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PubMed1990

The in situ immune response in popliteal lymph nodes of mice after macrophage depletion. Differential effects of macrophages on thymus-dependent and thymus-independent immune responses.

Mice were subcutaneously (SC) injected in the left hind footpad with dichloromethylene diphosphonate (Cl2MDP)-containing liposomes to eliminate macrophages lining the subcapsular sinus (SCS) and those in the medulla of draining popliteal lymph nodes (PLN). In order to study the effect of depletion of these macrophages on the in situ immune response in the PLN, liposome-treated mice were SC injected in the same footpad with thymus-independent (TI) type 1 antigen trinitrophenylated lipopolysaccharide (TNP-LPS), TI-type 2 antigen TNP-Ficoll or thymus-dependent (TD) antigen TNP-keyhole limpet haemocyanin (TNP-KLH). No major differences were observed in antibody-serum titers of liposome-treated and control animals. After primary as well as secondary immunization with the TD-antigen TNP-KLH, an increase in the number of antibody-forming cells (AFC) was found and the peak of response was delayed in the PLN of liposome-treated animals. Such differences were not observed with the TI-antigens. These results indicate that macrophages lining the SCS and those in the medulla of the PLN are not essential for the induction of an immune response. The positive effect of macrophage-depletion on the number of AFC may be explained by competition for the antigen by macrophages and other antigen-presenting cells.

Animals↗
PubMed1987

On the interactions between macrophages and developmental stages of Schistosoma mansoni: the cytotoxic mechanisms involved in macrophage-mediated killing of schistosomula in vitro.

In an in vitro cytotoxicity assay, mouse adherent peritoneal exudate macrophages (APEM), harvested 8-10 weeks post Schistosoma mansoni infection caused sizable (greater than 90%) specific killing of schistosomula. This cidal effect was not diminished by the addition of scavengers of oxidative burst products to the cytotoxicity assay, albeit macrophages from schistosome-infected mice produced more H2O2 than did macrophages from non-infected mice. Of inhibitors of lysosomal enzyme function and release added to the cytotoxicity assay, trypan blue (1 mg/ml) fully abolished the schistosomulicidal effect; hydrocortisone (100 micrograms/ml) was partly effective, and gold salts (1 mg/ml) were ineffective. A cidal effect was not apparent in the absence of L-arginine nor in the presence of excess (greater than 400 micrograms/ml) L-arginine, L-lysine or L-ornithine. Arginase (5 U/ml) totally abrogated the schistosomulicidal effect. The findings suggest that a macrophage protein of a lysosomal origin, dependent on arginine for its reaction and/or production, may be involved in the in vitro killing of schistosomula by macrophages from S. mansoni-infected mice.

Animals↗
PubMed2000

Expression and regulation of macrophage inflammatory protein-2 gene by vanadium in mouse macrophages.

Environmental and occupational exposure to vanadium (V) dusts results in inflammation mainly confined to the respiratory tract. Macrophages apparently play an important role in mediating the inflammation via the production of many chemokines. In the current study, we investigated whether vanadium can regulate the gene expression of a CXC chemokine macrophage inflammatory protein-2 (MIP-2), and to determine the molecular mechanisms controlling MIP-2 gene expression. A mouse macrophage cell line RAW 264.7 was treated with sodium metavanadate (NaVO3) at the dose of 0.5, 5, or 10 microg/mi V. Northern blot analysis showed that induction of MIP-2 mRNA expression was in a dose-dependent manner. To define the time course of the inflammatory response, RAW 264.7 cells were exposed to 5 microg/ml V, MIP-2 mRNA in macrophages increased markedly as early as 1 h after treatment, maximally induced at 4 h and reduced to 2-fold above control levels by 6 and 8 h. The protein levels of MIP-2 in conditioned media, measured by enzyme-linked immunosorbent assay (ELISA), was well correlated with the levels of MIP-2 mRNA following all of the treatments in the study. In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS). To further investigate transcriptional regulation of the MIP-2 gene expression by vanadium, we performed RNA decay assay by measuring the half-life of MIP-2 mRNA. Co-treatment of macrophages with the transcriptional inhibitor actinomycin D at 5 microg/ml following exposure to 5 microg/ml V for 4 h revealed complete stabilization of vanadium-induced MIP-2 mRNA and no sign of mRNA degradation, at least, for 6 h, in comparison to the half-life of MIP-2 mRNA was approximately 2.5 h by bacterial lipopolysaccharide (LPS) treatment, supporting post-transcriptional stabilization as the predominant role of MIP-2 gene expression. In conclusion, these observations demonstrate that in vitro vanadium can induce MIP-2 mRNA expression, mediating, at least in part, via the production of ROS. In addition, the increase in MIP-2 mRNA level involves, most likely, post-transcriptional control via increased mRNA stability.

