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PubMed1972

Staphylococcidal capability of rabbit peritoneal macrophages in relation to infection and elicitation: induction and elicitation of activated macrophages.

The capability of macrophages to inactivate ingested staphylococci can be augmented when repeated infection is followed by specific elicitation with staphylococcal lysate. The increase in staphylococcidal capability with specific elicitation after infection is not dramatic but is statistically significant. The percentage of change in staphylococcidal capability after infection and specific elicitation is systematically related to the staphylococcidal capability of the populations of macrophages in the same rabbits studied prior to infection. When the capability of the initial populations of macrophages has been high, the percentage of change after infection and elicitation may be slight or even negative. When the staphylococcidal capability of the initial population of macrophages in a given rabbit has been low, there is typically a significant increase in this capability after infection and elicitation. It is shown at the cellular level that it is possible to evoke a population of activated macrophages, by a procedure which is analogous to procedures reported as useful in human practice.

Animals↗
PubMed1988

Production of colony-stimulating factors (CSFs) during infection: separate determinations of macrophage-, granulocyte-, granulocyte-macrophage-, and multi-CSFs.

After infection of mice with Listeria monocytogenes, elevated levels of colony-stimulating factors (CSFs) in the serum were quantitated by six different assays: ability to stimulate colony formation, the proliferation of 2 suspension of bone marrow cells (both measuring total colony-stimulating activity), a radioimmunoassay for macrophage-CSF (CSF-1), the WEHI-3B differentiation assay for granulocyte-CSF, and proliferation of 32D-c1-3 and FDC-P1 cell lines (specific for multi-CSF and either multi- or granulocyte-macrophage-CSFs, respectively). The great bulk of serum colony-stimulating activity represented macrophage- and granulocyte-CSFs, with small but measurable amounts of granulocyte-macrophage-CSF. The degree of elevation of serum CSF depended on the infecting dose used and the numbers of bacteria growing in the spleens and livers of the two mouse strains compared, i.e., L. monocytogenes-resistant C57BL/10 and susceptible BALB/cJ. The increase in serum CSFs occurred before the peak in bone marrow granulocyte-macrophage progenitors and before the reduction in bacterial numbers which follows the onset of specific cell-mediated immunity.

Animals↗
PubMed1992

Adherence of Legionella pneumophila to guinea pig peritoneal macrophages, J774 mouse macrophages, and undifferentiated U937 human monocytes: role of Fc and complement receptors.

Legionella pneumophila, the causative agent of Legionnaires' disease, is a facultative intracellular pathogen of alveolar macrophages. Although previous studies have demonstrated that specific antibody facilitates uptake of L. pneumophila by phagocytic cells, the role of complement has been unclear. Thus, we have examined the relative contributions of Fc gamma- and complement receptor-mediated adherence to guinea pig peritoneal macrophages, U937 human monocytic cells, and J774 mouse macrophage cells. Opsonization of L. pneumophila (Philadelphia 2) with polyclonal immunoglobulin G promoted maximum adherence to guinea pig macrophages. In contrast, incubation in the presence of 20% fresh nonimmune human serum from a single donor did not promote adherence. The results obtained with U937 and J774 cells paralleled those obtained with guinea pig macrophages. In the absence of specific antibody, opsonization with guinea pig complement did not enhance adherence of the Philadelphia 1, Philadelphia 2, or Knoxville strain. However, when complement was added to heat-inactivated, specific antiserum, a fourfold increase in the number of adherent organisms was observed. Blocking studies utilizing membrane receptor-specific monoclonal antibodies demonstrated that both Fc and complement receptors mediated adherence of organisms treated with complement in the presence of specific antibody. These results suggest that complement augments adherence of L. pneumophila only when acting in concert with specific antibody.

Animals↗
PubMed1989

Insertional activation of N-myc by endogenous Moloney-like murine retrovirus sequences in macrophage cell lines derived from myeloma cell line-macrophage hybrids.

Hybrids formed from a myeloma cell line, NS1, and macrophages initially show myeloma properties but later, after loss of the parental macrophage genome and consequent loss of myeloma characteristics, express macrophage properties. Molecular studies demonstrated that macrophage properties in the hybridomas originate from the NS1 parental cells (M. Setoguchi, S. Yoshida, Y. Higuchi, S. Akizuki, and S. Yamamoto, Somatic Cell Mol. Genet. 14:427-438, 1988). In such hybrids, N-myc was activated by insertion of endogenous Moloney-like retrovirus sequences into mouse N-myc exon 3 when the hybrids gained macrophage properties. Interestingly, expression of N-myc took place in all aged hybrids. These results suggest that such unique insertional mutagenesis occurs in a regionally specific manner and that expression of N-myc may play a role in hematopoietic lineage conversion.

