bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monocytes and Neutrophils Oxidize Low Density Lipoprotein Making It Cytotoxic
Authors: Cathcart Martha K , Morel Diane W , Chisolm Guy M 
Published: January 2018

Abstract
Free radicals are believed to be involved in leukocyte induced tissue injury. The present studies were performed to determine whether low density lipoprotein (LDL) might serve as a mediator of tissue injury after leukocyte induced free radical oxidation of LDL. Our results show that incubation of LDL with monocytes or polymorphonuclear leukocytes (PMN) leads to oxidation of the lipoprotein rendering it toxic to proliferating fibroblasts. Monocyte activation enhances these effects. Butylated hydroxytoluene (BHT), vitamin E (vit E) and glutathione (GSH) virtually prevent the oxidation of LDL and the formation of cytotoxic LDL, indicating that these alterations are mediated by leukocyte-derived free radicals. This is the first demonstration that short-lived free radicals emanating from phagocytic cells could mediate cell injury through the action of a stable cytotoxin formed by the oxidation of LDL. The fact that lipoproteins can transfer a cytotoxic effect from leukocytes to proliferating cells reveals a pathway for cell destruction which may have implications in atherosclerotic plaque progression, macrophage mediated toxicity to tumor cells and tissue injury by inflammatory processes.
An Inhibitory Factor Against Monocyte Spreading in the Sera of Patients With Systemic Lupus Erythematosus
Authors: Baba Toru , Ochiya Takahiro , Baba Akiko , Yamaguchi Koji , Yaoita Hideo , Uyeno Kenichi 
Published: January 2018

Abstract
The effect of the sera of patients with systemic lupus erythematosus (SUE) on monocyte function was studied using cell spreading as an indicator. Monocyte spreading induced by exogenous stimuli was shown to be inhibited by SLE sera. Gel filtration of SLE sera on Sephadex G-200 revealed that the factor responsible for this inhibition had a molecular weight of about 50,000. Pretreatment of monocytes with the inhibitory factor led to suppression of cell spreading induced by subsequent stimulation, but this hyporeactivity was reversible. Spreading of monocytes was rapidly aborted by the addition of this inhibitory factor. Thus, the inhibitory factor appeared to affect monocyte itself, but its effect seemed to be transient.
Sequential Histochemical Staining for Resident and Recruited Macrophages
Authors: Bugelski Peter J 
Published: January 2018

Abstract
A new histochemical technique is described that permits differentiation of resident from recruited macrophages by staining of paraffin sections of tissues from rats and mice. Resident macrophages are identified by their ability to phagocytose and retain intravenously injected colloidal Prussian blue. New macrophages that emigrate into tissue are identified by phagocytosis of a second colloid, iron dextran. Paraffin sections of formalin-fixed tissues are sequentially stained for the presence of the two colloids with different chromogens, the endogenous pseudo-peroxidase activity of colloidal Prussian blue used to catalyze the polymerization of diaminobenzidine and after conversion of iron dextran to Prussian blue, the second colloid used to catalyze the polymerization of tetramethylbenzidine. The staining results in resident macrophages staining brown while newly recruited macrophages stain blue. The studies have shown that colloidal Prussian blue is stable in vivo and neither loses its catalytic activity nor undergoes extensive redistribution. They also show that the technique can be used to measure Kupffer cell recruitment stimulated by complete Freund's adjuvant in rats and tumor-associated macrophage recruitment in subcutaneous and spontaneous liver metastases in mice.
Zymosan-Stimulated Production of Phosphatidic Acid by Macrophages: Relationship to Release of Superoxide Anion and Inhibition by Agents That Increase Intracellular Cyclic AMP
Authors: Channon Jacqueline Y , Leslie Christina C , Johnston Richard B. 
Published: January 2018

Abstract
Murine peritoneal macrophages (mΦ) respond to unopsonized zymosan with the production of superoxide anion (O2-). We investigated the involvement of phospholipid turnover in the transduction mechanism for this phenomenon. Zymosan-stimulated mΦ produced increased amounts of phosphatidic acid (PA); the increase was first detected at 1.5 min and continued for 10 min of incubation. Production of O2- was not detected until between 2 to 4 min after stimulation, and continued to increase through 60 min. Inhibition experiments suggested that these two processes were linked. Theophylline (theo)/ dibutyrylcyclic AMP (dbcAMP) and theo/prostaglandin E2 (PGE2) inhibited O2- production at every time point (79% and 80% inhibition, respectively, at 4 min). Corresponding inhibition of PA production was also achieved at every time point (85% by theo/dbcAMP; 67% by theo/PGE2 at 4 min). These results are compatible with a role for phospholipid remodeling in the transduction process associated with the respiratory burst. Results suggest that the phospholipid species could be phosphatidylcholine (PC) as well as phosphatidylinositol (PI).
Induction of Chemotaxis in Mouse Peritoneal Macrophages by Activators of Protein Kinase C
Authors: Laskin Debra L , Gardner Carol R , Laskin Jeffrey D 
Published: January 2018

