bluuebunny/crossref_metadata_2025_split huggingface dataset:
Restoration of Prostaglandin Releasing Macrophage Populations in Lethally Irradiated Mice With Spleen Cells From Bone Marrow-Depleted Donors
Authors: Shibata Yoshimi , Volkman Alvin 
Published: January 2018

Abstract
Previous studies in mice severely depleted of bone marrow cells by 89Sr showed persistent monocytopenia and impaired expression of prostaglandin E2-releasing splenic macrophages (PGSM) despite the occurrence in the spleen of more than 10-fold increases in pluripotential stem cells and Mo colony-forming cells. To determine whether the observed deficits were due to a lack of precursors of blood monocytes and PGSM in the spleens of 89Sr-treated mice, radiation chimeras were established by iv infusion of 2 × 106spleen cells from 89Sr donor CBA/J or semisyngeneic B6CB F1 hybrid mice into lethally γ-irradiated CBA/J recipients. Blood monocyte levels were greater than normal by day 14 and PGSM induced by Corynebacterium parvum were demonstrated by day 28. These restored Mø populations expressed the donor haplotype detected in vitro with haplotypespecific monoclonal anti-H-2K plus complement. “Sr treatment of the chimeras resulted in profound depletion of monocytes and PGSM. The data indicate that the spleen of the 89Sr-treated mouse, which is an ineffective source of circulating monocytes and PGSM, contains cells which can generate both of these populations following infusion into lethally irradiated recipients. Since the bone marrow of such recipients was capable of being repopulated, the aggregate observations suggest that functional bone marrow is obligatory for the generation of blood monocytes and PGSM populations.
Influence of Lactoferrin on the Function of Human Polymorphonuclear Leukocytes and Monocytes
Authors: Gahr Manfred , Speer Christian P , Damerau Bernd , Sawatzki Günther 
Published: January 2018

Abstract
Polymorphonuclear leukocytes (PMN) exposed to highly purified human lactoferrin (from colostrum) exhibit an increased random motility (at least 2.5-fold) and are primed to produce more superoxide [12.1 ± 1.2 nmol O2-/min/106 PMN preincubated with lactoferrin (0.5 mg/ml) against 6.4 ± 2.3 with cells without lactoferrin after FMLP stimulation]. The action of lactoferrin seemed to be specific, because it could be abolished by simultaneous addition of antilactoferrin antibody. Addition of transferrin and iron salts to PMN was without effect. Between iron-poor and iron-saturated lactoferrin there was no difference in influence on PMN function except for a higher FMLP stimulated superoxide production by iron-saturated lactoferrin. Aggregation, degranulation (β-glucuronidase, lysozyme), and bacterial killing were not influenced by lactoferrin. Incubation of monocytes and monocyte-derived macrophages with lactoferrin did not alter their motility or their superoxide production rates. Our findings indicate that PMN become more effective after exposure to lactoferrin by having a greater motility and producing superoxide at a faster rate.
Role of Degranulation in Activation of the Respiratory Burst in Human Neutrophils
Authors: Manara F Suzi , Chin Jean , Schneider Donald L 
Published: January 2018

Abstract
The neutrophil response to infection and inflammation includes membrane fusion or degranulation and activation of the membranous respiratory burst oxidase. The role of degranulation in the activation of the burst was explored in resting and activated cells. Exposed membrane proteins of intact cells were labeled with impermeant reagents. Phorbol ester-activated neutrophils and enucleated cells which are granule depleted both exhibit increased labeling with [125l]lactoperoxidase over that of resting cells. The binding of antibodies to granule membranes by cells activated with phorbol ester or treated with cytochalasin B and lithium chloride were similarly increased. These data indicate that insertion of granule membrane into the cell membrane occurs during activation and enucleation of neutrophils.
Hyperosmolarity, known to inhibit degranulation, also exhibited an inhibitory effect on the respiratory burst oxidase in the presence of phorbol ester or latex. Pre-treatment of cells with phorbol ester followed by an increase in osmolarity, however, still resulted in activation. Temperatures below 17°C abruptly and simultaneously abolish degranulation and activation of the respiratory burst oxidase. Pre-treatment of neutrophils with phorbol ester at 37°C, followed by measurement of oxidase activity at decreased temperatures, on the other hand, revealed a linear Arrhenius plot above and below 17°C. These results suggest that membrane fusion or degranulation is a step in activation of the respiratory burst.
Plasma Membrane Appearance of Phosphatidylethanolamine in Stimulated Macrophages
Authors: Sandra Alexander , Cai Jun 
Published: January 2018