Amino Acid Sequence↗
PubMed1998

Extracellular matrix modulates macrophage functions characteristic to atheroma: collagen type I enhances acquisition of resident macrophage traits by human peripheral blood monocytes in vitro.

Activated resident macrophages sustain atheroma, and a high macrophage content is associated with plaque vulnerability. Factors leading to differentiation and activation of these blood-derived cells remain largely uncharacterized. We investigated the contribution of interaction with collagen type I, the predominant component of atherosclerotic matrix, to differentiation and modulation of characteristic macrophage functions, including intracellular lipid accumulation and production of the typical matrix-degrading enzyme matrix metalloproteinase (MMP)-9. When used as an adhesion substrate for human peripheral blood monocytes in vitro, collagen type I increased monocyte differentiation, assessed by analysis of CD71 expression and cell spreading. Culturing on collagen type I doubled the number of differentiated monocytes at 24 hours (44.9+/-1.4% versus 18.4+/-1.7% on uncoated dishes, P<.001, n=3 independent experiments) and was a stronger stimulus for differentiation than phorbol myristate acetate, a known inducer of monocyte differentiation. The effect of substrate on intracellular accumulation of modified lipoproteins was assessed by quantitative confocal microscopy of monocytes incubated with fluorescent acetylated LDL. The collagen type I substrate also doubled the number of macrophages containing intracellular lipid and significantly increased the individual intracellular loading. Monocytes cultured on collagen type I also released more MMP-9 than did cells plated directly on plastic. The role of monocyte spreading was further assessed by treatment with colchicine, an inhibitor of cytoskeletal function, or with genistein, a nonspecific inhibitor of tyrosine kinases, shown to participate in cell adhesion. Cell spreading was inhibited in 72.3+/-6.7% of colchicine-treated and in 62.4+/-6.4% of genistein-treated monocytes (n=3, P<.01 in both cases). The same conditions also decreased secretion of MMP-9, and genistein reduced the number of acetylated LDL-containing cells (from 286+/-7 to 184+/-8 cells/mm2 with genistein, n=3, P<.001). Data showed a strong correlation (r>.98) between monocyte spreading on collagen type I and intracellular lipid accumulation. Our results indicate that interaction with vascular matrix may play an important role in differentiation of peripheral blood monocytes into resident lipid-laden macrophages, which act as central stimulators throughout the natural history of atheroma.

Arteriosclerosis↗
PubMed2000

Adenovirus-mediated gene transfer of a secreted form of human macrophage scavenger receptor inhibits modified low-density lipoprotein degradation and foam-cell formation in macrophages.

BACKGROUND: Macrophage scavenger receptors (MSRs) play an important role in the pathogenesis of atherosclerosis. Therefore, local modulation of MSR activity could have a beneficial effect on atherogenesis. METHODS AND RESULTS: We cloned a secreted "decoy" MSR (sMSR) that contains an extracellular portion of the human MSR type AI and constructed an adenoviral vector that directs high-level expression of sMSR in macrophages under the control of the human CD68 promoter. Expression of the sMSR protein inhibited the degradation of (125)I-labeled acetylated LDL and oxidized LDL by murine macrophages up to 90%. sMSRs also reduced acetylated LDL degradation in MSR knockout mouse peritoneal macrophages by 60% to 80%, which suggests that the decoy construct can compete for the uptake mediated via other related scavenger receptors. In addition, sMSRs inhibited foam-cell formation in murine macrophages in the presence of cytochalasin D. The mechanism of inhibition is through ligand binding to the sMSRs, which prevents the ligand binding to MSRs on cell membranes. CONCLUSIONS: The demonstration that recombinant adenovirus-mediated gene transfer of decoy sMSRs can block foam-cell formation suggests a possible new strategy for gene therapy of atherosclerosis and for the treatment of lipid accumulation after arterial manipulations.

Adenoviridae↗
PubMed1991

Presence of platelet-derived growth factor in normal and fibrotic lung is specifically associated with interstitial macrophages, while both interstitial macrophages and alveolar epithelial cells express the c-sis proto-oncogene.

