bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development, Differentiation, and Maturation of Macrophages in the Fetal Mouse Liver
Authors: Naito Makoto , Takahashi Kiyoshi , Nishikawa Shin-lchi 
Published: January 2018

Abstract
Primitive macrophages emerged in the sinusoidal lumen of the fetal mouse liver at 10 days of gestation before the Initiation of hepatic hematopoiesis and matured into fetal macrophages. In the culture of cell suspensions from the fetal liver with LP3-conditioned medium, monocyte colonies were formed, but monocytopoiesis was poor in the early stage of hepatic hematopoiesis in vivo. In the culture of cell suspensions obtained from the fetal liver at 10 days of gestation on the monolayer of a mouse bone marrow stromal cell line, ST2, primitive/fetal macrophage colonies were formed before the development of monocyte/macrophage colonies and showed differentiation of primitive macrophages into fetal macrophages without passing through the stage of promonocytes and monocytes. At this time, the fetal cardiovascular system was connected with the vitelline vein just before the formation of the liver. With the progress of gestation, a monocytic cell series was observed to develop and form a monocyte/macrophage population. This was confirmed by in vitro studies with an LP3-conditioned medium and on a monolayer of ST2. Thus, it appears that there exist two different macrophage populations, a primitive/ fetal macrophage population and a monocyte/macrophage population in hepatic hematopoiesis. It also appears that fetal macrophages are differentiated from primitive macrophages which are colonized into the fetal liver from the yolk sac or which develop in loco, presumably from hematopoietic stem cells.
Lipopolysaccharide (LPS) Alters Phosphatidylcholine Metabolism in Elicited Peritoneal Macrophages
Authors: Grove Robert I , Allegretto Nick J , Kiener Peter A , Warr Glenn A 
Published: January 2018

Abstract
We investigated the effects of LPS on mouse peritoneal macrophage phospholipids using radiolabeled precursors. LPS (200 ng/ml) stimulated incorporation of [32P] into all classes of phospholipids within 0.5 hr, and after 2 hr the increase was 60% greater than controls. Separation of the phospholipid classes by thin-layer chromatography revealed a selective increase in incorporation of label into phosphatidylcholine (PC) (90% increase compared to approximately 50% in the other phospholipids). In macrophages labeled with [3H]-choline, LPS stimulated both the incorporation of label into PC and the release of incorporated label into the medium. The time dependencies of stimulated [3H] release and [32P] incorporation were similar. These data are consistent with the hypothesis that LPS activates macrophages via a PC-specific phospholipase-dependent mechanism.
Calcium Is Required for PMA Induced Superoxide Release From Human Neutrophils
Authors: Ishihara Y , Rosolia D L , McKenna P J , Peters S P , Albertine K H , Gee M H 
Published: January 2018

Abstract
Experiments were designed to reexamine the relationship between extracellular calcium and superoxide generation in phorbol myristate acetate (PMA) stimulated neutrophils exploiting a newly adapted method to measure superoxide anion (O2-) generation from adherent cells stimulated at high and low cell density. Human neutrophils were plated in microtiter wells in cell densities of either 0.2 or 2.0 million cells/well. Superoxide release was measured sequentially over 60 min by reduction of ferricytochrome c. Cells were maintained in 1 mM Ca++ or 0 mM Ca++ Hanks' buffer for 60 min prior to activation as well as during measurement of O2-. In 1 mM Ca++, 2.0 million adherent neutrophils released 10.7 ± 1.2 nmol O2- in 20 min (n=4). O2- release was not significantly different for high density cells incubated and stimulated in 0 mM Ca++. In the presence of 1 mM Ca++, 0.2 million adherent neutrophils released 6.3 ± 0.5 nmols O2- in 20 min. With cells stimulated at low density, PMA stimulated O2- release was significantly decreased (3.0 ± 0.6 nmol O2- in 20 min) as was the initial rate of secretion of O2- in the absence of extracellular calcium. Basal release of superoxide was also greater in the presence of 1 mM Ca++ (0.96 nmol/20 min) compared to basal release in 0 mM Ca++ (0.22 nmol/20 min). Additional experiments with 0.2 million cells/well showed that extracellular Ca++ was required during stimulation with PMA and that prior incubation of cells for up to 60 min in 0 mM Ca++ had no effect on O2- release measured in the presence of calcium. Furthermore, PMA stimulated O2- was independent of verapamil (10-5–10-7 M), suggesting that voltage-dependent calcium channels do not participate in this response. The planar areas for unstimulated neutrophils in 0 mM Ca++ increased after addition of PMA. Unstimulated cells in 1 mM Ca++ tended to be larger and planar areas did not increase after PMA. These studies demonstrate that PMA stimulated O2- secretion is dependent on extracellular calcium particularly when adherent neutrophils are stimulated at low cell density. Furthermore, extracellular calcium at a concentration of 1 mM primes neutrophils by increasing basal secretion of O2- and increasing superoxide release after a maximum stimulating dose of PMA.
Synergistic Effect of Interferon-γ and Tumor Necrosis Factor-α on Antiviral Activity and (2′–5′) Oligo (A) Synthetase Induction in a Myelomonocytic Cell Line
Authors: Wietzerbin Juana , Gaudelet Corinne , Catinot Liliane , Chebath Judith , Falcoff Rébéca 
Published: January 2018