Acetylcysteine↗
PubMed2002

Early vascular permeability in murine experimental peritonitis is co-mediated by resident peritoneal macrophages and mast cells: crucial involvement of macrophage-derived cysteinyl-leukotrienes.

The initial phase of zymosan-induced peritonitis involves an increase of vascular permeability (peak at 30 min) that is correlated with high levels of vasoactive eicosanoids, namely, prostaglandins (PGI2 and PGE2) of cyclooxygenase-1 origin (as estimated by RT-PCR) and cysteinyl-leukotrienes. Previously, we showed that the increase of vascular permeability can be attributed only partially to mast cells and their histamine, as seen in mast cell-deficient WBB6F1-W/Wv mice. Thus we aimed to identify the major cellular source(s) that mediate vasopermeability, as well as particular vasoactive mediators operating in this model. For this purpose, some mice were selectively depleted of either peritoneal macrophages or mast cells, and/or they were treated with several pharmacologic inhibitors of cyclooxygenase- and lipoxygenase-metabolic pathways. More-over, macrophage-depleted mast cell-deficient WBB6F1-W/Wv mice and their controls (+/+) were used. The macrophage depletion always caused a profound decrease of both vascular permeability and lipid-mediator levels, which was particularly pronounced for leukotrienes, whereas the effects of mast-cell depletion were less severe. The macrophage/mast-cell co-mediation of vasopermeability was also revealed in thioglycolate-induced peritonitis, as well as the macrophage origin of cysteinyl-leukotrienes. Taken together, these findings demonstrate that the resident peritoneal macrophages are in fact the main contributors to the vasopermeability at the early stages of zymosan-induced peritonitis.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Uptake and incorporation of saturated and unsaturated fatty acids into macrophage lipids and their effect upon macrophage adhesion and phagocytosis.

Murine thioglycollate-elicited peritoneal macrophages were cultured in the presence of a variety of fatty acids added as complexes with bovine serum albumin. All fatty acids tested were taken up readily by the cells and both neutral and phospholipid fractions were enriched with the fatty acid provided in the medium. This generated a range of cells enriched in saturated, monounsaturated or polyunsaturated fatty acids, including n-3 acids of fish oil origin. Saturated fatty acid enrichment enhanced macrophage adhesion to both tissue culture plastic and bacterial plastic compared with enrichment with polyunsaturated fatty acids. Macrophages enriched with the saturated fatty acids myristate or palmitate showed decreases of 28% and 21% respectively in their ability to phagocytose unopsonized zymosan particles. Those enriched with polyunsaturated fatty acids showed 25-55% enhancement of phagocytic capacity. The greatest rate of uptake was with arachidonate-enriched cells. Phagocytic rate was highly correlated with the saturated/unsaturated fatty acid ratio, percentage of polyunsaturated fatty acid and index of unsaturation, except for macrophages enriched with fish-oil-derived fatty acids; they showed lower phagocytic activity than expected on the basis of their degree of unsaturation. These results suggest that membrane fluidity is important in determining macrophage adhesion and phagocytic activity. However, in the case of phagocytosis, this effect may be partially overcome if the cells are enriched with fish-oil-derived fatty acids. Thus it may be possible to modulate the activity of cells of the immune system, and so an immune response, by dietary lipid manipulation.

Animals↗
PubMed1999

Regulation of macrophage inflammatory protein-2 gene expression by oxidative stress in rat alveolar macrophages.