Normal lung structure is maintained by the presence of mesenchymal cells and their extracellular matrix products. The slow normal turnover of these cells is disrupted in fibrotic disorders, resulting in the in situ accumulation of mesenchymal cells and their extracellular matrix leading to a progressive alveolar wall thickening. Idiopathic pulmonary fibrosis (IPF) is a chronic fibrotic disorder of the lung characterized by a diffuse interstitial and intra-alveolar inflammation dominated by macrophages and polymorphonuclear neutrophils. Evaluation of alveolar macrophages (AM) obtained by bronchoalveolar lavage has previously shown that AM from normal individuals spontaneously release small amounts of platelet-derived growth factor (PDGF), a chemotactic and growth factor for mesenchymal cells, whereas AM from IPF patients spontaneously release increased amounts of biologically active PDGF, suggesting its involvement in mesenchymal cell accumulation. However, other cells such as endothelial cells and vascular smooth muscle cells can also release PDGF in vitro. In order to specify PDGF location in lung parenchyma, open lung biopsies from normal individuals and IPF patients were examined by immunohistochemistry using an anti-PDGF antibody and by in situ hybridization using PDGF A-chain and B-chain gene probes. In normal as well as in fibrotic lung, PDGF was only present in relation with interstitial macrophages but not with any other inflammatory cells or mesenchymal cells. Furthermore, the percentage of PDGF-positive macrophages in IPF was 3-fold increased in comparison to normal lung. In addition, the percentage of PDGF-positive macrophages was the same in fibrotic and nonfibrotic areas of IPF lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1996

Proteolytic cleavage and activation of pro-macrophage-stimulating protein by resident peritoneal macrophage membrane proteases.

Macrophage stimulating protein (MSP), which is secreted as biologically inactive pro-MSP, is activated to MSP by cleavage at a single peptide bond. Our objectives were to determine the form of MSP in circulating blood and to study proteolytic activation of pro-MSP by its target cell. Western blot of immunoaffinity-purified serum MSP showed that all the protein was pro-MSP, without detectable MSP. The circulating form of the protein is therefore pro-MSP, and conversion to MSP does not occur when blood is shed. Incubation of radiolabeled pro-MSP with murine peritoneal macrophages caused proteolytic cleavage to predominantly inactive fragments. Among several protease inhibitors, soybean trypsin inhibitor was one of two that inhibited nonspecific cleavage and revealed a macrophage proteolysis of pro-MSP, and certain concentrations enhanced cleavage to mature MSP. Macrophage membranes had nonspecific and specific pro-MSP proteolytic activity, which was not present in macrophage culture fluids. The results suggest that control of MSP activity can occur at the level of the target cell by proteolytic cleavage of pro-MSP to mature MSP or to inactive fragments.

Animals↗
PubMed1993

Liposome-mediated macrophage depletion: an experimental approach to study the role of testicular macrophages in the rat.

Liposome-entrapped dichloromethylene diphosphonate was injected locally into the right testes of adult rats. This treatment, which has been found to deplete resident macrophages in some other organs, reduced the number of testicular macrophages by at least 90%. Testicular weight and seminiferous tubule morphology were unaffected by liposome treatment. Leydig cell testosterone secretion gradually declined in the macrophage-depleted testes, and there was a compensatory increase in Leydig cell size and testosterone secretion in the contralateral saline-injected testes. These observations suggest that macrophages influence Leydig cell function locally. It is concluded that liposome-mediated depletion of testicular macrophages may serve as an experimental model with which to study the physiological role of these cells.

Animals↗
PubMed1979

Macrophages in experimental and human brain tumors. Part 1: Studies of the macrophage content of experimental rat brain tumors of varying immunogenicity.

Although the presence of lymphoreticular cells within tumors has been recognized for over 100 years, it is only within the last decade that the concept has arisen that standard histological examination techniques may lead to an underestimation of the true extent of tumor infiltration by lymphoreticular cells, and particularly by macrophages. The macrophage content of certain systemic tumors has been correlated with their immunogenicity and growth characteristics. Since the central nervous system is to some extent an "immunologically privileged site" and contains within it specialized reticuloendothelial cells called microglia, the authors determined the macrophage content of three rodent brain-tumor cell lines, and attempted to correlate this macrophage content with their immunogenicity and growth characteristics. Their findings indicate a direct correlation between the immunogenicity and macrophage content of these three neural tumor cell lines.

Animals↗
PubMed1979

Macrophages in experimental and human brain tumors. Part 2: studies of the macrophage content of human brain tumors.

