cells. Furthermore, the data suggest it may be appropriate to distinguish monocyte activation, in which cells at a given maturational stage develop a heightened ability to perform a particular function, from changes in the functional repertoire of cells acquired as a consequence of lymphokine-induced differentiation.

Cell Line↗
PubMed1988

Induction of adenosine deaminase and 5' nucleotidase activity in cultured human blood monocytes and monocytic leukemia (THP-1) cells by differentiating agents.

The in vitro effect of short-term culture as well as the effect of retinol (ROH), retinoic acid (RA), muramyl dipeptide [( Abu']MDP), lipopolysaccharide (LPS), and gamma interferon (IFN-gamma) on the induction of the purine metabolic enzymes, adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5'nucleotidase (5NT) in human peripheral blood monocytes (HPBM) was examined. HPBM isolated by centrifugal elutriation were cultured for up to 96 h. Following an initial time lag of 24 h, mean ADA activity from seven separate experiments as measured in nmoles/10(6) cells/h increased from a baseline of 31.3 +/- 9.3 to 57.8 +/- 16.4 (P less than 0.005) at 72 h and to 72 +/- 21.5 (P less than .025) by 96 h. 5NT activity increased from a baseline of 2.2 +/- 0.9 to a maximum of 44 +/- 10.1 by 72 h and then declined to 29 +/- 18 (P less than 0.005) by 96 h, while no significant change in PNP activity was observed. HPBM incubated for 3 d with optimal concentrations of LPS, RA, and IFN-gamma had increases in ADA and 5NT activity ranging from three- to 10-fold compared to HPBM cultured in media alone, whereas no effect was observed with ROH and [Abu']MDP. RA, but not ROH, significantly enhanced ADA activity in a monocytic leukemia cell (THP-1) line. Addition of RA or the tumor promoter, phorbol 12-myristic 13-acetate (PMA), to HPBM or THP-1 cells resulted in significant increases in 5NT activity with opposite effects on ADA activity. These findings suggest that the biological mechanisms associated with differentiation in normal and malignant monocytes seem to be related and that the sequence and degree to which the various differentiation agents induce the enzyme elevations are also related to the mechanisms of activation/differentiation.

5'-Nucleotidase↗
PubMed1988

Endotoxin abolishes the induction of alpha 2-macroglobulin synthesis in cultured human monocytes indicating inhibition of the terminal monocyte maturation into macrophages.

Monocytes were prepared from human blood and allowed to differentiate into macrophages in vitro. Synthesis and secretion of the potent proteinase inhibitor alpha 2-macroglobulin is strongly induced during maturation of monocytes into macrophages establishing alpha 2-macroglobulin as a differentiation marker protein. When the monocytes were incubated with endotoxin (S. typhi) in a concentration as low as 100 ng/ml, induction of alpha 2-macroglobulin synthesis was completely abolished indicating impaired monocyte/macrophage differentiation by lipopolysaccharides (LPS). In contrast to alpha 2-macroglobulin, synthesis of alpha 1-proteinase inhibitor in mononuclear phagocytes was stimulated by endotoxin.

Cell Differentiation↗
PubMed1989

Granulocyte-monocyte-colony-stimulating factor augments the cytotoxic capacity of lymphocytes and monocytes in antibody-dependent cellular cytotoxicity.

Human peripheral blood mononuclear cells (lymphocytes and monocytes) were preincubated for 0-24 h with human recombinant granulocyte-monocyte-colony-stimulating factor (GM-CSF) and used as effector cells in an 18 h antibody-dependent cellular cytotoxicity (ADCC) assay with SW948 (a human colorectal carcinoma cell line) as target cells and mAb 17-1A. A significant increase in the lytic capability was noted after 0.5-2 h of preactivation while longer preincubation times did not significantly increase the lytic potential. GM-CSF at 0.01 microgram/ml induced the best tumor cell lysis while higher concentrations were inhibitory. GM-CSF pretreatment induced a statistically significant increase in the lytic capacity of both monocytes and lymphocytes in ADCC as well as in the spontaneous cytotoxicity.

Antibodies, Monoclonal↗
PubMed1981

Monocyte count, monocyte chemotaxis and chemotactic factor inactivator in gastric cancer patients.

The monocyte count in the peripheral blood, chemotactic responsiveness (MCR) and chemotactic factor inactivator (CFI) were measured in 66 patients with gastric cancer. Monocyte counts in advanced gastric cancer patients were significantly increased. MCR was significantly depressed in gastric cancer patients in the advanced stage of the disease, as compared with findings in the control groups. Sixty-seven percent of the patients with stage IV carcinoma had abnormally depressed responses. The CFIs were significantly higher in gastric cancer patients than in the control groups, and there was a positive correlation between the degree of inhibition and extent of cancer progress. These data support the hypothesis that qualitative and quantitative abnormalities of circulating monocytes, as macrophage precursors, may hinder immunological host defense mechanisms.