Abstract
Mouse peritoneal macrophages were labeled with [1-3H]ethanolamine, and the presence of radioactive [3H]phosphatidylethanolamine (PE) at the plasma membrane was monitored by reacting the cells with trinitrobenzene sulfonic acid (TNBS) under nonpenetrating conditions. Macrophages stimulated with either the calcium ionophore A23187 or zymosan demonstrated a larger proportion of radiolabeled PE in the plasma membrane than control, nonstimulated cells. In experiments in which macrophages were labeled with ethanolamine for increasing times, appearance of membrane 3[H]PE was stimulated as early as after 2 hr of labeling. Macrophages labeled for 24 hr, then stimulated and returned to fresh medium still reflected a higher amount of membrane 3[H]PE at 2 hr after the stimulation, suggesting stimulation results in long-term alterations in plasma membrane lipids. Protease-peptone-elicited macrophages, which are not stimulated by zymosan or ionophore, did not exhibit an increase in membrane 3[H]PE upon stimulation. The size of the TNBS-accessible radiolabeled PE pool increased proportionately with a second stimulation; however, a subsequent labeling of the cells with TNBS after brief warming increased the TNBS-accessible pool in control cells only. As shown in previous studies, macrophage stimulation resulted in an increased incorporation of lipid precursors into phospholipid. The mass of plasma membrane Tnp-PE relative to mass of PE was not increased in ionophore-treated macrophages in contrast to a small (~22%) increase in zymosan-treated cells. These results are suggestive of alterations in lipid synthesis in stimulated macrophages and possible long-term changes in the structure and function of the plasma membrane of macrophages following stimulation.
Regulation of Interferon Production by Human Monocytes: Requirements for Priming for Lipopolysaccharide-Induced Production
Authors: Hayes Mark P , Enterline Joan C , Gerrard Theresa L , Zoon Kathryn C 
Published: January 2018

Abstract
Macrophages are uniquely responsive to bacterial lipopolysaccharide (LPS) for activation of a number of host defense functions and production of bioactive mediators. One potentially important mediator produced by LPS-stimulated macrophages is interferon (IFN-α/β). In contrast to murine observations, we have observed that freshly isolated human monocytes, purified by counter-current centrifugal elutriation, do not produce interferon in response to LPS. This is not due to a lack of response to LPS, as assessed by the induction of other monokines, or to an incapacity for IFN production, since IFN was inducible by poly-l,C treatment of monocytes in the absence of any other exogenous stimulus. However, human monocytes can be primed for the production of IFN in response to LPS if they are cultured in the presence of either granulocyte-macrophage colony stimulating factor (GM-CSF) or interferon-γ (IFN-γ). The IFN secreted is of the α subtype. Monocytes primed with GM-CSF or IFN-γ also maintained LPS responses for production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1). M-CSF did not prime monocytes for LPS-induced IFN production, although it did enhance production of TNF-α and promoted monocyte survival. Northern analysis indicated that the induction of IFN-α by LPS was regulated primarily at the mRNA level. The highly regulated production of IFN-α by monocytes/macrophages has important implications for autocrine action of interferons in the activation and differentiation of these cells.
Selective Inhibition of Natural Killer but not Natural Cytotoxic Activity in a Cloned Cell Line by Delta-9-Tetrahydrocannabinol
Authors: Wang Min , Richards Allen L , Friedman Herman , Djeu Julie Y 
Published: January 2018

Abstract
Natural killer (NK) and natural cytotoxic (NC) activities are spontaneously generated against certain tumors in vitro and their contribution to tumor immunity is being extensively investigated. We report here that the interleukin-2 (IL-2)–dependent murine cell line, NKB61A2, which we recently found to express both NK and NC functions, can be modulated selectively by 9δ-tetrahydrocannabinol (THC). THC, a major psychoactive metabolite of marijuana, could significantly inhibit NK activity without altering NC activity in NKB61A2 cells. Inhibition of NK function occurred at a post-binding stage because effector/target conjugation was unaffected by THC. With regard to NC function, neither the cytotoxic activity of the cells nor release of tumor necrosis factor was interrupted by THC. Therefore, THC may provide a useful tool for dissociating the mechanism of NK and NC activities within a single population of cells.
Metabolism of Leukotriene B4 via Reduction Into Dihydro-Leukotriene B4 in Human Monocytes, Alveolar Macrophages, and U-937 Cells
Authors: Schönfeld W , Kasimir S , Knöller J , Jablonski K , König W 
Published: January 2018

