bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin-1 Inhibitor Production by Human Mononuclear Leukocytes and Leukocyte Subpopulations Exposed to Respiratory Syncytial Virus: Analysis and Comparison With the Response to Influenza Virus
Authors: McCarthy Donna O , Domurat Frank M , Nichols Joan E , Roberts Norbert J 
Published: January 2018

Abstract
Net interleukin-1 (IL-1) inhibitor activity is induced by exposure of purified human monocytes-macrophages to respiratory syncytial virus (RSV). Furthermore, IL-1 inhibitor activity was produced by monocytes-macrophages exposed to RSV in the presence of lymphocytes, that is, by unseparated mononuclear leukocytes (MNL). Purified RSV-exposed lymphocytes, as well as the lymphocytes exposed within MNL preparations, produced net IL-1 inhibitor activity. In contrast, net IL-1 activity was produced when purified monocytes-macrophages or unseparated MNL were exposed to influenza virus. The RSV-induced IL-1 inhibitors demonstrated antiproliferative effects on mitogen-stimulated human lymphocytes as well as on the mouse thymocytes used in standard assays. The results raise the possibility that such antiproliferative activity is mediated, at least in part, by monocytes-macrophages. The data also suggest that IL-1 inhibitors produced by MNL after exposure to RSV may contribute along with other factors to the recurrence of RSV infection in immune individuals.
Virus-Transformed Macrophage-Like Cell Line as Tool for Eicosanoid Research
Authors: Wessel K , Kaever V , Ostertag W , Bitter-Suermann D , Resch K 
Published: January 2018

Abstract
The ability of a virus-transformed murine macrophage like cell line HA 38 to produce different eicosanoid metabolites was examined. HA 38 cells release similar amounts of prostaglandins and leukotrienes as did murine peritoneal macrophages in response to both physiological and non-physiological stimuli. Enzyme systems known to be involved in the regulation of eicosanoid synthesis are expressed. HA 38 cells thus are a well defined macrophage model system and are well suited to study eicosanoid synthesis in macrophages and effects of drugs on the prostaglandin and leukotriene synthesis pathways.
Feline Hybridoma Growth Factor/lnterleukin-6 Activity
Authors: Ohashi Takashi , Goitsuka Ryo , Ono Kenichiro , Hasegawa Atsuhiko 
Published: January 2018

Abstract
An assay system was developed to measure feline hybridoma growth factor (HGF)/interleukin-6 (IL-6) activity in biological samples containing many kinds of cytokines by using the proliferation of the newly established mouse-rat hybridoma clone. B3B1. The proliferative response of this B3B1 clone was IL-6-specific, and could not be promoted by other cytokines including IL-1, IL-2, IL-3, and granulocyte-colony-stimulating factor (G-CSF), The anti-human B-cell stimulatory factor 2 (BSF-2)/IL-6 antiserum did not neutralize feline HGF/IL-6 activity in conditioned media prepared from feline con A-stimulated splenocytes and unstimulated alveolar macrophages, indicating antigenic differences between species. Feline HGF/IL-6 was eluted into the fractions corresponding to a molecular weight of 30,000–40,000 in gel filtration, and into the fractions at a salt concentration of 0.2–0.3 M NaCI in anion exchange chromatography. The physicochemical properties of feline HGF/IL-6 were slightly different from those of murine and human IL-6.
Killing of Mycobacterium smegmatis by Macrophages From Genetically Susceptible and Resistant Mice
Authors: Denis Michel , Forget Adrien , Pelletier Micheline , Gervais Francine , Skamene Emil 
Published: January 2018

Abstract
The bactericidal function of macrophages was investigated in congenic mice expressing the phenotype of susceptibility (B10.A, Bcgs) or resistance (B10.A.Bcgr) to mycobacterial infection. When splenic and peritoneal macrophages from these two mouse strains were infected in vitro with Mycobacterium smegmatis, the Bcgr macrophages were shown to inactivate M. smegmatis more efficiently than their Bcgs congenic counterparts. The mechanisms of this superior antimycobacterial activity was studied further. Addition of catalase did not abolish killing to a significant degree in either allelic type of macrophage, suggesting that hydrogen peroxide production was not involved in the killing activity controlled by the Bcg gene. Activation of Beg macrophages by exposure to crude lymphokines rendered them equally as efficient as their Bcgr counterparts in their capacity to destroy M. smegmatis. This finding suggests that both the genetically resistant and susceptible macrophages have the potential to kill M. smegmatis in vitro. This potential is expressed constitutively by the Bcgr but not Bcga macrophages and can be induced, by lymphokine treatment, in the Bcga macrophages. In a final set of experiments, the macrophage killing of M. smegmatis was evaluated as a test system to type for the Bcg gene allelic type in vitro, using a set of AXB and BXA recombinant inbred strains of mice. Results obtained show that typing of AXB/BXA recombinant inbred strains for the trait of bactericidal activity vs. M. smegmatis in vitro revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium bovis BCG in vivo.
Priming of Polymorphonuclear Granulocytes by Lipopolysaccharides and Its Complexes With Lipopolysaccharide Binding Protein and High Density Lipoprotein
Authors: Vosbeck Klaus , Tobias Peter , Mueller Heinz , Allen Rodger A , Arfors Karl-E , Ulevitch Richard J , Sklar Larry A 
Published: January 2018