Adult↗
PubMed2001

Human monocytes and monocyte-derived macrophage phagocytosis of serotype III group B streptococci strains.

In this report group B streptococci (GBS) strains 90356 and 80340 isolated from liquor and vagina, respectively, were placed into contact with human peripheral blood monocytes (PBM) and macrophages derived from monocytes (MDM) by differentiation in vitro. The increased expression of CD16 and CD68 by macrophages cultured for 7 days compared with adherent monocytes supported the distinct maturation status of these cells. The number of viable intracellular bacteria of the 90356 strain was observed after 2 h of incubation with PBM (P < 0.001) and 0.5 h with MDM (P < 0.001). MDM cells seemed to present a more efficient mechanism of bacterial destruction of GBS type III, isolated from a case of meningitis. Viable cells of strain 80340, isolated from the vagina, were not detected in significant numbers in PBM and MDM phagocytic cells. These findings add to our current understanding of the roles played by multiple receptor-ligand systems in the uptake and pathogenesis of group B streptococci infection. Survival strategies of GBS, which interfere with macrophage bactericidal functions, might exist.

Antigens, CD↗
PubMed1995

Adhesion properties of Mono Mac 6, a monocytic cell line with characteristics of mature human monocytes.

Progress in the understanding of blood cell--endothelial cell interactions has been achieved by the development of in-vitro model systems. We describe adhesion properties of the recently established human monocytic cell line Mono Mac 6. These cells showed increased adherence to unstimulated and tumour necrosis factor (TNF)-alpha (50 U/ml) stimulated human umbilical vein endothelial cells (HUVEC) (9.4% +/- 0.4% and 56.5% +/- 3.3%), as compared to U937 cells (2.6% +/- 0.8% and 40.0% +/- 8.4%). The values were similar to freshly isolated human blood monocytes (18.8% +/- 7.5% and 55.7% +/- 9.3%, respectively). Maximal binding was 6.2 +/- 0.6 Mono Mac 6 cells per HUVEC, which was 34% less than U937 cells (8.9 +/- 0.3). The lower number of adherent Mono Mac 6 cells per HUVEC could be due to their larger size, as assessed by flow cytometry. Blocking experiments with monoclonal antibody (mAb) directed against E-selectin, VCAM-1 and ICAM-1 on HUVEC and CD11b or CD14 on Mono Mac 6 cells demonstrated the contribution of these molecules to Mono Mac 6 adherence. Reduced binding after 24 h parallels the decline of E-selectin expression in HUVEC. Linearity of cell binding was confirmed from 0.2 x 10(6) to 1.0 x 10(6) Mono Mac 6 cells. Expression of CD11b and CD14 in Mono Mac 6 cells and in isolated human monocytes but not in U937 cells leading to interaction with ICAM-1 on HUVEC appears to be responsible for the increased adhesion of Mono Mac 6, as compared to U937 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗
PubMed1985

Monocyte function in cervical carcinoma: plasma inhibitor of monocyte chemotaxis.

Blood monocyte function was tested in 43 untreated patients with carcinoma of the cervix (stages Ib to IIIb) and 50 age-matched controls. Monocyte counts, adhesion to glass, spreading on glass, phagocytosis and killing of Candida albicans, and chemotaxis under agarose were not significantly different between the patient and control groups. In 65% of a further series of 17 patient/control pairs, the plasma of cervical carcinoma patients was shown to contain a cell-directed inhibitor of monocyte chemotaxis. The accumulated evidence indicates that production of such factors by malignant tumors is an important mechanism in counteracting mononuclear phagocyte defense.

Candida albicans↗
PubMed1990

Inhibition of TPA-induced monocytic differentiation in THP-1 human monocytic leukemic cells by staurosporine, a potent protein kinase C inhibitor.

THP-1 is a factor-indepencent, monocytic leukemia cell line which differentiates into adherent macrophages upon treatment with 12-O-tetra-decanoylphorbol-13-acetate (TPA). Unlike its normal counterparts, THP-1 cells display only minimal levels of proto-oncogene c-FMS RNA which encode for membrane M-CSF receptors. Northern blot analysis showed that the c-FMS mRNA levels in THP-1 cells was greatly enhanced during TPA-induced monocytic differentiation. Despite the acquisition of functional activities and induction of c-FMS transcripts after TPA treatment, no surface M-CSF receptors were detected on the THP-1 cells. The inducing activity associated with TPA was completely abrogated when THP-1 cells were pretreated with staurosporine, a potent protein kinase C (PK-C) inhibitor. It is concluded that the activation of the PK-C system is a part of the metabolic cascade essential for the initiation of monocytic differentiation in THP-1 cells.