Abstract
The biological effects of leukotriene B4 (LTB4) within the microenvironment are controlled by rapid inactivation. In this regard human granulocytes convert LTB4 into ω-oxidated products (20-OH-LTB4 and 20-COOH-LTB4); moreover, we recently described the formation of unpolar metabolites of LTB4 in human tonsillar and lung macrophages. By means of high performance liquid chromatography (HPLC) we identified the main metabolite of LTB4 as dihydro-LTB4 (5,12-dihydroxyeicosatrienoic acid). Studies on a lymphocyte (74–78%), monocyte (19–22%), and basophil (&lt;4%) containing cell fraction isolated from peripheral blood as well as peripheral monocytes purified by elutriation centrifugation revealed evidence that these cells metabolize LTB4 to a very low degree if incubated immediately after isolation. However, after culture for 24–72 h these cells showed a strongly increased capacity to metabolize LTB4. The pattern of metabolites in this cell fraction was identical to bronchoalveolar macrophages (purity &gt;95%). Similarly, the LTB4-reductase was expressed in differentiated human monocytic U-937 cells almost 5–7 h after the addition of dimethylsulfoxide (1.3%) or phorbol-myristate-acetate (16 nM). The expression of this pathway was blocked in the presence of cycloheximide (10 μg/ml) whereas actinomycin (3.8 μg/ml) had no effects. Dihydro-LTB4 was further metabolized by granulocytes probably via ω-oxidation; therefore, several metabolites could be detected by radioactive high performance liquid chromatography (HPLC) after incubation of bronchoalveolar cells consisting of macrophages and granulocytes with 3H-LTB4. Our data provide evidence for a unique role of macrophages to control the level of LTB4 by generation as well as metabolism into dihydro-LTB4.
Modulation of Tumor Necrosis Factor and Gamma Interferon Production by Cocaine and Morphine in Aging Mice Infected With LP-BM5, a Murine Retrovirus
Authors: Chen Guan-jie , Watson Ronald Ross 
Published: January 2018

Abstract
The actions of retroviral infections, aging, and cocaine and morphine injection on cytokine production were investigated in C57BL/6 female mice. Retroviral infection with LP-BM5 murine leukemia virus was further developed as a model of murine acquired immunodeficiency syndrome (AIDS). The effects of cocaine and morphine on gammainterferon (IFN) and tumor necrosis factor (TNF) production in vivo and with isolated spleen cells were measured by a sandwich enzyme-linked immunosorbent assay (ELISA) method. Serum IFN was generally not detected in any group except mice injected with saline and young mice infected with LP-BM5 virus. Splenocytes from mice with murine AIDS produced less IFN when stimulated in vitro by ConA. In aged mice, IFN production by spleen cells was severely suppressed by retroviral infection. Cocaine had a tendency to suppress IFN production by stimulated cells in vitro. Morphine tended to reduce IFN production by spleen cells from retrovirally infected animals.
The serum TNF level in mice with murine AIDS was elevated creating higher levels in morphine and morphine plus cocaine treated uninfected mice while cocaine injection eliminated serum TNF. When stimulated in vitro by lipopolysaccharides (LPS), splenocytes from mice with murine AIDS also produced more TNF than uninfected controls. TNF production in vitro and in vivo was significantly increased by retroviral infection. Therefore, results indicate that cocaine and retroviral infection modulate TNF and IFN production.
Murine Peritoneal Macrophage Gangliosides Inhibit Lymphocyte Proliferation
Authors: Berenson Charles S , Ryan John L 
Published: January 2018