The authors have analyzed 47 tumors of the central nervous system (11 glioblastomas, nine meningiomas, three medulloblastomas, 12 assorted primary neural tumors, and 12 brain metastases) for their content of macrophages. Cell suspensions were prepared by enzymatic digestion and macrophages were quantitated by IgGEAC rosette formation. Adsorption of sensitized indicator cells (EA) to sections of tumor was used as a measure to determine the distribution of IgGFc receptor-positive cells within the tumors and to serve as a control for selective release of IgGFc receptor-positive cells by enzyme digestion. The 11 glioblastomas had a mean macrophage content of 45% (range: 8% to 78%), the nine meningiomas had a mean of 44% (range: 5% to 81%), the three medulloblastomas a mean of 6% (range 2% to 15%), and the metastatic tumors a mean of 24% (range: 4% to 70%). Adsorption of EA demonstrated that IgGFc receptor-positive cells were distributed throughout the tumor mass, although different types of patterns were observed. There was an excellent correlation between the percent of IgGEAC positive cells in suspensions and the extent of EA adsorption to the tumor sections. Compared to systemic neoplasms, most nervous system tumors have a high macrophage content. It is possible that the high macrophage content of brain tumors is related to their immunogenicity, and may be a partial explanation for tha rarity of brain-tumor metastases.

Brain Neoplasms↗
PubMed1976

The function of macrophages in antigen recognition by guinea pig T lymphocytes. III. Genetic analysis of the antigens mediating macrophage-T lymphocyte interaction.

Activation of immune T lymphocytes by antigen-pulsed macrophages is mediated by the Ia antigens of the guinea pig MHC or the products of closely linked genes. Studies using combinations of macrophages and T cells derived from outbred animals with different Ia antigens and/or Ir gene products have demonstrated that sharing of Ir gene products between macrophage and T cells is not sufficient for effective macrophage-T cell interaction. The role of the Ia antigens in the absence of the linked Ir gene products could not be directly examined because we were unable to identify an animal which bore the full complement of Ia antigens in the absence of the Ir gene that is normally associated with them. The results of these studies support the concept of the functional expression of the Ir gene product in the macrophage.

Animals↗
PubMed1992

Chemotactic response of macrophages to Acanthamoeba castellanii antigen and antibody-dependent macrophage-mediated killing of the parasite.

The chemotactic potential of antigens of Acanthamoeba castellanii for macrophages and the ability of naive and immune rat peritoneal macrophages to kill A. castellanii in vitro were assessed. The amoebolytic capacity of immune rat serum and complement was also examined. No parasite was killed in the presence of heat-inactivated naive rat serum. Low numbers of parasites were lysed in the presence of heat-inactivated immune rat serum, whereas significantly greater numbers of parasites were lysed in the presence of nonheat-inactivated naive and immune rat serum. Macrophages from naive rats were capable of lysing some parasites. However, the amoebolytic capability of these cells was significantly increased in the presence of serum from immune rats. Regardless of the source of serum used, macrophages from immune rats demonstrated about twice the amoebolytic proficiency of cells from naive rats. Macrophages from naive rats showed their highest capacity for lysing amoebae when incubated in the presence of gamma interferon and immune rat serum. The greatest overall proficiency in lysing parasites was displayed by cells from immune rats incubated with A. castellanii in the presence of gamma interferon and nonheat-inactivated serum from immune rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acanthamoeba↗
PubMed1990

Macrophage deactivating factor and transforming growth factors-beta 1 -beta 2 and -beta 3 inhibit induction of macrophage nitrogen oxide synthesis by IFN-gamma.

Macrophage deactivating factor (MDF) and three members of the transforming growth factor-beta family (TGF-beta 1, -beta 2, and -beta 3) blocked the ability of IFN-gamma to induce release of reactive nitrogen intermediates from mouse peritoneal macrophages. Raising the concentration of IFN-gamma did not diminish the potency of the inhibitors (50% inhibition by approximately 7 nM MDF, 2 pM TGF-beta 1, 4 pM TGF-beta 2, and 8 pM TGF-beta 3). These inhibitors partially blocked induction of nitrite release in macrophages activated with the combination of IFN-gamma plus TNF-alpha, but were incapable of inhibiting when macrophages were activated by the combination of IFN-gamma plus LPS. MDF and TGF-beta 1, -beta 2, and -beta 3 inhibited IFN-gamma-induced nitrite release only if present during the induction phase; once IFN-gamma-nitrite release had commenced, addition of the same cytokines was no longer inhibitory. Maximum inhibition of synthesis over a 48-h period required that the inhibitors be present during the first 3 h of induction. Thus, cytokines can suppress as well as induce macrophage synthesis of reactive nitrogen intermediates, products with cytotoxic, antimicrobial, and vasodilatory properties.

