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PubMed1993

ATP- and UTP-induced currents in macrophages and macrophage polykaryons.

We have investigated the currents induced by extracellular ATP (ATPo), extra-cellular UTP, and other related compounds in macrophages. At potentials of -20 to -60 mV, a typical response to ATPo puffs consists of a fast-activating inward current followed by a transient outward current. The phenomenon lasts 5-20 s, but for sustained exposure to ATP the inward current persists for up to 10 min (our longest recording time). Both currents are inhibited by Mg2+, suggesting that the phenomenon is mediated by ATP4-. The outward current can be ascribed to a Ca(2+)-dependent K+ conductance, and release of Ca2+ from intracellular stores is at least in part responsible for this current. The inward current has a reversal potential of approximately 0 mV, and it is nonspecific for monovalent cations. UTP, a nucleotide that induces an increase in the cytoplasmic concentration of free Ca2+ but does not permeabilize macrophages, and ATP-gamma-S can also induce inward and outward current similar to those described for ATP, but higher doses are required. Adenosine and AMP produce no detectable effect, whereas ADP induces a small outward current. The implications of these results to the phenomenon of ATPo-induced permeabilization of macrophage membranes to large molecules are discussed.

Adenosine↗
PubMed2000

Role of alveolar macrophages in innate immunity in neonates: evidence for selective lipopolysaccharide binding protein production by rat neonatal alveolar macrophages.

As the first line of defense against inhaled substances, alveolar macrophages (AM) play a crucial role in maintaining lung homeostasis. This is achieved via phagocytosis of foreign material and the secretion of a wide range of mediator molecules, including those involved in neutrophil recruitment. Neonates are known to manifest increased susceptibility to lung infections, and we hypothesize that this may be due in part to a deficiency in the function of AM. We report here that although recruitment of neutrophils into the respiratory tract of newborn animals in response to Moraxalla catarrhalis exposure is greatly delayed and diminished, AM from newborn animals have greater phagocytic capacity when compared with those from adult animals. Additionally, newborn AM respond normally to lipopolysaccharide (LPS) via production of a variety of chemokines, including macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, monocyte chemotactic protein-1, gro/ cytokine-induced neutrophil chemoattractant, MIP-2, and tumor necrosis factor-alpha. We have also demonstrated an LPS inducible expression of messenger RNA for LPS binding protein (LBP) in neonatal AM that was not observed in AM from adult animals or in peritoneal macrophages. We speculate that local production of LBP by AM may be a significant factor in the neonatal immunologic response to infections, providing a compensatory mechanism for the deficiency in specific neonatal immunity during this period of development when the newborn is being exposed to a range of potentially pathogenic materials for the first time.

Animals↗
PubMed2001

Human lung tissue macrophages, but not alveolar macrophages, express matrix metalloproteinases after direct contact with activated T lymphocytes.

Human alveolar macrophages (AM) and lung tissue macrophages (LTM) have a distinct localization in the cellular environment. We studied their response to direct contact with activated T lymphocytes in terms of the production of interstitial collagenase (MMP-1), 92-kD gelatinase (MMP-9), and of TIMP-1, one of the counter-regulatory tissue inhibitors of metalloproteinases. Either AM obtained by bronchoalveolar lavage or LTM obtained by mincing and digestion of lung tissue were exposed for 48 h to plasma membranes of T lymphocytes previously activated with phorbol myristate acetate and phytohemagglutinin for 24 h. Membranes of activated T cells strongly induced the production of MMP-1, MMP-9, and TIMP-1 exclusively in LTM but not in AM, whereas membranes from unstimulated T cells failed to induce the release of MMPs. Both populations of mononuclear phagocytes spontaneously released only small amounts of MMPs and TIMP-1. Similar results were obtained when MMP and TIMP-1 expression was analyzed at pretranslational and biosynthetic levels, respectively. Blockade experiments with cytokine antagonists revealed the involvement of T-cell membrane-associated interleukin-1 and tumor necrosis factor-alpha in MMP production by LTM upon contact with T cells. These data suggest that the ability of lung macrophages to produce MMPs after direct contact with activated T cells is related to the difference in phenotype of mononuclear phagocytes and cell localization. In addition, these observations indicate that cell-cell contact represents an important biological mechanism in potentiating the inflammatory response of mononuclear phagocytes in the lungs.