Abstract
Two activators of calcium and phospholipid dependent protein kinase (protein kinase C), the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and the synthetic diacylglycerol, 1-oleoyl-2-acetylglycerol (OAG), were compared as chemotactic agents for mouse peritoneal macrophages. Both of these compounds were found to induce Chemotaxis in the macrophages to a similar extent in a time and dose dependent manner. Induction of Chemotaxis was observed in the concentration range of 10-100 nM for TPA and 25-250 μM for OAG. Two structurally related synthetic sn 1,2-diacylglycerols, 1,2-dioctanoylglycerol (diC8) and 1,2-didecanoylglycerol (diC10), were also found to be chemotactic for macrophages, while monoacylglycerol (2-monoolein) was inactive. Of the diacylglycerols, OAG was found to be the most active followed by dlC8 and diC10. In contrast to TPA, the synthetic diacylglycerols had no effect on superoxide anion release by the cells, suggesting that the mechanism of superoxide anion release by TPA in macrophages is distinct from Chemotaxis. Phorbol-12,13-diacetate, a biologically inactive phorbol ester analog that inhibits the binding of TPA to its cellular receptors, inhibited macrophage Chemotaxis induced by TPA, the synthetic diacylglycerols, and the complement fragment, C5a. Taken together, our results suggest that Chemotaxis in macrophages may be mediated by activation of protein kinase C.
Differential Protein Synthesis by Murine Peritoneal Macrophages Elicited by Various Stimuli
Authors: Tannenbaum Charles S , Nurmi-McKernan Lisa , Largen Michael T 
Published: January 2018

Abstract
Protein synthetic patterns of murine peritoneal macrophages were analyzed by two-dimensional Polyacrylamide gel electrophoresis (2D PAGE) of 35S methionine-labeled proteins. While the protein synthetic patterns exhibited by resident, inflammatory, and activated macrophages had numerous common features that distinguished them from the other normal non-macrophage cell types examined, unique proteins also characterized each macrophage population from the others. The accumulation by resident macrophages of proteins 23, 25, and 37 distinguished them from elicited cells, as did the former's more abundant synthesis of proteins 54 and 52. The protein synthetic patterns of inflammatory thioglycollate- and proteose peptone-elicited macrophages were strikingly similar, save for the former's greater levels of accumulation of proteins 14 and 28, and the letter's more pronounced expression of p23.5. Peritoneal macrophages elicited by treatment with heat-killed Propionibacterium acnes, the live, attenuated Mycobacterium bovis strain BCG, Listeria monocytogenes, and the protozoan flagellate Trypanosoma rhodesiense, all exhibited tumoricidal activity in 16-h or 72-h functional assays. They shared a common protein synthetic profile that differentiated them from the synthetic patterns characteristic of the non-tumoricidal resident and inflammatory macrophages. These tumoricidal macrophages were unique in synthesizing a protein(s) of approximate molecular weight 26,000 daltons. A time-course study employing P. acnes-activated peritoneal macrophages indicated that p26 accumulation decayed with tumoricidal capacity as a function of time in culture, although no direct correlation between lytic activity and p26 expression could be definitively established. Peritoneal macrophages elicited with proteose peptone were not directly tumoricidal but were rendered so upon in vitro treatment with nanogram amounts of bacterial lipopolysaccharide. The accumulation of low levels of p26 by the newly explanted proteose peptone-elicited macrophages suggests the possibility that this protein characterizes macrophage populations primed as well as triggered for tumoricidal activity.
Alveolar Macrophage/Peripheral Blood Monocyte-Derived Factors Modulate Proliferation of Primary Lines of Human Lung Fibroblasts
Authors: Jordana Manel , Newhouse Michael T , Gauldie Jack 
Published: January 2018