Chemokines are important mediators in the development of inflammation. Our previous work demonstrated that an oxidative stress can up-regulate mRNA expression of a CC chemokine macrophage inflammatory protein (MIP)-1alpha in rat alveolar macrophages. In the present study, we further investigate whether an oxidative stress can regulate the gene expression of a related CXC chemokine MIP-2, involved in both neutrophil chemotaxis and activation. A rat alveolar macrophage cell line (NR8383) was exposed to 10 microg/ml bacterial lipopolysaccharide (LPS) and MIP-2 mRNA levels dramatically increased after 4 hr of stimulation. This increase by LPS was attenuated by co-treatment with the antioxidants N-acetylcysteine and dimethylsulphoxide, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species. To assess directly the role of oxidative stress on regulation of MIP-2 mRNA expression, macrophages were exposed to H2O2. MIP-2 mRNA levels had significantly increased after 1 hr exposure to 0.5 mm H2O2, were maximally increased after 4 hr and decreased after 6 hr. Co-treatment of macrophages with the transcriptional inhibitor actinomycin D eliminated the H2O2-induction of MIP-2 mRNA, implicating a role for transcriptional activation in increased expression of MIP-2. Genomic cloning of the rat MIP-2 gene 5'-flanking region has identified a consensus nuclear factor-kappaB (NF-kappaB) binding site. Gel-mobility shift assays revealed NF-kappaB binding to the MIP-2 promoter/enhancer sequence was induced by H2O2. LPS treatment for 4 hr also significantly activated NF-kappaB binding, which could also be attenuated by pretreatment with N-acetylcysteine at the doses that reduced MIP-2 mRNA expression. The half-life of MIP-2 mRNA transcripts was also increased by H2O2 treatment. These observations indicate that MIP-2 gene expression is subject to both transcriptional and post-transcriptional control in response to an H2O2 oxidative stress.

Animals↗
PubMed1999

Splenic marginal metallophilic macrophages and marginal zone macrophages are the major interferon-alpha/beta producers in mice upon intravenous challenge with herpes simplex virus.

The interferon (IFN)-alpha/beta-producing cells (IPCs) are localized predominantly in the spleen, in particular in the marginal zones (MZ), in C57BL/6 mice injected intravenously (i.v.) with UV-inactivated herpes simplex virus (HSV). We defined the phenotype of these murine IPCs using simultaneous immunohistochemical labelling of intracellular IFN-alpha/beta and various surface antigens. We found that the IPCs in the MZ are not dendritic cells because they did not express major histocompatibility complex (MHC) class II and CD11c molecules. Furthermore, they did not express antigenic markers typical for T cells, B cells or red pulp macrophages. In contrast, the majority of IPCs were stained by the anti-sialoadhesin monoclonal antibody (MoAb) SER-4, which is specific for marginal metallophilic macrophages. In addition, a minor part of the IPCs with a more outward localization in the MZ were stained by a MoAb specific for MZ macrophages. We conclude that the massive IFN-alpha/beta production in the MZ of the spleen upon in vivo stimulation by HSV is mainly exerted by marginal metallophilic macrophages and to a lesser extent by MZ macrophages.

Animals↗
PubMed1999

The effect of testicular macrophages, macrophage-conditioned medium and interleukin-1alpha on bank vole Leydig cell steroidogenesis.

It has already been accepted that the function and activity of the testis is regulated not only by gonadotrophins, but also by many locally produced factors and by cell-cell interactions. That is why the aim of our work was to determine whether macrophages and/or their products have an influence on Leydig cell steroidogenic activity. The source of Leydig cells and macrophages were male bank voles of spring and autumn generations, reared in 18 light:6 dark or 6 light:18 dark (18L:6D or 6L:18D) conditions for 7-8 weeks. The Leydig cells were growing in monocultures or in co-cultures with macrophages (testicular or peritoneal), either as control or hCG-stimulated ones. To some of the cultures 6 IU/ml of interleukin 1alpha (IL-1alpha) was added. After then the cells were analysed morphologically, histochemically, and radioimmunologically. In the present study we found many differences in morphology and steroidogenic activity of Leydig cells obtained from different photoperiods. Leydig cells from a long day formed monolayer contrary to the cells from a short one growing as single cells or in clusters. Moreover, Leydig cells from a long photoperiod produced more testosterone and were sensitive to the stimulatory effect of both testicular macrophages and testicular macrophage-conditioned medium. They were also more sensitive to the inhibitory influence of IL-1alpha.

Androgens↗
PubMed2000

Protein kinase C-regulated dynamitin-macrophage-enriched myristoylated alanine-rice C kinase substrate interaction is involved in macrophage cell spreading.