Abstract
TNF was not observed to have an antiviral effect on either HL60 or U937 cells. However, it did significantly enhance interferon (IFN)-γ-mediated antiviral activity in U937 cells. Treatment of U937 cells with IFN-γ enhanced (2′–5′) oligo (A) synthetase activity (2.5-fold) but treatment with TNF did not Combined treatment with TNF-α + IFN-γ increased this activity dramatically (20–40-fold). This increase correlated with the very large increase in the (‘2–5’) oligo (A) synthetase mRNA level in U937 cells. No such effects were observed in HL60 cells. Furthermore, binding studies and cross-linking analysis showed that IFN-γ modulated TNF-α receptors in U937 cells without altering their properties, but did not do so in HL60 cells.
Macrophages From C3H/HeJ Mice Require an Additional Step To Produce Monokines: Synergistic Effects of Silica and Poly(I:C) in the Release of Interleukin 1
Authors: Souvannavong Vongthip , Adam Arlette 
Published: January 2018

Abstract
Resident macrophages from C3H/HeJ mice, in contrast with those of other strains of mice such as BDF1 mice, did not release a 35 kD m.w. factor having macrophage replacing activity (FRM) or interleukin 1 (IL-1) when, respectively, cultured alone or in the presence of silica. C3H/HeJ macrophages were nevertheless capable of producing an intracellular IL-1-like activity. In addition, after a two-step activation process, macrophages from BDF1 mice spontaneously released IL-1, whereas silica was required to induce the release of IL-1 from similarly treated C3H/HeJ macrophages. Such in vivo primed and in vitro stimulated macrophages failed to release FRM. In contrast, poly(l:C) was able to induce the release of FRM by C3H/HeJ macrophages but not that of IL-1; moreover, the addition of silica to poly(l:C)-stimulated cells led to an IL-1 release similar to that obtained with normal mice treated with silica alone. Since poly(l:C) is able to elicit the production of interferons (IFN), the involvement of IFNs was investigated in poly(l:C) activity. Neither IFN-α/β nor IFN-γ, when used alone or in the presence of silica, could induce the release of IL-1 by C3H/HeJ macrophages. In addition, antibodies to IFN-α/β and IFN-γ were unable to affect the poly(l:C) and silica induced release of IL-1. Thus, the signal provided by poly(l:C) does not appear to be mediated by IFN(s).
Tumoricidal Effector Mechanisms of Murine BCG-Activated Macrophages: Role of TNF in Conjugation-Dependent and Conjugation-Independent Pathways
Authors: Klostergaard Jim , Stoltje Paul A , Kull Frederick C 
Published: January 2018

Abstract
The roles of secreted and membrane-associated TNFs were investigated in activated macrophage cytolysis of L929, EMT-6, and P815 targets. While all three targets were susceptible to cytolysis in coculture, an anti-TNF antiserum blocked lysis of L929 and EMT-6 but not of the P815 targets. Of the three targets, recombinant human or mouse TNF could only lyse the L929 target; despite the fact that a role for TNF was invoked in lysis of EMT-6 targets in coculture, the latter was strongly resistant to soluble rTNF, even at concentrations 30–40-fold higher than the Ka for Its TNF-receptor. Cytolysis of the L929 target occurred when it was cocultured with BCG-activated macrophages even when these effector cells did not secrete TNF, either due to prior chemical crosslinking or to lack of exposure to a triggering level of lipopolysaccharide. Furthermore, by introduction of the anti-TNF antiserum over a dose-range, it was shown that macrophage cytolysis both of L929 and EMT-6 targets occurred in the absence of bioavailable, fluid-phase TNF. Thus, even for targets susceptible to fluid-phase TNF, TNF-dependent, direct macrophage-mediated cytolysis appears to be a function independent of secreted TNF and one that utilizes effector-target contact to express the action of a membrane form of the molecule.
Binding of the T Cell Activation Monoclonal Antibody Ta1 to Dipeptidyl Peptidase IV
Authors: Barton Randall W , Prendergast Jay , Kennedy Charles A 
Published: January 2018