Abstract
Human peripheral blood neutrophils are primed, or enabled to respond to formyl peptide. by prior exposure to bacterial lipopolysaccharide (LPS). The activity of LPS and the size of its aggregates are altered by plasma constituents such as high density lipoprotein (HDL) and the recently discovered acute phase reactant lipopolysaccharide binding protein (LBP) Tobias et al.: J. Exp. Med. 164,777, 1986]. The ability of LPS, LPS–LBP, and LPS–HDL complexes to activate a number of cellular responses have been compared. LPS–LBP and LPS–HDL were prepared using LBP and HDL from rabbit serum. LPS from Salmonella minnesota Re595 and its LPS–LBP and LPS–HDL complexes differed in their ability to prime PMN O2− production in response to formyl peptide (f-Nle-Leu-Phe-Nle-Tyr-Leu [FNLPNTL]). Human PMN prepared under conditions in which O2 production is minimal (&lt;1 nmol O2−/106 PMN/10 min) after exposure to 10-7 M FNLPNTL can be primed with 0.1–100 ng/ml LPS in a dose- and time-dependent manner to produce up to 12 nmol O2−/106 PMN/10 min. LBP complexation accelerated the priming induced by LPS, whereas HDL complexation retarded it. Priming was accompanied by a parallel two- to threefold increase in formyl peptide receptor number as determined by FACS analysis of fluoresceinated FNLPNTL binding and SDS-PAGE autoradiographic analysis of photoaffinity ligand binding. Thus binding of LPS to plasma proteins changes the response of the PMN to LPS and may represent one way in which the response of the PMN is regulated during infection. Since LBP concentrations change during an acute phase response, complexation of LPS with LBP is a mechanism that may regulate neutrophil responses in vivo during inflammation.
Differential Tumor Necrosis Factor Production by Human Monocyte Subsets
Authors: Szabo Gyongyi , Miller-Graziano Carol L , Wu Jia-Yan , Takayama Thomas , Kodys Karen 
Published: January 2018

Abstract
The human monocyte (MØ) subset rosetting with anti RH-coated human erythrocytes via high-affinity, 72 kD receptors (FcRI+), contains the PGE2-producing immunosuppressive subpopulation, while the non-rosetting MØ subset (FcRI-) is the major plasminogen activator-producing and antigen-presenting MØ. This study gives additional evidence for the functional disparity of the FcRI- and FcRI+ MØ subsets. We are demonstrating that the normal human MØ subset isolated by rosetting via the FcRI receptor (FcRI+) produces greater quantities of tumor necrosis factor (TNF) than the non-rosetting (FcRI-) MØ. TNF production by the FcRI+ MØ subset is greater than that of the FcRI- MØ subset whether secreted (P &lt; .001) or cell-associated (P &lt; .001) TNF is assessed. The rosetting MØ subset that expresses high densities of FcRI (FcRI+) produced the majority of normal human peripheral blood MØ TNF whether the stimulation was an interferon gamma (IFNγ) prime followed by MDP or followed by interleukin-2 (IL-2). The Fc rosetting technique itself resulted in some TNF induction in the FcRI+ MØ subset accounting for some of the increased TNF production of this subset. However, increasing the stimulation level of the FcRI very-low-density (FcRI-) MØ subset did not induce it to produce TNF levels equivalent to the moderately stimulated FcRI+ MØ subset. These data, therefore, imply that only stimulation through the type I Fcγ receptor can augment or induce TNF activity. The difference in the MØ subset's TNF response remained even after the FcRI- MØ subset received a 2.5-fold increase in stimulation with the classical MØ induction regimen of IFNγ plus bacterial cell wall product. Although stimulation of the FcRI+ MØ subset via crosslinking of their FcRI receptors might represent a unique TNF stimulation pathway, this stimulation does not occur in the low-density FcRI (FcRI-) MØ subset, again indicating functional disparity between these subsets. Greater TNF production by the FcRI+ MØ subset was induced concomitant to elevation of its prostaglandin E2 production. Since both TNF and PGE2 are increased in some patient groups, a pathological shift in the FcRI+ versus FcRI- MØ ratio in these patients coupled to the functional differences in FcRI+ and FcRI+ MØ subsets could be one mechanism for the development of immunoincompetence.
Repopulation of Macrophages in Popliteal Lymph Nodes of Mice After Liposome-Mediated Depletion
Authors: Delemarre F G A , Kors N , Kraal G , van Rooijen N 
Published: January 2018

