bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolism of platelet-activating factor in neutrophils isolated from Pichinde virus–infected guinea pigs
Authors: Qian Changgeng , Liu Ching-Tong , Peters Clarence J 
Published: January 2018

Abstract
Metabolism of platelet-activating factor (PAF) was studied in cultured polymorphonuclear neutrophils (PMNs) obtained from Pichinde virus–infected strain 13 guinea pigs. Neutrophils obtained from control and infected guinea pigs on postinoculation days 10 and 14 were incubated with [3H]lyso-PAF, [3H]PAF, or [3H]acetate. After incubation for 1 h at 37°C, formation of [3H]acyl-PAF from either [3H]lyso-PAF or [3H]PAF increased significantly in PMNs from infected guinea pigs compared to control PMNs. Furthermore, total radioactivity from [3H]lyso-PAF or [3H]PAF was higher in PMNs from infected animals than in those from controls. However, compared to PAF production by control PMNs, production of PAF by infected PMNs was unchanged. These results suggest that PMNs may not be the major source of increased blood PAF levels during Pichinde viral disease.
Differential effects of CD4+ and CD8+ cells in acute, systemic murine candidosis
Authors: Coker Lee A , Mercadal Carmen M , Rouse Barry T , Moore Robert N 
Published: January 2018

Abstract
Monoclonal antibody (mAb) depletion was used to assess contributions of CD4+ and CD8+ cells in resistance to systemic murine Candida albicans infection. Depletion of CD8+ cells did not influence either survival or mean survival time (MST); however, depletion of CD4+ cells significantly enhanced both survival and MST. Combined depletion of both CD4+ and CD8+ cells significantly lengthened the MST but did not enhance survival. A protective influence of CD8+ cells could be deduced but, to be manifested, required depletion of an overshadowing immunopathologic CD4+ response.
In vitro modulation of the toxicity associated with the use of zidovudine on normal murine, human, and murine retrovirus-infected hematopoietic progenitor stem cells with basic fibroblast growth factor and synergistic activity with interleukin-1
Authors: Gallicchio Vincent S , Hughes Nedda K , Hulette Ben C 
Published: January 2018

Abstract
The antiviral drug used in the treatment of acquired immunodeficiency syndrome, zidovudine, has proved effective in ameliorating the morbidity and mortality associated with human immunodeficiency virus infection. However, associated with zidovudine is the development of severe bone marrow toxicity manifested by anemia, neutropenia, and occasionally thrombocytopenia. We report the results of studies that demonstrate the ability of basic fibroblast growth factor (B-FGF) to reduce zidovudine toxicity to several classes of hematopoietic progenitors (granulocyte-macrophage, CFU-GM; megakaryocyte. CFU-Meg; and erythroid, BFU-E) from normal murine, human, and murine retrovirus–infected bone marrow cells when cocultured with zidovudine in vitro. Optimal response to B-FGF was observed at a dose concentration of 10 ng/ml. The specificity of B-FGF was demonstrated in the presence of protamine sulfate, an effective inhibitor of B-FGF mitogenic activity. In addition, synergistic activity of B-FGF on zidovudine-induced hematopoietic stem cell toxicity was observed in the presence of interleukin 1 (IL-1) (30 ng/ml). These studies demonstrate that B-FGF is capable of reducing the hematopoietic toxicity associated with zidovudine and that such an effect can be amplified in the presence of IL-1.
Stimulation of human monocyte and polymorphonuclear cell iodination and interleukin-1 production by epigallocatechin gallate
Authors: Sakagami Hiroshi , Asano Kazuhito , Hara Yukihiko , Shimamura Tadakatsu 
Published: January 2018

Abstract
(-)Epigallocatechin gallate (EGCg) stimulated iodination of human peripheral blood monocytes, polymorphonuclear cells (PMN), and human promyelocytic leukemic HL-60 cells, dependent on time, dose, and temperature. However, EGCg did not affect iodination of nonadherent peripheral blood mononuclear cells, red blood cells, or 11 other cultured cell lines. Although various immunoregulators such as lipopolysaccharide (LPS), opsonized zymosan, 12-O-tetradecanoylphorbol-13-acetate (TPA) and tumor necrosis factor stimulated PMN iodination to varying degrees, their ability to stimulate monocyte iodination was much lower than that of EGCg. Washout experiments demonstrated that contact with EGCg for &lt; 60 min irreversibly stimulated PMN and monocyte iodination. EGCg also potently stimulated the production of interleukin-1-like factor by monocytes. The data suggest that EGCg is a strong in vitro stimulant of human phagocytes.
Platelet activating factor stimulates intracellular calcium transients in human neutrophils: involvement of endogenous 5-lipoxygenase products
Authors: Rediske John J , Quintavalla Joe C , Haston William O , Morrissey Michael M , Seligman Bruce 
Published: January 2018