Abstract
The monoclonal antibodies, Ta1 and IOT15, define T cell activation cell surface markers and have been assigned to the CD26 leukocyte differentiation antigen cluster. Dipeptidyl peptidase IV (DPP IV, EC 3.4.14.5) is an exoaminopeptidase that, among leukocytes, is expressed almost exclusively on activated T cells. Comparative binding studies showed that the Ta1 mAb binds to DPP IV purified from human placenta as well as in extracts of the human YT lymphoid cell line and of CD3 stimulated normal human peripheral blood mononuclear cells. The mAb IOT15 did not bind to DPP IV from any source even upon repeated incubations. Western blot analysis of YT cell extracts revealed that Ta1 and IOT15 bound to distinctly different molecular weight molecules. Immunofluorescent cell surface capping experiments showed that capping of the IOT15 did not alter the surface distribution of the Ta1 fluorescence. The capping results combined with the DPP IV binding results indicate that IOT15 and Tal mAb's bind to different, apparently unassociated, molecules on the surface of T cells and that only Ta1 binds the T cell surface enzyme DPP IV.
Assessment of Chemokinetic Behavior of Inflammatory Lung Macrophages in a Linear Under-Agarose Assay
Authors: Newton-Nash Debra K , Tonellato Peter , Swiersz Melanie , Abramoff Peter 
Published: January 2018

Abstract
Migration of cells in response to a chemoattractant gradient is influenced by directed migration (chemotaxis) and stimulated random motility (chemokinesis). The present study quantitated the chemokinetic motility of normal and inflammatory lung macrophages by performing the linear under-agarose assay in the presence of uniform concentrations of chemoattractant. Under these conditions, cell motility can be likened to a molecular diffusion process. Mathematical analyses which describe molecular diffusion were then applied, allowing the quantitation of the parameter, μ, the cellular equivalent to the molecular diffusivity constant. Determination of changes in μ as a function of chemoattractant concentration revealed that the chemokinetic motility of alveolar macrophages recovered during the early stages of acute pulmonary inflammation was greater than that of normal alveolar macrophages and macrophages recovered later in the inflammatory response. The correlation of differences in macrophage chemokinesis with macrophage maturation and the relevance of these differences to macrophage accumulation during inflammation are discussed.
Multiple Receptors on Human Monocytes Are Involved in Adhesion to Cultured Human Endothelial Cells
Authors: Carlos Timothy M , Dobrina Aldo , Ross Russell , Harlan John M 
Published: January 2018

Abstract
Monocytes exhibit significant basal (unstimulated) adherence to human umbilical vein endothelium (HUVE), which is only partially inhibited by an anti-CD18 monoclonal antibody (mAb) (60.3). We examined factors modulating the residual, CD18-independent monocyte binding to HUVE by pretreating monocytes with mAb 60.3 to eliminate CD18-dependent binding. Basal adherence was reduced from 32% ± 2% to 14% ± 2% with mAb 60.3 (means ± SE of eight experiments; P &lt; 0.01). mAb 60.3-treated monocytes were incubated with tumor necrosis factor-γ (TNF-α), interleukin-1 (IL-1), lipopolysaccharide (LPS), N-formylmethionyl-leucyl-phenylalamine (FMLP), or phorbol myristate acetate (PMA). Only PMA affected CD18-independent binding. Pretreatment with PMA alone reduced adherence to 21% ± 2% (mean ± SE of eight experiments; P &lt; 0.01). In conjunction with mAb 60.3, PMA virtually eliminated monocyte adherence to HUVE (7% ± 1%, mean ± SE of eight experiments; P &lt; 0.01). We also examined CD18-independent monocyte binding to endothelial-leukocyte adhesion molecules (E-LAMs) induced by pretreatment of HUVE with LPS. Monoclonal antibody 60.3-treated monocytes increased adherence from 14% ± 2% with unstimulated HUVE to 37% ± 2% with LPS-stimulated HUVE (mean ± SE of four experiments; P &lt; 0.01). Monocytes pretreated with both mAb 60.3 and PMA increased adherence from 5% ± 1% with the unstimulated HUVE to 18% ± 1% with the LPS-stimulated HUVE (mean ± SE of four experiments; P &lt; 0.01). This result implies the presence of a CD18-independent and PMA-insensttive receptor on human monocytes for an E-LAM induced by LPS. In summary, we have identified two CD18-independent mechanisms of monocyte adherence to HUVE; a PMA-sensitive mechanism mediating basal adherence and a PMA-insensitive mechanism involved in binding to E-LAMs.
Decreased Fc Receptor Expression on Macrophages Following Simple Hemorrhage as Observed by Scanning Immunoelectron Microscopy
Authors: Rana M Waheed , Ayala Alfred , Dean Richard E , Chaudry Irshad H 
Published: January 2018