Abstract
Pulmonary fibrosis is characterized by an alteration in lung collagen synthesis and deposition, as well as by increased fibroblast proliferation. It is also characterized by an intermittent influx of immune and inflammatory cells in the lung. To investigate the nature of the target cell in this disorder, we established a series of primary lines of human adult lung fibroblasts and studied the effect of mediators released from activated normal human alveolar macrophages (AM) and peripheral blood monocytes (PBM) on the proliferation of both normal lung fibroblasts and fibroblasts established from lung tissue of patients with active fibrosis. Our data show that monocyte supernatants containing a 15-18 kD monokine from either AM or PBM inhibits growth of logarithmic phase proliferating lung fibroblasts in a dose-dependent manner. This effect can be entirely abrogated by treating the fibroblasts with indomethacin and is reconstituted by adding exogenous PGE2. A study of the kinetics of this interaction shows that exposure to monocyte supernatant for 30 min to 1 hr is sufficient to cause significant inhibition of fibroblast proliferation and that this effect can be halted, but not reversed, at any stage by incubation with indomethacin. We also show that fibroblasts derived from patients with pulmonary fibrosis are affected more quickly by exposure to the mediators, although the final extent of inhibition seen at each concentration of mediators is similar in normal and “fibrotic” fibroblasts. These studies indicate that activated AM or PBM release cytokines (including IL-1) which inhibit the growth of proliferating normal and fibrotic fibroblasts through activation of the intrinsic arachidonic acid pathway of this cell and also that this effect requires a continuous activation of this pathway to be fully expressed.
Defective Production of Reactive Oxygen Intermediates by Tumor-Associated Macrophages Exposed to Phorbol Ester
Authors: Ghezzi Pietro , Erroi Annalaura , Acero Raffaella , Salmona Mario , Mantovani Alberto 
Published: January 2018

Abstract
Macrophages were isolated from poorly immunogenic metastatic sarcomas (mFS6 and MN/MCA1) of C57BL/6 origin. Tumor-associated macrophages (TAM) showed little release of superoxide when exposed to phorbol myristate acetate. When exposed to a phagocytic stimulus (zymosan), TAM released appreciable amounts of superoxide. TAM had a lower number of specific binding sites for phorbol esters than resident or caseinate-elicited peritoneal macrophages, but had normal NADPH-cytochrome C reductase. The tumor environment, possibly through previously demonstrated products of neoplastic cells, may influence the functional status of in situ macrophages and, thus, impair host anti-tumor and anti-microbial defense mechanisms.
Self-Renewal of Pulmonary Alveolar Macrophages: Evidence From Radiation Chimera Studies
Authors: Tarling John D , Lin Hsiu-san , Hsu Shin 
Published: January 2018

Abstract
Radiation-induced chimeric mice were used to study the origin of pulmonary alveolar macrophages. Unlike in other studies, these radiation chimeras were prepared by using a special fractionated irradiation regimen to minimize the killing of alveolar macrophage colony-forming cells, putative local stem cells. For this study CBA mice with or without T6 chromosome marker were used. Under this experimental condition, the majority of alveolar macrophages in mitosis are of host origin even after 45 weeks. These data suggest that alveolar macrophages are a self-renewing population under normal steady-state conditions.
New Method for the Measurement of Eosinophil Migration
Authors: Håkansson Lena , Westerlund Dorothea , Venge Per 
Published: January 2018

Abstract
A new application of the Boyden chamber method for the measurement of eosinophil migration, without the need of eosinophil isolation, has been developed. A cell suspension containing a mixture of granulocytes, neutrophils to the greater part, was used. The eosinophils were identified by staining their granules with Chromotrope 2R. The method made it possible to study the migration of eosinophils from normal individuals without eosinophilia. Control experiments demonstrated that the chemotactic and chemokinetic response of eosinophils in the granulocyte mixture was in accordance with the response of isolated eosinophils from the same donor. Normal eosinophils demonstrated a significant chemotactic response to C5f, platelet-activating factor (PAF), leukotriene B4 (LTB4), and f-meth-leu-phe (f-MLP). Furthermore, PAF was demonstrated to be significantly more eosinophil chemotactic than neutrophil chemotactic.
Macrophage Cell Line B6MP102 Resembles Peritoneal Macrophages in Tumor Cell Recognition and Killing
Authors: Chapes Stephen K , Didier Elizabeth S , Tompkins Wayne A F 
Published: January 2018