Abstract
Macrophages lining the subcapsular sinus (SCS) and those located in the medulla of popliteal lymph nodes (PLN) of mice were eliminated after subcutaneous (s.c.) injection of dichloromethylene diphosphonate (CI2MDP)-containing liposomes. No effect of liposome-entrapped CI2MDP could be seen on nonphagocytic cells, e.g., interdigitating cells (IDC) and B- and T-lymphocytes. One month after injection the eliminated subsets of macrophages were still absent. After 2 mo a small number of macrophages had reappeared along the SCS and in the medulla of the PLN of a few animals. Complete repopulation of the PLN with macrophages was observed only after 5 mo.
This extremely long repopulation time could be shortened drastically by local administration of Freund's complete adjuvant (FCA). A small number of macrophages reappeared along the SCS and in the medulla 1 wk after FCA and after 3 wk the repopulation of the PLN with macrophages was complete. Such rapid repopulation of macrophages was not achieved after s.c. injection of paraffin oil or paratyphoid vaccine.
These results indicate that the normal rate of influx of mononuclear phagocytes into the PLN is low, but that it can be sped up after administration of FCA.
Effects of Polymyxin B on Superoxide Anion Release and Priming in Human Polymorphonuclear Leukocytes
Authors: Aida Yoshitomi , Pabst Michael J , Rademacher Jonella M , Hatakeyama Tamiko , Aono Masao 
Published: January 2018

Abstract
We studied the effect of a potent inhibitor of protein kinase C, polymyxin B (PMXB), on superoxide anion (O−2 release by human polymorphonuclear leukocytes (PMNL). PMXB was compared with another inhibitor of protein kinase C, 1-(5-isoquinoline-sulfonyl)-2-methyl piperazine (H-7). Both PMXB and H-7 inhibited phorbol myristate acetate (PMA)-stimulated O−2 release. Formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated O−2 release by cytochalasin B–treated PMNL was not inhibited significantly by either PMXB or H-7. 1-Oleoyl-2-acetyl-glycerol (OAG,25–100 μM) stimulated PMNL to release O−2 with a long lag-time (8–10 min). Although H-7 inhibited OAG-stimulated O−2 release, PMXB augmented the OAG-stimulated response by increasing rate and reducing lag time. The augmenting effect of PMXB was evident only when added after stimulation by OAG, with maximum effect observed at 3 min after addition of OAG. The augmenting effect was also seen with PMXB immobilized on agarose beads. PMXB did not affect the respiratory burst response to 1,2-dioctanoylglycerol. PMXB-augmented, OAG-stimulated O−2 release was inhibited by the addition of H-7 before OAG. In contrast to the effect on O−2 release, OAG-stimulated protein phosphorylation was inhibited similarly by either PMXB or H-7, when these agents were added 3 min after stimulation by OAG. These results suggested that initial activation of protein kinase C by OAG is essential for O−2 release, but that PMXB acts in a manner independent from protein kinase C to augment OAG-stimulated O−2 release. When priming by OAG for enhanced O−2 release (as opposed to direct stimulation of O−2 release) in FMLP-stimulated PMNL was examined, PMXB inhibited O−2 release in OAG-primed PMNL, suggesting that protein kinase C is involved in priming of PMNL by OAG.
Oxidative Metabolism in the Alveolar Macrophage: Analysis by Flow Cytometry
Authors: Kobzik Lester , Godleski John J , Brain Joseph D 
Published: January 2018