CD40 Ligand↗
PubMed2006

Heat stress response results in increased macrophage inflammatory protein-2 concentration in a lipopolysaccharide-exposed macrophage cell line.

Pretreatment with heat confers cardiopulmonary protection in endotoxemic animals. This mechanism may be through suppression of pro-inflammatory mediator production. The objectives of this study were to determine the effect of heat stress on tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 (MIP-2) in a lipopolysaccharide-exposed macrophage cell line and to study the relationship between TNF-alpha and MIP-2 production. Heat pretreatment resulted in decreased TNF-alpha transcription and translation by lipopolysaccharide-exposed macrophages; and increased MIP-2 concentration without additional effect in transcription. Administration of TNF-alpha antibody prior to exposure to lipopolysaccharide resulted in increased MIP-2 concentration suggesting that TNF-alpha acts to down-regulate MIP-2 production. The mechanism by which heat stress causes an increase in MIP-2 concentration may be secondary to its suppressing effect on TNF-alpha production.

Animals↗
PubMed2000

Endo180, an endocytic recycling glycoprotein related to the macrophage mannose receptor is expressed on fibroblasts, endothelial cells and macrophages and functions as a lectin receptor.

Endo180 was previously characterized as a novel, cell type specific, recycling transmembrane glycoprotein. This manuscript describes the isolation of a full length human Endo180 cDNA clone which was shown to encode a fourth member of a family of proteins comprising the macrophage mannose receptor, the phospholipase A(2) receptor and the DEC-205/MR6 receptor. This receptor family is unusual in that they contain 8-10 C-type lectin carbohydrate recognition domains in a single polypeptide backbone, however, only the macrophage mannose receptor had been shown to function as a lectin. Sequence analysis of Endo180 reveals that the second carbohydrate recognition domain has retained key conserved amino acids found in other functional C-type lectins. Furthermore, it is demonstrated that this protein displays Ca(2+)-dependent binding to N-acetylglucosamine but not mannose affinity columns. In order to characterize the physiological function of Endo180, a series of biochemical and morphological studies were undertaken. Endo180 is found to be predominantly expressed in vivo and in vitro on fibroblasts, endothelial cells and macrophages, and the distribution and post-translational processing in these cells is consistent with Endo180 functioning to internalize glycosylated ligands from the extracellular milieu for release in an endosomal compartment.

Amino Acid Sequence↗
PubMed2004

Effect of various catechins on the IL-12p40 production by murine peritoneal macrophages and a macrophage cell line, J774.1.

Interleukin-12 (IL-12) is a heterodimeric cytokine comprising p40 and p35 subunits produced mainly by monocytes and macrophages, and plays an essential role in the regulation of the differentiation of Th1 cells. Green tea polyphenols exhibit potent anti-oxidative activities and anti-inflammatory effects by modulating cytokine production. We investigated the effect of catechins on IL-12p40 production in murine macrophages induced by bacterial lipopolysaccharide (LPS). Pretreatment with several catechins at doses of 0.3-30 microM suppressed IL-12 p40 production by murine peritoneal exudate cells (PEC) and J774.1 cells in a dose-dependent manner. Decreases in protein production were primarily due to down-regulation of the transcription of IL-12p40 mRNA. Of the various catechins, (-)-epigallocatechin gallate (EGCG) was the most potent inhibitor, followed by (-)-gallocatechin gallate (GCG) and (-)-epicatechin gallate (ECG). EGCG inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS-induced phosphorylation of p44/p42 extracellular signal-related kinase (ERK). In addition, both EGCG and GCG inhibited LPS-induced degradation of IkappaBalpha with concomitant inhibition of nuclear protein binding to NF-kappaB site and synthesis of IRF-1. These results suggest that gallate-containing catechins, particularly EGCG, inhibits LPS-induced IL-12p40 production in murine macrophages by inhibiting p38 MAPK while enhancing p44/p42 ERK, leading to the inhibition of IkappaBalpha degradation and NF-kappaB activation.

Animals↗
PubMed1987

Increase in macrophage progenitor cell number in femoral marrow of mice after continuous infusion or repeated injections of a macrophage colony-stimulating factor.