Abstract
Gangliosides have been shown to act as immunoregulatory agents by altering proliferative responses of lymphocytes to both antigens and mitogens. Most early studies have utilized brain gangliosides and have required high concentrations. The role of endogenous gangliosides from macrophages has remained unexplored. In this study, thioglycollate-elicited murine peritoneal macrophage gangliosides were purified and added to cultures of murine lymphocytes. Nanogram amounts caused a profound inhibition of LPS-induced DNA synthesis of splenocytes and of purified B lymphocytes, without demonstrable cellular toxicity. No effect was seen using asialo-GM1. This effect was present across a wide range of lipopolyssacharide (LPS) doses. Nanogram amounts of macrophage gangliosides also inhibited concanavalin A (ConA)-mediated lymphocyte proliferation. Inhibition of LPS-induced mitogenesis was present even if gangliosides were removed from the extracellular environment after 15–60 min of incubation prior to the addition of LPS. This inhibition was reversible with incubation of ganglioside pre-treated lymphocytes in medium containing serum. These inhibitory properties of macrophage gangliosides are distinct from those found in studies using brain gangliosides, and support a potential role for macrophage gangliosides as negative modulators of lymphocyte proliferation.
The Liver and the Hematolymphoid System: I. The Regulation of Nylon-Passed Spleen Cell Proliferation by Active Factors Released From Syngeneic Nonparenchymal Liver Cells
Authors: Mabuchi Ayako , Komuro Toshiro , Saizawa Takashi , Sakamoto Toshiki , Watari Eiji , Yokomuro Kozo 
Published: January 2018

Abstract
Nylon-passed spleen cells were found to proliferate when cultured with syngeneic nonparenchymal adherent liver cells and their culture supernatants. The supernatants contained IL-1, IL-6, GM-CSF, and IFN (α + β) activities but not IL-2 and IL-3 activities. The IFN level was higher in early culture sup (2–24 hr) than in later culture sup (48–72 hr). Proliferation was greatly increased by anti-IFN (α + β) serum in the spleen cells cultured in the earlier sup. This antiserum increased the spleen cell proliferation only slightly in the later culture sup. This suggests that nonparenchymal liver cells produce two factors, one having a suppressor, and the other an enhancer action, with IFN being one of the suppressor factors. With culture time, DNA synthesis of spleen cells increased and IL-2 and IL-3 activities were generated in the culture sup. Cells proliferated during culture were found to be morphologically lymphocytes, granulocytes, and macrophages. The mechanisms by which nonparenchymal liver cells regulate the hematolymphoid system are discussed based on our observations.
Involvement of Fibronectin and Its Receptor in Human Lymphocyte Proliferation
Authors: Klingemann Hans G , Kohn Fred R 
Published: January 2018

Abstract
Adhesion between lymphocytes and antigen-presenting cells is necessary for the development of certain immune reactions. We have previously shown that fibronectin (FN) added to mixed lymphocyte cultures (MLC) can restore a decreased lymphocyte proliferation in immunocompromised individuals. Using highly purified cell populations from peripheral blood for depletion and adding back experiments we show here that exogenous FN enhanced proliferation only when allogeneic monocytes were co-cultured with responder lymphocytes. Although lymphocyte proliferation in MLC was augmented by FN, there was no preferential proliferation of any particular major lymphocyte subpopulation in cultures supplemented with FN as compared to control cultures lacking its addition. Antibody against the FN receptor (FN-R) of the β1 integrin family, as well as Arg-Gly-Asp containing peptide, could inhibit alloantigen-induced lymphocyte proliferation in a concentration-dependent manner. Anti–CD3-lnduced proliferation was inhibited by anti–FN-R antibody but not Arg-Gly-Asp peptide whereas no inhibition was seen with the phytohemagglutinin (PHA)-induced lymphocyte proliferation. This study presents further evidence that FN and its receptor (α5β1) are involved in the augmentation of T-cell responsiveness to proliferative stimuli.
Involvement of Cytokines in Determining Resistance and Acquired Immunity in Murine Tuberculosis
Authors: Denis Michel 
Published: January 2018

Abstract
Herein we demonstrate that continuous infusion of either TNF-α or IFN-γ (104 U/day) via osmotic micropumps leads to an increased resistance of mice infected with a lethal dose (107) of M. tuberculosis H37Rv, associated with a decreased microbial growth in all target organs. This result was reinforced by the finding that infusion of antibodies against TNF-α or IFN-γ greatly enhanced susceptibility of naive mice to tuberculosis. In a final set of experiments, using neutralizing antibodies, we show that IFN-γ, not TNF-α is involved in determining acquired resistance against murine tuberculosis, as seen by the fact that acquired immunity is resistant to anti-TNF-α antibodies, yet sensitive to anti-IFN-γ antibodies. This suggests a role for both IFN-γ and TNF-α in determining innate resistance whereas IFN-γ may be the mediator of the anamnestic response.
Fibronectin fragments stimulate tumor necrosis factor secretion by human monocytes
Authors: Beezhold Donald H , Personius Christine 
Published: January 2018