Abstract
We evaluated the reagents dichlorofluorescin (DCFH) and hydroethidine (HE) for use in flow cytometric analysis of the respiratory burst of alveolar macrophages and monocytes. DCFH and HE are non-fluorescent precursors which can be oxidized intracellularly to the fluorescent compounds dichlorofluorescein and ethidium.
Alveolar macrophages (AMs) loaded with either DCFH or HE were analyzed after phorbol myristate acetate (PMA) stimulation. The results, expressed as fmol/cell oxidation product (DCF or ethidium) after fluorometric standardization of the flow cytometer. show that both DCFH (273 ± 48, mean increase over control ± SE, fmol/cell, N = 9) and HE (416 ± 54, N = 11) detected the substantial respiratory burst of hamster AMs. Similar results were obtained with normal human AMs. By using multiparameter analyses, the oxidative response of AMs ingesting opsonized fluorescent latex beads was measured in subpopulations ingesting increasing numbers of particles. A graded increase in oxidation of both DCFH and HE was found in response to increasing phagocytosis. Ingestion of fluoresceinated staphylococcal bacteria caused similar changes in HE-loaded AMs. Inhibition of respiration with antimycin showed that approximately 95% of the increased oxidative metabolism of hamster AMs ingesting opsonized beads or bacteria was mitochondrial. The remaining 5% (10–40 fmol/cell) is membrane-derived oxidative activity quantitatively similar to that measured in assays of extracellular release of H2O2.
Monocytes loaded with either DCFH or HE also showed substantial increases in fluorescence after PMA stimulation (mean % increase over control ± SE at 30 ruin: 464 ± 104, DCFH, 505 ± 156, HE). While DCHF is known to measure H2O2, HE is less well characterized. Exposure of cells to an extracellular source of both superoxide anion (O2-) and H2O2, xanthine oxidase-xanthine, resulted in marked oxidation of intracellular HE. Addition of both superoxide dismutase and catalase blocked this oxidation, indicating that HE can detect both O2- and H2O2. These agents can be useful probes for precise analysis of oxidative metabolism during phagocytosis in AMs and other mononuclear phagocytes.
The Short and Happy Life of Neutrophil Activation
Authors: Becker Elmer L 
Published: January 2018

Abstract
This is largely a history of attempts from approximately 1960 until about 1980–81 to understand the mechanisms by which neutrophils are activated by chemotactic factors to induce chemotaxis and granule secretion. As such, it deals with the growth of our knowledge of neutrophil chemotactic factors and their receptors; the importance and role of cation fluxes, especially Ca2+, microfilaments and microtubules, membrane potential, cyclic nucleotides, and the start of our recognition of the importance of arachidonic acid and phospholipid metabolism and protein phosphorylation. In a very real sense this is a history of the origins of our present realization that reactions and functions which had been considered specific to the neutrophil are to be thought of as similar or identical to general biological and physiological processes such as muscle contraction, cellular secretion, etc.
Estimation of In Vivo Reticuloendothelial System Phagocytic Activity in Rats by Direct Blood Clearance Techniques and Nuclear Scintigraphy
Authors: Goyal Deepi G , Gutowski Karol A , Merion Robert M 
Published: January 2018

Abstract
There has been considerable interest in the examination off reticuloendothelial system phagocytic blockade. In this study, the kinetics of phospholipid liposome-mediated and intraperitoneal silica-mediated phagocytic blockade were examined using five methods off analysis off in vivo 99mTc-labeled albumin clearance and reticuloendothelial cell uptake. Two direct blood sampling techniques revealed significant impairment in 99mTc-labeled albumin clearance after treatment with silica (P &lt; 0.05), while liposome treatment was not associated with such impairment. A method utilizing nuclear scintigraphy for the determination of blood clearance was incapable of detecting silica-mediated blockade but demonstrated significant impairment by liposomes at 2 hr (P &lt; 0.001), 6 hr (P &lt; 0.05), and 24 hr (P &lt; 0.001). Gamma camera imaging methods for determination of hepatic uptake demonstrated significant (P &lt; 0.05) and reversible impairment of 99mTc-labeled albumin uptake by liposomes. The most promising of these techniques utilizes deconvolutional analysis off liver region of interest time–activity curves to correct for continuously changing blood concentrations of tracer and for intracellular tracer processing and catabolism. Measurements of reticuloendothelial system phagocytic activity should include methods that take into account the observed discrepancies between blood clearance determinations and reticuloendothelial cell uptake.
Superoxide Anion Generation in the Liver During the Early Stage of Endotoxemia in Rats
Authors: Bautista Abraham P , Mészáros Károly , Bojta Julia , Spitzer John J 
Published: January 2018