Macrophage spreading requires the microtubule cytoskeleton and protein kinase C (PKC). The mechanism of involvement of the microtubules and PKC in this event is not fully understood. Dynamitin is a subunit of dynactin, which is important for linking the microtubule-dependent motor protein dynein to vesicle membranes. We report that dynamitin is a Ca(2+)/calmodulin-binding protein and that dynamitin binds directly to macrophage-enriched myristoylated alanine-rice C kinase substrate (MacMARCKS), a membrane-associated PKC substrate involved in macrophage spreading and integrin activation. Dynamitin was found to copurify with MacMARCKS both during MacMARCKS purification with conventional chromatography and during the immunoabsorption of MacMARCKS using anti-MacMARCKS antibody. Vice versa, MacMARCKS was also found to cosediment with the 20 S dynactin complex. We determined that the effector domain of MacMARCKS is required to interact with the N-terminal domain of dynamitin. MacMARCKS and dynamitin also partially colocalized at peripheral regions of macrophages and in the cell-cell border of 293 epithelial cells. Treatment with phorbol esters abolished this colocalization. Disrupting the interaction with a short peptide derived from the MacMARCKS-binding domain of dynamitin caused macrophages to spread and flatten. These data suggest that the dynamitin-MacMARCKS interaction is involved in cell spreading. Furthermore, the regulation of this interaction by PKC and Ca(2+)/calmodulin provides a possible regulatory mechanism for cell adhesion and spreading.

Adenosine Triphosphatases↗
PubMed2002

Role of mitogen-activated protein kinase activation in the production of inflammatory mediators: differences between primary rat alveolar macrophages and macrophage cell lines.

Stimulation of macrophages has been shown to activate all three families of mitogen activated protein kinases (MAPKs). However, variable results are reported in the literature with respect to the particular kinases activated with any given stimulus. In this study, the role of activation of MAPKs was examined in the production of inflammatory mediators by measuring the phosphorylation of the kinases and their ability to phosphorylate specific substrates in rat primary alveolar macrophages, a rat alveolar macrophage cell line (NR8383), and two mouse monocytic cell lines (RAW 264.7 and J774A.1). In the three cell lines examined, all three families of MAPKs were activated upon stimulation with either lipopolysaccharide (LPS) or LPS plus interferon-gamma; in contrast, only ERK1/2 was activated in primary rat alveolar macrophages upon stimulation with LPS. Inhibition of ERK1/2 activation by the MEK inhibitor PD98059 abrogated nitric oxide and tumor necrosis factor-alpha (TNF-alpha) production in primary rat alveolar macrophages, but the p38 inhibitor SB203580 had no effect on the production of these two inflammatory mediators. These observations indicate that MAPK activation is cell specific and explain some of the conflicting results reported in the literature. These studies emphasize the need to exercise caution in extrapolating data from cell lines to primary cells.

Animals↗
PubMed1975

Macrophage-lymphocyte interaction. II. Antigen-mediated physical interactions between immune guinea pig lymph node lymphocytes and syngeneic macrophages.

The effect of specific antigen on the development of physical interactions between lymph node lymphocytes (LNL) obtained from animals which had been immunized to that antigen and macrophages was examined. We found that the presence of antigen, either limited to the macrophage () or free in the medium, profoundly increased the degree of ) or free in the medium, profoundly increased the degree of Mphi-LNL interaction observed. This enhanced interaction was dependent on the coincidence in the cultures of Mphi bearing antigen and LNL from animals specifically immunized to that antigen. Although antigen-independent interactions developed equally well between syngeneic and allogeneic combinations of lymphocytes and macrophages, antigen mediated interactions required that macrophages and lymphocytes be syngeneic. Prolongation of antigen-mediated Mphi-LNL interactions resulted in the induction of LNL DNA synthesis, initially involving those lymphocytes physically associated with antigen-bearing Mphi. These studies are interpreted to indicate that physical interaction between immune lymphocytes and antigen-bearing Mphi represents a morphological correlate of the functional activation of immune lymphocytes. Further, it is suggested that the physical events involved in lymphocyte proliferation may proceed sequentially from antigen-independent reversible binding of lymphocytes by macrophages to prolonged antigen-stabilized interaction eventuating in the triggering of specifically immune lymphocytes.

Animals↗
PubMed2004

Transmission of macrophage-tropic HIV-1 by breast-milk macrophages via DC-SIGN.