Alkaloids↗
PubMed1985

Prostaglandin and thromboxane biosynthesis in isolated platelet-free human monocytes. I. A modified procedure for the characterization of the prostaglandin spectrum produced by resting and activated monocytes.

We have developed a technique to isolate monocytes from human peripheral blood. The technique takes special care of completely eliminating platelets which are usually present in other preparations. Monocytes obtained in good yields (2.5-5.0 X 10(5) cells/ml blood), were found to be 70-80% pure on the basis of morphological and histochemical criteria. Contamination was largely due to the presence of lymphocytes. Monocytes were incubated in the presence or absence of arachidonic acid and TXB2, PGE2 and 6-keto-PGF1 alpha were measured by specific and sensitive radio-immunoassays. It was found that when cells were incubated for up to 1 hr, the production of PGs was low or absent even in the presence of 10 microM arachidonic acid in the incubation medium. However, when incubations were carried out for 24 hrs in the presence of at least 1% fetal calf serum a dramatic increase in TXB2 production occurred, with levels as high as 150 ng X 10(6) cells. The ratio TXB2/PGE2 was around 3, while 6-keto-PGF1 alpha was produced at a much lower level. In the same conditions, when care was taken to evaluate PGs already present in fetal serum and/or cross reactivity due to media generally employed, purified human lymphocytes appeared unable to produce detectable levels of the three PGs tested.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Monocyte chemoattractant protein 1: a potential regulator of monocyte recruitment in inflammatory disease.

The appearance of specific types of leukocytes in inflammatory infiltrates may be governed by cell-specific chemoattractants called chemokines. In particular, monocyte chemoattractant protein 1 (MCP-1) has been implicated in diseases characterized by monocyte-rich infiltrates, including atherosclerosis, rheumatoid arthritis and multiple sclerosis. While we are beginning to understand the structural determinants that govern the activities of MCP-1 in vitro, we know much less about its physiological functions in vivo and its pathogenetic role in disease. However, recent data from genetically modified mice have begun to place MCP-1 in a central position in monocyte trafficking and activation.

Amino Acid Sequence↗
PubMed1992

Ovarian steroids modulate human monocyte tumor necrosis factor alpha messenger ribonucleic acid levels in cultured human peripheral monocytes.

OBJECTIVE: To determine whether tumor necrosis factor alpha (TNF-alpha) messenger ribonucleic acid (mRNA) levels in human peripheral monocytes are regulated by ovarian steroids. DESIGN: Human granulosa-luteal cells and cultured, activated human peripheral monocytes were subjected to Northern blot analysis for TNF-alpha mRNA. SETTING: Academic research laboratory. PATIENTS: Two human female volunteers of reproductive age and in the luteal phase of the menstrual cycle. RESULTS: Human granulosa-luteal cells produce TNF-alpha mRNA. Physiological levels of progesterone (P) and estradiol (E2) modulate TNF-alpha mRNA from peripheral blood monocytes with an apparent inverse relationship between steroid concentration and TNF-alpha message. CONCLUSIONS: Progesterone and E2 at physiological concentrations regulate TNF-alpha mRNA production. The P antagonist mifepristone (RU486) and the E2 agonist/antagonist tamoxifen modulate total TNF-alpha mRNA levels, suggesting involvement of specific receptors.

Cells, Cultured↗
PubMed1986

Monocyte bone degradation: in vitro analysis of monocyte activity in patients with juvenile rheumatoid arthritis.

We examined the ability of the mononuclear phagocyte in vitro to degrade 45Ca-labeled bone particles to determine whether this assay allowed us to monitor disease activity in patients with juvenile rheumatoid arthritis. The monocytes from patients with juvenile rheumatoid arthritis receiving no anti-erosive therapy (n = 10) degraded significantly more bone than did cells obtained from normal controls (n = 10, P less than 0.001) or patients with juvenile rheumatoid arthritis receiving either gold thioglucose (n = 4, P less than 0.001) or D-penicillamine (n = 6, P less than 0.005). In two patients monitored for either 8 or 11 months, results of monocyte assays were found to parallel the clinical course. We conclude that in vitro monocyte bone degradation assays may provide a means of assessing joint activity in patients with juvenile rheumatoid arthritis. Further, this study and others indicate that mononuclear phagocytes are capable of causing erosive changes.

Adolescent↗