Continuous intraperitoneal infusion of a macrophage colony-stimulating factor (M-CSF or CSF-1) for 6 d resulted in a 2.3-fold increase in the frequency of progenitor cells (CFUc) of macrophages in femoral marrow in C3H/HeN mice but there was no significant increase in the number of blood leukocytes in these animals. Infusion of bacterial lipopolysaccharide (LPS) also increased femoral macrophage CFUc frequency to the same extent as the above. Furthermore, the effect of the M-CSF preparation was much less pronounced in LPS-resistant C3H/HeJ mice than in LPS-sensitive C3H/HeN mice. The results show that the effect of M-CSF on bone marrow CFUc is marginal, even when it is administered in large amounts in the animals.

Animals↗
PubMed1990

Suppression of alveolar macrophage membrane receptor-mediated phagocytosis by model and actual particle-adsorbate complexes. Initial contact with the alveolar macrophage membrane.

Alveolar macrophages were treated with carbon blacks and adsorbates in order to evaluate the biologic effect of adsorbate, adsorbent and adsorbate-adsorbent complexes. Their capacity to phagocytize a subsequent challenge via the Fc-membrane receptor was quantified. Phagocytosis was suppressed in a dose-related manner with increasing concentrations of both carbon blacks and adsorbates. Carbon black N339 covered with 0.5 monolayers of the adsorbates suppressed phagocytosis more than N339 without the adsorbates. Increasing the adsorbate acrolein coverage from 0.5 to greater than 2.0 monolayers suppressed phagocytosis in a dose-related manner. Finally, samples of diesel particulate matter collected from an engine operated on a pure hydrocarbon fuel with various oxidizers, air (PSU #1) and an oxidizer free of nitrogen (N-free) were tested. Treatment of the macrophages with PSU #1 had a negligible effect on phagocytosis whereas the N-free sample suppressed phagocytosis in a dose-related manner. The data show that alveolar macrophage Fc-receptor-mediated phagocytosis is affected by: carbon black and adsorbate identity and concentration, coverage of the carbon black with adsorbates, and the oxidizer used in the generation of particles emitted by a diesel engine.

Adsorption↗
PubMed2004

Bismuth uptake in rat testicular macrophages: a follow-up observation suggesting that bismuth alters interactions between testicular macrophages and Leydig cells.

Recent studies suggest that bismuth accumulates in Leydig cells. In addition, a reduced level of serum testosterone and a statistically significant reduction of Leydig cells have been observed. It was therefore hypothesized that Bi has a direct toxic effect on rat Leydig cells. We have now developed a method for double labeling of bismuth and ED-2 (a marker for testicular macrophages). The present data demonstrate that the heavily bismuth-loaded cells in rat testis, originally interpreted as being Leydig cells, are bismuth-loaded macrophages. Consequently, our data suggest a modified hypothesis regarding bismuth-induced interactions between testicular macrophages and Leydig cells.

Animals↗
PubMed1975

Distribution of cytophilic and anti-macrophage antibody on the macrophage surface.

The binding of cytophilic antibody to the macrophage surface results in patterns of distribution similar to those obtained when specific anti-macrophage antibody is used. These patterns are (a) diffuse circumferential binding at 4 degrees C, and (b) capping at 37 degrees C. The non-random distribution of the cytophilic antibody suggests that it binds to certain well-defined sites on the macrophage membrane.

Animals↗
PubMedDate not supplied

Inhibition of yeast phagocytosis by dexamethasone in macrophage cultures: reversibility of the effect and enhanced suppression in cultures of stimulated macrophages.

This investigation was initiated to characterize further the ability of 1 microM dexamethasone to suppress the ingestion of heat-killed Saccharomyces cerevisiae particles in cultures of murine resident peritoneal macrophages. Time course studies revealed that the inhibitory response required the continual presence of the steroid in the culture medium. In addition, increased inhibitory responses occurred after dexamethasone was supplied to previously untreated cultures of resident macrophages that became stimulated by differentiating in vitro. These findings indicate that glucocorticoids act directly on macrophages to decrease their phagocytic capacity, which in vivo would reduce host resistance.

Cells, Cultured↗
PubMed1997

Role of macrophages in experimental malaria: V--Effect of ethyl palmitate on macrophages in Plasmodium berghei infected mice.