Abstract
In this paper we describe the bone marrow-derived macrophage cell line B6MP102. We describe growth characteristics, responsiveness to biological response modifiers known to activate macrophages (MPs), and the ability of B6MP102—comparable to that of peritoneal MPs—to kill and discriminate tumor cells. We demonstrate that B6MP102 is easily maintained in culture in the presence of 15% L-M cell-conditioned media. We have found that the B6MP102 cell line is similar to in vivo-derived peritoneal MPs. These cells are responsive to biological response modifiers but are not spontaneously cytotoxic. They produce O− 2 in quantities comparable to that produced by peritoneal MPs, and they exhibit target ranges for direct killing similar to those of activated peritoneal MPs. In addition, B6MP102 is similar to MPs in mediating cytostasis. These latter two points are especially significant, suggesting that the mechanisms that MPs may use to distinguish and kill tumor cells are retained in the B6MP102 cell line. This makes the cell line a useful tool for studying MP-tumor cell interactions.
Identification of Nonadherent Mononuclear Cells in Human Cord Blood That Differentiate Into Macrophages
Authors: Santiago-Schwarz Frances , Fleit Howard B 
Published: January 2018

Abstract
We describe a population of nonadherent cells in neonatal cord blood that, upon in vitro cultivation, develop into monocyte-macrophages. These cells initially are negative for nonspecific esterase cytoplasmic activity, lack the monocyte marker MO.2, fall into smaller, nonmonocytic cell size areas, as determined by fluorescence-activated cell sorter (FACS)-assisted size analysis, and differentiate into macrophages under nonstimulatory culture conditions (in the absence of exogenous colony stimulating factors, &lt;0.1 ng/ml endotoxin, and growth in suspension). In contrast to the adherent, committed macrophage precursors in cord blood, which differentiate into macrophages after 2-3 days of culture, the nonadherent precursor does not acquire monocyte-macrophage characteristics until day 14 of culture. Earlier induction is achieved by adding the monocyte-activating agents lipopolysaccharide or 1,25 dihydroxyvitamin D3 to cultures.
Differential Presentation of Tolerogenic Immunoglobulin In Vivo by Macrophages and by a Lymphoid Dendritic Cell-Like Tumor Line
Authors: Phipps Richard P , Illig Karl , Schad Victoria , Bhimani Karim 
Published: January 2018

Abstract
Previous work indicated that macrophages and a lymphoid dendritic cell-like tumor line, P388AD.2, possessed a differential ability to present a haptenated immunoglobulin (tolerogen) in vitro. Macrophages presented fluorescein-conjugated sheep gamma globulin (FL-SGG) and elicited B-cell unresponsiveness. In contrast, P388AD.2 presented this normally tolerogenic signal as an immunogenic one and induced augmented anti-hapten antibody responses. The objective of the present study was to determine whether differential tolerogen presentation could occur in vivo using defined accessory cells pulsed with FL-SGG. Interestingly, the intravenous (IV) injection of FL-SGG-pulsed thioglycollate-elicited macrophages, which secreted prostaglandin E2, induced hapten-specific B-cell unresponsiveness in syngeneic recipients. One thousand times as much FL-SGG in soluble form was required to produce the same degree of unresponsiveness. In contrast to macrophage-elicited negative signalling, non-prostaglandin secreting P388AD.2, when pulsed with FL-SGG, induced hapten-specific responses 2-3 times control values. Moreover, as few as 2 × 104 FL-SGG-pulsed P388AD.2 induced significant augmentation of the anti-FL antibody response. The presentation of FL-SGG in an immunogenic fashion by P388AD.2 was rapid and long lasting since increased responses were demonstrated as early as 1 day or as long as 21 days after IV injection. P388AD.2 were not simply acting as a passive carrier, nor permitting host presentation of FL-SGG, since there were requirements for P388AD.2 viability, and for syngeneic recipients in order to generate augmented anti-FL antibody responses. Moreover, inappropriate presentation of FL-SGG by P388AD.2 injected into allogeneic recipients did not elicit positive or negative signalling. In order to demonstrate that the ability of P388AD.2 to present FL-SGG in an immunogenic fashion was not simply a property of all tumor cells, the P388D1 cell line was pulsed with FL-SGG and injected. Neither tolerance nor augmentation was induced. Overall these results demonstrate that the type of antigen-presenting cell which introduces the immune system to an immunoglobulin tolerogen is critical to the induction of B-cell unresponsiveness or priming.
Protective Effects of Tumor Necrosis Factor in Experimental Legionella pneumophila Infections of Mice via Activation of PMN Function
Authors: Blanchard D Kay , Djeu Julie Y , Klein Thomas W , Friedman Herman , Stewart William E 
Published: January 2018