Recent findings suggest that macrophage-tropic human immunodeficiency virus type 1 (HIV-1) produced in colostrum/early breast milk may hold a clue to determine the mechanisms of transmission of HIV-1 via breast-feeding. Here, we show that the majority of CD4(+) cells in the colostrum are CD14(+) macrophages expressing both chemokine receptors and DC-SIGN, a dendritic cell-specific receptor for HIV-1. The R5-type macrophage-tropic HIV-1 isolate NL(AD8) infected such breast-milk macrophages and caused them to secrete virus particles efficiently; however, the secreted virions showed only a weak transmissibility to their susceptible target, MAGIC-5 cells. When stimulated with interleukin-4, the breast-milk macrophages demonstrated a striking enhancement of expression of DC-SIGN and showed a strong capacity to transmit NL(AD8) virions to MAGIC-5 cells, which was specifically blocked by anti-DC-SIGN-specific antibody. These results suggest that HIV-1 virions captured by DC-SIGN, but not secreted cell-free virions, may be more efficiently transmitted to other compartments, such as the gastrointestinal tract, through acidic gastric juice.

Adult↗
PubMed2004

High concentrations of circulating macrophage migration inhibitory factor in patients with severe blunt trauma: Is serum macrophage migration inhibitory factor concentration a valuable prognostic factor?

OBJECTIVE: To determine serum concentrations of macrophage migration inhibitory factor and other cytokines in severe blunt trauma patients in critical settings and to evaluate their association with patient outcome. DESIGN: Prospective, observational study. SETTING: Emergency department and surgical intensive care unit of a university hospital. PATIENTS: Fifty-four severe blunt trauma patients with systemic inflammatory response syndrome requiring intensive care, emergency surgical intervention, or both were enrolled in the study. Forty-four patients with minor injuries were the controls. INTERVENTIONS: Serum macrophage migration inhibitory factor concentrations were measured in the emergency department <4 hrs postinjury (day 1) and the surgical intensive care unit 24 hrs later (day 2). Blood samples for determination of tumor necrosis factor-alpha, interleukin-6, interleukin-8, and interleukin-10 were measured both in patients with severe blunt trauma and in controls. The Acute Physiology and Chronic Health Evaluation II, Injury Severity Score, Revised Trauma Score, and Trauma Revised Injury Severity Score were used for clinical evaluation of trauma severity. MEASUREMENTS AND MAIN RESULTS: Serum macrophage migration inhibitory factor concentrations were higher in severe blunt trauma patients than in controls; were significantly correlated with Acute Physiology and Chronic Health Evaluation II, Revised Trauma Score, and Trauma Revised Injury Severity Score scores in severe blunt trauma patients but not in controls; and were higher in nonsurvivors than in survivors. CONCLUSIONS: Our data suggest that the serum macrophage migration inhibitory factor concentration is higher in severe blunt trauma and that it reflects the severity of trauma. The serum macrophage migration inhibitory factor concentration might be a valuable predictor for the outcome of severe blunt trauma.

APACHE↗
PubMed2004

Effect of tacrolimus on the expression of macrophage scavenger and nuclear hormone receptors in THP-1-derived human macrophages.

BACKGROUND: Data indicate that tacrolimus and cyclosporine A (CsA) differentially affect the risk of atherosclerosis. The results of our recent in vitro studies of clinically relevant CsA concentrations demonstrated the modulation of macrophage scavenger receptors (MSRs) involved in atherogenesis. This work evaluated the effects of clinically relevant tacrolimus concentrations on the expression of the MSR genes CD36 and CD68, SR-A and SR-BII, lectin-like oxidized low-density lipoprotein receptor-1, the nuclear hormone receptors peroxisome proliferator-activated receptor (PPAR)gamma and liver-X-receptor-alpha, and the cholesterol efflux pump ABCA1 in the in vitro human THP-1 macrophage model. METHODS: The cells were cultured and differentiated into macrophages. Macrophages were treated with the tacrolimus to assess gene expression in a time-dependent (1, 2, 4, 8, and 24 hr) and dose-dependent (concentrations [micrograms/liter] corresponding to the trough [15], peak [30], and 4 x peak [120]) manner using reverse-transcriptase polymerase chain reactions. The gene expression levels of interest were normalized to GAPDH expression in each sample to provide semiquantitative reverse-transcriptase polymerase chain reaction results. Additional immunoblotting studies demonstrated protein expression of CD36, PPARgamma, and ABCA1. RESULTS.: The gene expression of CD36, SR-BII, and lectin-like oxidized low-density lipoprotein receptor-1 were down-regulated, and ABCA1 was up-regulated. CD68, SR-AI, liver-X-receptor-alpha, and PPARgamma were regulated in a dose-dependent manner. Protein expression of CD36 was down-regulated, and PPARgamma and ABCA1 were relatively unchanged. CONCLUSIONS: Tacrolimus seems to regulate MSRs, nuclear hormone receptors, and ABCA1 in THP-1 macrophages. These results differ from previous findings with CsA and may provide insight into the mechanisms of posttransplant atherosclerosis.