Ethyl palmitate (EP) was used as a macrophage cytotoxin. The response of P. berghei after exposing the macrophage to EP was opposite to what was seen with other agents like Silica, Antimacrophage serum and Freund's complete adjuvant. EP at dose of 5 mg and above decreased the survival period (SP), median survival day (MSD) and parasite density 24 hrs. before death (K values). Prepatent period (PP) was lower at doses 10 mg and 20 mg per day for 5 days before challenge compared to their corresponding controls. EP at a dose of 5 mg and above was found to be toxic to host, mice. EP in dosage of 3 mg per mouse administered 48 hrs. before challenge resulted in an increase in the mean survival period, survival rate (30%) and decrease in the mean parasitaemia per day when compared with the corresponding control. The interfering agents affected differently both the host and/or parasite. A proper modulation of the macrophage during the course of infection may help the host in surviving this lethal infection.

Animals↗
PubMed2000

Macrophage inflammatory protein 1alpha attenuates the toxic effects of temozolomide in human bone marrow granulocyte-macrophage colony-forming cells.

Macrophage inflammatory protein 1alpha (MIP-1alpha) is a chemokine that may act principally by preventing hemopoietic cells from entering G1, thereby attenuating the cytotoxic effects of cell cycle-specific chemotherapeutic agents. Here we examine the effect of MIP-1alpha on the sensitivity of human granulocyte-macrophage hemopoietic progenitor cells (granulocyte-macrophage colony-forming cells; GM-CFCs) with the cytotoxic effects of antitumor agents that act mainly via alkylation at the O6 position of guanine in DNA. Mononuclear cell preparations from human bone marrow were used in an in vitro GM-CFC colony-forming assay. The GM-CFC survival from individual patients displayed a range of sensitivities to the methylating agent temozolomide [(Tz) 20-55% survival at 10 microg/ml Tz]. However, in all 16 cases, MIP-1alpha (50 ng/ml) protected against GM-CFC killing: survival in the presence of MIP-1alpha ranged from 65-97% at 10 microg/ml Tz, with GM-CFCs being 1.5-4.5-fold more resistant than control cells from the same patient. The highest levels of protection were seen in the GM-CFCs with the highest sensitivity in the absence of MIP-1alpha. Similar degrees of protection were seen for the methylating agent streptozotocin, but no protection was detected for the chloroethylating agents carmustine or mitozolomide in the samples for which there was protection against the toxic effects of Tz. Whereas the mechanism of this effect remains to be established, the results may have potential immediate clinical application in the attenuation of hematological toxicity after administration of methylating antitumor agents.

Antineoplastic Agents, Alkylating↗
PubMed2000

Significance of macrophage chemoattractant protein-1 in macrophage recruitment, angiogenesis, and survival in human breast cancer.

Tumor cells stimulate the formation of stroma that secretes various mediators pivotal for tumor growth, including growth factors, cytokines, and proteases. However, little is known about the local regulation of these soluble mediators in the human tumor microenvironment. In this study, the local expression of cytokines, chemokines, and angiogenic factors was investigated in primary breast cancer tissue. The concentrations of interleukin (IL)-1, IL-4, IL-6, IL-10, IL-12, tumor necrosis factor (TNF)-alpha, IFN-gamma, IL-8, macrophage chemoattractant protein (MCP)-1, epithelial-neutrophil activating peptide-78, vascular endothelial growth factor, and thymidine phosphorylase (TP) were measured in 151 primary breast cancer extracts by ELISA. Tumor-associated macrophages (TAMs) were also examined by immunohistochemistry with anti-CD68 antibodies. The correlation between soluble mediators and the relationship between TAM count and soluble mediators were evaluated. MCP-1 concentration was correlated significantly with the level of vascular endothelial growth factor, TP, TNF-alpha, and IL-8, which are potent angiogenic factors. IL-4 concentration was correlated significantly with IL-8 and IL-10. On the other hand, an inverse association was observed between TP and IL-12. The level of MCP-1 was associated significantly with TAM accumulation. In the immunohistochemical analysis, MCP-1 expression was observed in both infiltrating macrophages and tumor cells. Prognostic analysis revealed that high expression of MCP-1, as well as of VEGF, was a significant indicator of early relapse. These findings indicate that interaction between the immune network system and angiogenesis is important for progression of human breast cancer, and that MCP-1 may play an important role in the regulation of angiogenesis and the immune system.