Abstract
Infiltration of polymorphonuclear neutrophils (PMN) in the rat liver 3 hr after an intravenous (IV) injection of a sublethal dose of Escherichia coli lipopolysaccharide (LPS) was observed without any significant alteration in the total number of Kupffer and endothelial cells. Since previous studies have demonstrated that phagocytic cells in the liver were in a state of metabolic activation under similar experimental conditions, we investigated the in vitro generation of superoxide anion (O2-) by this cell type following the administration of LPS. Kupffer cells from normal rats did not release O2-, in contrast to those obtained from LPS-treated rats. The generation of O2- by Kupffer cells from endotoxic rats was elevated from 3.0 ± 1.9 nmol/106 cells/60 min (mean ± SD) in the absence of macrophage (Mφ) activators, to 5.0 ± 2.36, 11.33 ± 5.40, and 4.33 ± 0.90 in the presence of opsonized zymosan, phorbol myristate acetate (PMA), and the calcium ionophore A23187, respectively. Hepatocytes from normal or endotoxic rats did not produce detectable O2-. Endothelial cells from LPS-treated rats generated &lt; 0.8 nmol/106 cells in the presence of zymosan. PMN that accumulated in the livers of endotoxic rats released O2- only in the presence of zymosan (8.12 ± 5.40), PMA (15.43 ± 5.84), or A23187 (1.70 ± 0.12). The O2- generation by blood monocytes and PMN increased significantly after endotoxin administration and in the presence of activators. These results suggest that the hypermetabolic state of phagocytic cells in the liver shortly after LPS treatment may be correlated with the increased generation of O2-. The latter may subsequently contribute to the induction of hepatic injury in endotoxemia.
Surface Characteristics, Morphology, and Ultrastructure of Human Adherent Lymphokine-Activated Killer Cells
Authors: Melder Robert J , Walker Elizabeth R , Herberman Ronald B , Whiteside Theresa L 
Published: January 2018

Abstract
Human adherent lymphokine-activated killer (A-LAK) cells represent a population of highly cytotoxic, interleukin-2 (IL-2)-activated peripheral blood lymphocytes that have large granular lymphocyte (LGL) morphology and display natural killer (NK) cell-associated surface markers (CD3-CD56+). The ultrastructure of A-LAK cells also is consistent with that of highly activated NK cells. After their initial isolation, continued culture of A-LAK cells in the presence of IL-2 resulted in cyclic shifts between adherent and nonadherent phases with about 90% of the cells floating and non-adherent. All of these A-LAK cells were spheroidal with numerous villi and pseudopodia. In the adherent phase, A-LAK cells were motile, moving along the solid surface at a speed of about 1 μm per minute, and polar, with a ruffled leading edge at one end of the cell and a terminal tuft of villi at the opposite end. Transmission electron microscopy of these cells also demonstrated a high degree of Internal polarity, with the nucleus at the leading edge of the cell and richly granulated cytoplasm at the terminal end. Extensive cytoskeletal structures, multivesicular bodies, and an active Golgi complex characterized these cells. A-LAK cells in the adherent phase were found to express numerous point contacts (podosomes) and larger adherence structures containing polymerized actin, which appear to be important for interactions of these cells with the substrate. Increased expression of adhesion molecules in association with surface structures mediating adherence is also responsible for effective binding of A-LAK cells to solid surfaces.
Dependence on Ca2+ of Lipoprotein Lipase Stability
Authors: Goldman Rachel 
Published: January 2018

Abstract
Macrophages continuously secrete lipoprotein lipase (LPL) into the culture medium. When LPL was collected from thioglycollate-elicited peritoneal macrophages (Tg-Mø) or J774.1 cells over a 4 h period in Ca2+ and Mg2+-free Dulbecco's modified Eagle's medium (d-DMEM) the activity in the collection medium was reduced by 40–62% and 23%, respectively, as compared to that expressed in full medium (DMEM). Ca2+ supplementation during the collection period in d-DMEM augmented LPL activity in the medium; about 1 mM Ca2+ was required for attainment of activity comparable to that expressed in DMEM. Addition of Ca2+ during the assay did not enhance LPL activity collected into d-DMEM. Addition of EGTA to the assay mixture reduced LPL activity by 34–60% and when present in the collection medium, EGTA led to a reduction in enzyme activity greater than 90%. A 4 h incubation of Tg-Mø in 3 mM EGTA led to an almost complete loss of intracellular Ca2+ (measured by efflux of 45Ca2+ from preloaded cells), yet there was no change in the overall synthesis and secretion of proteins and in the phagocytic capability of the cells. LPL activity in the enzyme collection medium after its removal from cell monolayers was stable at least up to 4 h at 0°C and at 23°C. Activity was progressively lost with increased temperatures: up to 40% loss at 37°C in 4 h. Addition of EGTA to the above medium led to an enhanced rate of irreversible enzyme inactivation: 76–86% loss of activity in 4 h at 37°C. No inactivation was observed at 0°C and at 23°C in the presence of EGTA. The results indicate a critical role for Ca2+ in enzyme stabilization.