Animals↗
PubMed1990

Ultrastructural localization of a macrophage-restricted sialic acid binding hemagglutinin, SER, in macrophage-hematopoietic cell clusters.

Resident bone marrow macrophages in hematopoietic clusters have previously been shown to express a novel lectin-like sheep erythrocyte receptor, SER, which mediates binding of unopsonized sheep erythrocytes via recognition of sialylated glycoconjugates and may interact with sialylated ligands on murine bone marrow cells. In this study, the distribution of SER on macrophages within hematopoietic clusters was localized by a monoclonal antibody, SER-4, by immunofluorescence and immunoelectron microscopy. SER was found to be diffusely localized at the contact zones between macrophages and erythroblasts, whereas the receptor was highly concentrated at the contacts between macrophages and developing myelomonocytic cells. These data suggest that SER on resident bone marrow macrophages interacts differentially with sialylated ligands on developing myeloid cells and that this may influence their development.

Animals↗
PubMed1989

Effect of cisplatin, lipopolysaccharide, muramyl dipeptide and recombinant interferon-gamma on murine macrophages in vitro. I. Macrophage-mediated tumor cell lysis.

Murine macrophage monolayers treated with cisplatin, lipopolysaccharide (LPS), muramyl dipeptide (MDP) or recombinant interferon-gamma (rIFN gamma) were observed to have significantly increased tumoricidal activity. rIFN gamma had synergistic effects with cisplatin, LPS or MDP in activating macrophages. However, MDP showed much more pronounced synergism with cisplatin and LPS than with rIFN gamma. Supernatants collected from these activated macrophage monolayers also showed increased tumoricidal activity. Tumor cell lysis mediated by cisplatin-treated macrophages did not require priming with rIFN gamma though it may be necessary as a first signal for the increased macrophage activation with LPS and MDP.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1989

Experimental murine schistosomiasis mansoni: hyperplasia of the mono-macrophage cell lineage and stimulation of myeloid proliferation by peripheral macrophages.

1. Normal and schistosome-infected mice were similar in terms of the total number of bone marrow myeloid cell precursors and their proliferative capacity in vitro when stimulated with supernatants of L-929 cells containing M-CSF. 2. Delayed differentiation of bone marrow neutrophil granulocytes and blood monocytosis of infected animals were consistent with a modification in the differentiation of bone marrow myeloid precursors, favoring the production of a mono-macrophage cell lineage. 3. Macrophages isolated from periovular granulomas secreted a considerable stimulatory activity for the proliferation of the mono-macrophagic cell lineage, whereas peritoneal macrophages from the same animals had only a very low stimulatory activity. 4. We conclude that systemic hyperplasia of mono-macrophagic cells in schistosomiasis may be related to their increased release from the bone marrow and to their peripheral amplification in inflammatory tissue infiltrate as a consequence of the local production of stimulatory activity for their proliferation.

Animals↗
PubMed1989

Increased expression of class II antigens of the major histocompatibility complex on alveolar macrophages and alveolar type II cells and interleukin-1 (IL-1) secretion from alveolar macrophages in an animal model of silicosis.

Silicosis is a chronic progressive granulomatous and fibrotic lung disease caused by inhaled silica. Although the causative agent is known, the pathogenesis, especially the immunologic response, is not well understood. We examined two important components of cell-mediated immune responses in the lungs of rats with silica-induced lung disease, i.e., class II (Ia) antigen expression and IL-1 production. The relative density of Ia was examined on isolated alveolar macrophages and type II cells with a solid-phase cellular radioimmunoassay and the percent of Ia positive cells was determined by an indirect immunofluorescent technique. There was a three-fold increase of Ia expression on the alveolar macrophages and nearly a two-fold increase on type II cells from rats with silicosis compared to normal rats. The percent of alveolar type II cells positive for Ia increased by 20%, and the alveolar macrophages increased by 40%. IL-1 in supernatants from cultured alveolar macrophage was measured by the amount of DNA synthesis in an IL-1 dependent cell line (D10). A six-fold increase in IL-1 secretion was noted in macrophage supernatants derived from silica-treated animals. We conclude that in this animal model of silicosis, a local amplification of cell-mediated immune responses may be instrumental in the pathogenesis.

Animals↗