Adult↗
PubMed1992

Coexpression of type I and type II human macrophage scavenger receptors in macrophages of various organs and foam cells in atherosclerotic lesions.

Macrophage scavenger receptors are trimeric membrane glycoproteins implicated in the pathologic deposition of cholesterol in arterial walls during atherogenesis. Two types of cDNAs for functional human receptors have been cloned, but their physiologic roles remain obscure. To study the expression of these receptors, the authors generated antibodies against scavenger receptor type-specific synthetic peptide. Immunohistochemical examination using these antibodies and other anti-human receptor antibodies shows that type I and type II receptor proteins can be detected in foam cells in various stages of atherosclerosis, most evidently in fatty streaks. Co-expression of the two types of receptor protein was also detected in macrophages of various organs. Both types of the protein were detected on the surface and the membrane of endosomes in macrophages. These results indicate that both type I and type II scavenger receptors are expressed and functionally active in physiologic and pathologic conditions.

Arteriosclerosis↗
PubMed1990

Induction and regulation of IL-4 receptor expression on murine macrophage cell lines and bone marrow-derived macrophages by IFN-gamma.

IL-4 is a T cell-derived cytokine that regulates the induction of proliferation of resting B cells, and appears to act on various other cells involved in the immune response. The pluripotential effects of IL-4 are dependent on the interaction of IL-4 with its receptor (IL-4R). Although the regulation and metabolism of these receptors have been examined on B and T cells, little is known about the metabolism or regulation of the IL-4R on macrophages. In studying the dynamics of IL-4R expression on the murine macrophage-like cell line J774.16, we detected the presence of low numbers of high affinity IL-4R (234 +/- 38, Kd = 110 +/- 11 pM) on the surface membrane. However, upon exposure to IFN-gamma, a potent macrophage activating cytokine, there was a rapid upregulation (within 45 min) of IL-4R (2750 +/- 178) on the cell surface, with no change in receptor affinity (Kd = 205 +/- 37 pM). Maximum expression occurred at 2 to 4 h with no further increase in IL-4R expression over the next 48 h. Cells pulsed with IFN-gamma for 45 min displayed maximum IL-4R expression by 4 h. The induction of IL-4R by IFN-gamma was dose dependent: as little as 0.5 ng/ml of IFN-gamma was capable of inducing IL-4R expression, with optimal induction at 10 ng/ml. The addition of the metabolic inhibitors actinomycin D and cycloheximide before the addition of IFN-gamma indicated that both RNA transcription and protein translation were required for this upregulation to occur.

Animals↗
PubMed1989

[Macrophage activation by synthetic peptides. II. The effect of oxidative burst products on the fluorescence kinetics of macrophages stained with fluorescein diacetate].

Our previous study has shown that the intensity of macrophages in a medium containing fluorescein diacetate (FDA) retains a certain constant level ready to fall upon the addition of stimulants. The decrease in fluorescence was attempted to explain by secretion of oxygen metabolites during the activation process. The decrease in fluorescence is much smaller in the medium containing catalase and superoxide dismutase. Hydrogen peroxide (50 nM and higher) causes a reversible decrease in the fluorescent intensity of resting macrophages. These experiments suggest that the oxidative burst products may serve as regulators of the feedback control during macrophage activation.

Animals↗
PubMed1989

Structures on T cells and macrophages involved in interleukin 1 (Il-1) secretion by macrophages upon contact with syngeneic thymocytes.

We demonstrate, using a new rosette method of determination of interleukin 1 activity that macrophages secrete Il-1 upon contact with syngeneic thymocytes or with thymocytes homologous in the Ia region of MHC complex. The phenomenon takes place in the absence of foreign antigen. Blocking of class II MHC antigens on macrophages with monoclonal antibodies against structures of the T-cell receptor complex (alpha/beta T-cell receptor-TCR, CD3 and L3T4) inhibits production of Il-1 to the background level. We conclude that secretion of Il-1 from macrophages, upon contact with syngeneic thymocytes, is triggered by a T-cell signal following interaction: TCR-Ia molecules.

Animals↗