ATP Binding Cassette Transporter 1↗
PubMed1990

Microtiter plate assay for selecting "macrophage virulent" strains of Mycobacterium avium intracellulare mycobacteria in mouse pulmonary alveolar macrophages.

Currently used macrophage-mycobacterial in vitro infection models require substantial numbers of macrophages. We developed a miniaturized version of such a model, using microtiter plates, which is comparable to standardly published methods, is reproducible, and requires fewer macrophages. In addition to its ease of handling and its economy in time, number of animals, and supplies, this method is preferable when limited numbers of macrophages are available. We have used this assay as a means of selecting human derived isolates from patients with M. avium intracellulare pulmonary disease for their ability to infect and multiply in cultured mouse pulmonary alveolar macrophages.

Animals↗
PubMed1990

Macrophage heterogeneity in human fetal tissue. Fetal macrophages.

The immunophenotype of the macrophage population in human fetal tissue was studied, using a panel of monoclonal antibodies against cells of the macrophage/monocyte lineage. Using a double-labelling technique two main populations were observed in tissue from 14 weeks of estimated gestational age (EGA); EBM11+ DR+ and EBM11+ DR- cells of which a small proportion were also RFD7+. Most macrophages were negative with 3.9, an antibody specific for the adhesion molecule P150.95 and LP9 which is specific for a lysosomal enzyme. The exception to this was a small population of positive cells in the thymus. Small numbers of 3.9+ cells were also infrequently observed in tissue at and above 17 weeks of EGA, while occasional RFD9+ cells were only observed in most tissues, before this time. The higher percentage of macrophages were DR+ DQ- DP-, with a few DQ+ cells appearing at 15 weeks of EGA. In the thymus, DQ+ cells outnumbered DP+ cells especially in the medulla. These results indicate the heterogeneous and immature nature of the fetal macrophage population and point to the importance of age, tissue-specific factors and probable immune mediators in macrophage differentiation.

Antibodies, Monoclonal↗
PubMed1995

Immunohistochemical detection of macrophage-derived foam cells and macrophage colony-stimulating factor in pulmonary atherogenesis of cholesterol-fed rabbits.

In order to investigate the role of monocyte/macrophages and their relationship to the expression of macrophage colony-stimulating factor (MCSF) in pulmonary atherosclerosis, lungs were excised from rabbits that had been fed for 60 and 90 days on a diet containing 0.5% cholesterol. In the lungs, fatty streaks and elevated foam cell lesions predominated in the large or medium-sized elastic pulmonary arteries, while massive accumulation of foam cells in the intima of muscular arteries produced marked luminal narrowing and nearly complete occlusion. In these lesions, most of the foam cells were reactive with RbM2, a monoclonal antibody (mAb) against rabbit macrophages, while smooth muscle cell-derived foam cells were detected by mAb against smooth muscle actin in the deeper area of elevated foam cell lesions of elastic arteries. Ultrastructural observation confirmed the presence of monocytes in the intima, their differentiation into macrophages, and their transformation into foam cells in the atherosclerotic lesions. Immunohistochemical expression of MCSF was demonstrated in the endothelial cells, smooth muscle cells and foam cells. A minor macrophage-derived foam cell population was demonstrated to possess a proliferative capacity. These data suggest that MCSF is involved in the differentiation of monocytes into macrophages, their transformation into foam cells, and their proliferation during pulmonary atherogenesis.

Animals↗
PubMed1982

Role of macrophage activation and interferon in the resistance of alveolar macrophages from infected mice to influenza virus.

Lung macrophages from uninfected CD1 mice support the replication of influenza viruses (H1N1 and H0N1), but the cells from influenza-infected mice do not. The possible mechanisms of this resistance were investigated. Murine macrophages were "activated" in vitro with lipopolysaccharide and lymphokines, and in both cases activation was associated with resistance of cells to infection with influenza virus. Exposure of alveolar macrophages in vitro to 500 U of purified type I interferon per ml enhanced cell spreading and Fc receptor-mediated phagocytosis, suggesting macrophage activation, and protected the cells against infection with influenza virus. Alveolar macrophages were also protected by a soluble factor in the bronchoalveolar washings from influenza-infected mice. This effect was not virus specific and was abolished by anti-interferon serum.

Animals↗