Abstract
Fibronectin (Fn) is a high molecular-weight glycoprotein that can influence many aspects of monocyte function. The purpose of this study was to determine whether Fn could stimulate monocyte tumor necrosis factor (TNF) secretion. Monocytes were isolated from the peripheral blood of healthy volunteers by density gradient centrifugation and adherence to plastic (2 h). Plasma Fn was purified from the blood by gelatin-Sepharose affinity chromatography. Monocytes were stimulated with Fn for 18 h and the supernatants were assayed for TNF activity using the L929 bioassay. Intact Fn stimulated the secretion of TNF in a dose-dependent manner. Intact Fn–induced TNF secretion by monocytes was inhibited (50%) but not eliminated by the addition of the R-G-D–containing peptide GRGDSP. Limited proteolysis of the Fn molecule using insoluble chymotrypsin resulted in a fragment preparation that was dramatically more stimulatory than the intact Fn preparation. High-performance liquid chromatographic (HPLC) purification of the fragments demonstrated that at least two fragments were capable of stimulating TNF secretion. Further purification by affinity chromatography and HPLC localized the stimulatory activity to the 120-kd cell-binding fragment. The possibility that the stimulatory activity was the result of endotoxin contamination was ruled out using macrophages from C3H/Hej mice. These results suggest that Fn fragments are potentially important molecules for activation of monocytes and may stimulate monocyte cytotoxic activity.
In vivo testing confirms a blunting of the human cell-mediated immune mechanism during space flight
Authors: Taylor Gerald R , Janney Robert P 
Published: January 2018

Abstract
The cell-mediated immune (CMI) mechanism was evaluated in 10 space shuttle astronauts by measuring their delayed-type hypersensitivity response to seven common recall antigens. The Multitest CMI test system was used to administer antigens of tetanus, diphtheria, Streptococcus, Proteus, old tuberculin, Candida, and Trichophyton to the forearm 46 h before nominal mission termination; readings were conducted 2 h after landing. The mean number of reactions was reduced from 4.5 preflight to 3.0 inflight, and the mean reaction score was reduced from 21.4 to 13.7 mm inflight. The data presented suggest that the CMI system is still being degraded by space flight conditions on day 4 and that between day 5 and day 10, the depression maximizes and the system begins to adjust to the new conditions. The relation of these in vivo findings to previously reported in vitro results is discussed. J. Leukoc. Biol 51: 129–132; 1992.
Fc receptor expression, concanavalin A capping, and enzyme content of bovine neonatal neutrophils: a comparative study with adult cattle
Authors: Zwahlen Roland D , Wyder-Walther Marianne , Roth Daniel R 
Published: January 2018

Abstract
The increased susceptibility of newborns to infection may in part be related to impaired in vitro functions of neonatal polymorphonuclear neutrophils (PMNs). To evaluate early steps in the activation cycle of bovine PMNs we determined the expression of Fc receptors (FcRs) with an erythrocyte rosetting assay utilizing bovine anti-sheep immunoglobulin G2 IgG2 and the accumulation of ligand receptor complexes or “caps” with fluorochrome-coupled concanavalin A (Con A caps) on neutrophils from adult (A-PMN) and newborn (N-PMN) bovines. In addition, the levels of myeloperoxidase (MPO) and alkaline phosphatase (AP) were determined. FcR expression is reduced in N-PMNs (P &lt; .001), in contrast to results observed with human N-PMNs. Basal capping of Con A binding sites is reduced (P &lt; .05) in N-PMNs but is enhanced (P &lt; .001) upon pretreatment with colchicine (0.5, 5.0, and 50.0 μm). These findings are again contrary to results observed with human N-PMNs. Consistent with findings in human neonates, however, are reduced levels of cellular MPO (P &lt; .05) and elevated cellular AP (P &lt; .001) in the neonate. The functional significance of elevated AP levels and altered Con A capping in N-PMNs is unclear. However, diminished expression of FcR could potentially contribute to impaired adherence and phagocytosis of bacteria, and reduced activity of neutrophil MPO could indicate weaker microbicidal capacity of neonatal cells. The demonstrated impairment of N-PMN functions could potentially contribute to reducing the effectiveness of the cellular host defense system in neonatal calves.