Abstract
Although it is known that macrophage (Mφ) functions such as phagocytosis and antigen presentation are depressed following hemorrhage and resuscitaion, the mechanism remains unknown. The aim of this study was to determine, using scanning immunoelectron microscopic techniques, whether there is any alteration in the Fc receptors on the Mφ after hemorrhage. To study this, male C3H/HeN mice were bled to a mean blood pressure (BP) of 35 mm Hg and maintained at that pressure for 1 hr, then resuscitated with their own blood and adequate fluids. Twenty-four hrs later, Kupffer cells from livers and splenic adherent cells were isolated, incubated for 16 hr, and then exposed to polysterene beads conjugated with antimouse IgG that specifically binds to Fc receptors. The cells were then prepared for observation by scanning electron microscopy. At least 100 cells from each animal were examined. The number of Kupffer cells from posthemorrhage mice that exhibited specific receptor labeling was significantly decreased (41.0 ± 2.6, P &lt; 0.05) compared with control (64.2 ± 7.5). The number of splenic adherent cells from posthemorrhage mice exhibiting specific receptor labeling was also significantly decreased (35.7 ± 2.5, P &lt; 0.01) compared with control (61.2 ± 3.9). The internalization of markers was also seen in some cells. The cause of the decrease in receptor labeling following hemorrhage may be the loss, inactivation, and/or internalization of receptors. Thus the decreased number of functional macrophages may contribute to the depression of antigen presentation and to the enhanced susceptibility to sepsis following hemorrhage.
Effects of TNFα on the Expression of Class II MHC Molecules in Macrophages Induced by IFNγ: Evidence for Suppression at the Level of Transcription
Authors: Melhus O , Koerner T J , Adams D O 
Published: January 2018

Abstract
Tumor necrosis factor-α (TNFα) induces surface expression of class II major histocompatibility (MHC) molecules (la molecules) in many cells, including macrophage-like cell lines. When we tested the effects of this cytokine on murine peritoneal macrophages, TNFα had little effect on surface expression of la. The strong expression of such molecules induced by interferon-γ (IFN-γ) was, however, suppressed moderately by TNFα. These effects were reflected at the level of specific messenger RNA (mRNA) as detected by Northern blot analysis. Furthermore, the locus of control appears to be transcriptional; in nuclear run-on assays, TNFα suppressed the IFNγ-induced enhancement of transcription for the murine β-chain of l-A (l-Aβ.). Taken together the data suggest that TNFα has little effect on class II MHC genes and surface expression in murine peritoneal macrophages, that TNFα is a modest suppressant of such molecules when their levels are raised by IFNγ, and that these suppressive effects are mediated at the level of transcription.
Cystatin C and Cathepsin B Production by Alveolar Macrophages From Smokers and Nonsmokers
Authors: Warfel Alwin H , Cardozo Christopher , Yoo Ok Hi , Zucker-Franklin Dorothea 
Published: January 2018