Abstract
Tumor necrosis factor (TNF) was found in the lung lavage fluids of Legionella pneumophila-infected mice within 24 hr of intratracheal (i.t.) inoculation. Since this cytokine has been reported to activate polymorphonuclear leukocyte (PMN) function, the effect of TNF on the in vitro bactericidal capacity of PMN-enriched cultures was determined. Murine thioglycollate-elicited PMN which were treated with recombinant human TNF demonstrated augmented killing of L. pneumophila bacteria in vitro. Furthermore, treatment of PMN suspensions with cytokine-containing lung lavage fluid was found to enhance the bactericidal activity of PMN. The addition of anti-cachectin/TNF antibodies partially abrogated the stimulatory effects of the lavage fluid, suggesting that in vivo activation of PMN during the course of infection was likely, and that TNF was partially responsible for the enhanced bactericidal activity. In vivo treatment of animals with TNF resulted in significant protection of the animals from mortality. Furthermore, the rate of clearance of bacteria from the lung tissues of infected mice was increased in those animals treated with TNF, and correlated with the ability of this cytokine to protect the animals. These data suggest that the induction of TNF by Legionella bacteria during infection are involved in the non-specific host defense mechanisms, and that PMN activated by the TNF may be instrumental in clearing the organism from infected lung tissues, thereby protecting the animal.
Blastogenesis of Large Granular Lymphocytes in Nonlymphoid Organs
Authors: McIntyre Kim W , Natuk Robert J , Biron Christine A , Kase Kenneth , Greenberger Joel , Welsh Raymond M 
Published: January 2018

Abstract
High numbers of large granular lymphocytes (LGL) accumulate in the livers and peritoneal cavities of mice during the course of viral infection. Accumulation of natural killer (NK) cells at day 3 postinfection (p.i.) was shown to be radiation-sensitive, implying that proliferation was required for this response. Accumulation occurred in splenectomized mice, indicating that the spleen, known to be an organ for mature NK cell proliferation, was not the major source for liver and peritoneal NK/LGL.
Significant percentages (&gt; 25%) of the LGL found in the liver and peritoneal cavity following viral infection or interferon induction with poly-inosinic:pory-cytidylic acid were defined morphologically as blasts (large cells with prominent nucleoli and intensely basophilic cytoplasms containing azurophilic granules). Most blast LGL at day 3 p.i. were sensitive to administration of anti-asialo GM1 serum in vivo, were Lyt-2-, and were enriched in populations that lysed NK cell-sensitive targets in vitro, indicating that these were NK/LGL. At day 3 p.i., leukocytes from the liver and peritoneal cavity incorporated 3H-thymidine and bound to and killed NK cell-sensitive targets in single-cell cytotoxicity assays. These data suggest that NK/LGL undergo at least one round of division in the liver and peritoneal cavity during viral infection.
In contrast, blast LGL at day 7 p.i. were resistant to in vivo treatments with anti-asialo GM1 serum, were Lyt-2+, and were enriched in populations of cells that killed virus-infected histocompatible targets, indicating that they were cytotoxic T lymphocytes (CTL). These results suggest that both NK/LGL and CTL/LGL are capable of blastogenesis and presumed proliferation at sites of virus infection, providing a means for the in situ augmentation of a host’s cell-mediated antiviral defenses.
Cell Contact and Direct Transfer Between Co-Cultured Macrophages and Fibroblasts
Authors: Dean Michael F , Cooper John A , Stahl Philip 
Published: January 2018

Abstract
Mouse peritoneal macrophages formed attachments with β-glucuronidase deficient human fibroblasts within an hour after co-cultures were initiated. Some of these attachments were transitory, while in others macrophages remained in firm contact with fibroblasts for many hours. Attachment of one macrophage did not prevent attachment of others, since many fibroblasts made firm contact with four or five other cells. Not all macrophages, however, attached themselves to fibroblasts. Macrophages injected with Lucifer yellow did not transfer the dye to fibroblasts with which they had made contact, nor was there any reverse transfer from injected fibroblasts to macrophages. Lucifer yellow was, however, transferred rapidly from injected fibroblasts to other adjacent fibroblasts with which they had formed gap junctions. Macrophages whose lysosomes had been pre-loaded with FITC-dextran did transfer this ligand to recipient fibroblasts, where it became localised in a perinuclear pattern with many bright punctate patches adjacent to donor macrophages. Transfer of FITC-dextran was blocked when cells were separated by nucleopore membranes in an analogous manner to transfer of endogenous lysosomal β-glucurondiase.