Abstract
The capacity of alveolar macrophages (AM) obtained from smokers and nonsmokers to secrete cathepsin B and its inhibitor cystatin C was examined because of the concept that an imbalance in the production of proteolytic enzymes and/or their inhibitors could be responsible for the lung damage seen in smokers. Quantitation of immunoprecipitates on Western blots showed that the amount of total cystatin C secreted into the culture medium by AM of smokers was significantly greater than the amount secreted by cells obtained from nonsmokers, whereas the difference between the amount of cathepsin B secreted by the AM of smokers and that from nonsmokers did not appear significant. The cystatin C found in the medium conditioned by AM of nonsmokers appeared to be more heterogeneous in molecular size, presenting either as a single band of about 14 Kd or as a high-molecular-weight triplet of about 69 Kd, 63 Kd, and 57.3 Kd. Furthermore, in some cases there were single or doublet bands at 14 Kd as well as the high-molecular-weight triplets. In contrast, smokers AM-conditioned medium uniformly possessed both the low-and the high-molecular-weight cystatin C. Cathepsin B was not detected in Western blots at its reported molecular weights but was identified at the exact area occupied by the higher molecular weight cystatin C, i.e., at bands corresponding to 69 Kd, 63 Kd, and 57.3 Kd. Therefore, it is clear that in culture media of AM, cystatin C and cathepsin B are present as proteinase–antiproteinase complexes. The observation also suggests that in smokers an excess of cystatin C may be elaborated, which, if further substantiated, would show for the first time a likely role for this proteinase inhibitor in vivo.
Modulation of Mycobacterium avium Growth in Murine Macrophages: Reversal of Unresponsiveness to Interferon-Gamma by Indomethacin or Interleukin-4
Authors: Denis Michel , Gregg Evan O 
Published: January 2018

Abstract
The ability of soluble factors to modulate the growth of a virulent strain of Mycobacterium avium in murine peritoneal macrophages was studied. The virulent strain, TMC 702, grew progressively in the organs of susceptible BALB/C mice. In addition, this strain of M. avium grew progressively in untreated peritoneal macrophages. Treatment of macrophage monolayers with interferon-gamma (IFN-γ) did not change significantly the intracellular growth of M. avium. Addition of indomethacin to IFN-γ-treated macrophage monolayers rendered them significantly more bacteriostatic than macrophages treated with interferon alone, suggesting a role for prostaglandins in inducing unresponsiveness to IFN-γ in infected cells. Additionally, treatment with tumour necrosis factor-alpha led to a modest increase in bacteriostasis, as compared to untreated monolayers. Further experiments with recombinant interleukins showed that interleukin-4 (IL-4), on its own, could increase bacteriostatic activity against M.avium in a reproducible fashion. Experiments with interleukin combinations showed that IFN-γ and IL-4 treatment of macrophages rendered these cells almost fully bacteriostatic against M. avium. Inclusion of scavengers of reactive oxygen species did not modify the beneficial effect of IFN-γ and IL-4. Overall, our results suggest an important role for interleukins in modulating the interaction between virulent mycobacteria and murine macrophages.
Monokines Mediate Decreased Hepatic Glucocorticoid Binding in Endotoxemia
Authors: Bengtsson Torbjörn , Dahlgren Claes , Stendahl Olle , Andersson Tommy 
Published: January 2018

Abstract
Several studies indicate that the actin filament system is not only involved in cell motility, but also in the regulation of other neutrophil functions. The aim of the present investigation was to examine the mechanisms by which actin filament formation participates in the control of the respiratory burst and degranulation in human neutrophils. The approach taken was to use both an inhibitor (cytochalasin B) and a potentiator (tetracaine) of formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe)-induced actin polymerization. The total inhibition of fMet-Leu-Phe-induced actin polymerization in cytochalasin B-treated cells was accompanied by an impressive potentiation of both oxidase activity and degranulation (azurophilic and specific granules). However, preincubation with tetracaine, which causes an enhanced accumulation of F-actin in the periphery of fMet-Leu-Phe-stimulated cells, also augmented the rate and duration of peptide-induced superoxide anion production, but inhibited degranulation (specific granules). A likely explanation for the potentiating effects of cytochalasin B and tetracaine is provided by our observation that both of these substances reduced the acid-resistant binding of fMet-Leu-Phe (interpreted as a decrease in the internalization of fMet-Leu-Phe-receptor-complexes), resulting in an enhanced formation of second messengers (diacylglycerol). The findings that tetracaine potentiated the activity of the oxidase, whereas it inhibited degranulation (specific granules), suggest that actin polymerization per se plays a role in the latter process. Consequently, this study argues against the idea of a direct inhibitory effect of F-actin on chemotactic factor-induced oxidase activation, but supports an active role of actin filaments in the translocation and release of granule components.