Abstract
Stimulation of human neutrophils with platelet activating factor (PAF) resulted in a transient elevation of free cytosolic calcium. Neutrophils exhibited a two-component calcium response observed as a double peak when stimulated with &gt; 5 nM PAF. In contrast, leukotriene B4 (LTB4), C5a, or formylmethionyl-leucyl-phenylalanine stimulated only a single-peak calcium response. The double-peak calcium response was not elicited in human monocytes or differentiated U937 cells, which demonstrated a single peak. Pretreatment of neutrophils with a 5-lipoxygenase inhibitor or a specific LTB4-receptor antagonist selectively blocked the second calcium peak. These results suggest that PAF-mediated activation of human neutrophils results in the activation of the 5-lipoxygenase and the subsequent generation of LTB4. This LTB4 in turn elicits a secondary rise in calcium, which contributes to the overall response of neutrophils to PAF. These results demonstrate how LTB4 participates in the cellular responses elicited by PAF in human neutrophils.
Differentiation-dependent modulation of TNF production by PAF in human HL-60 myeloid leukemia cells
Authors: Rola-Pleszczynski Marek , Stankova Jana 
Published: January 2018

Abstract
Platelet-activating factor (PAF) can augment tumor necrosis factor (TNF) production by human monocytes in a bimodal manner, with two peaks of activation at picomolar and micromolar concentrations. These peaks are partially associated with monocyte subsets presenting different characteristics in terms of size, density, phenotypic markers, and [Ca2+]i mobilization responses. In the present study, we used the human promyelocytic leukemia cell line HL-60, at various times during differentiation with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] toward the monocyte lineage, in order to study the relation of cell differentiation to responsiveness to PAF in terms of cytokine production. TNF production was induced by pretreatment with interferon γ for 24 h and treatment with muramyl dipeptide. Although detectable TNF was produced by 4 day-differentiated cells, no effect was seen with PAF (10−16-10−6 M) at this or earlier stages. In contrast, 5 day–differentiated cells had a comparable baseline production of TNF but responded with a 2.5-fold increase to PAF with a single peak, maximal at 10−8 M. Moreover, 6 day- or 7 day-differentiated HL-60 cells showed a further increase in TNF production in response to PAF, and the response was bimodal, similar to that of the less dense subset of monocytes, with peaks at 10−14 and 10−7 M PAF. In parallel, undifferentiated HL-60 failed to respond to PAF in terms of [Ca2+]i mobilization. The earliest responsiveness to PAF (10−7 M) was observed by 4 days of treatment with 1,25(OH)2D3, and by day 7 the response to PAF became bimodal (10−14 and 10−7 M). These results indicate that myeloid cells acquire, during maturation toward the monocyte lineage, a progressive responsiveness to PAF in terms of [Ca2+]i mobilization and enhanced cytokine production, and they suggest that the heterogeneity in responses to PAF observed in normal monocytes may be related to their stage of differentiation or maturation.
Fucose-activated killer cells. I. Enhanced TNF-α mRNA accumulation and protein production
Authors: Staňková Jana 
Published: January 2018

Abstract
Our previous studies have shown that the monosaccharide α-l-fucose significantly enhances the cytolytic capacity of peripheral blood mononuclear leukocytes (PBMLs). To examine possible mechanisms through which fucose affects cytolytic activity, we studied the production of cytokines after α-l-fucose stimulation. In this report, we show that fucose induced a minor but significant augmentation of production of interleukin-2 (IL-2), but anti–IL-2 antibodies did not completely inhibit fucose-activated cytolysis. Fucose induced significantly higher secretion of TNF-α by both lymphocytes and monocytes. The nature of the lytic molecule detected in the TNF bioassay was verified with specific neutralizing antibodies. In addition, fucose induced the accumulation of TNF-α mRNA in a time-dependent manner with a peak at 8 h and a return to baseline values at 20 h after stimulation. In vitro nuclear transcription assays determined that fucose augmented the rate of transcription of the TNF-α gene, and inhibition of de novo transcription with actinomycin D indicated that the turnover rate of the TNF-α mRNA was not affected by fucose stimulation. We also determined that fucose did not modulate the mRNA expression of the pore-forming protein, a major lytic protein involved in lymphocyte cytotoxicity. Specific neutralizing antibodies indicated that TNF-α was not an effector molecule in fucose-activated killing of K562 or Raji target cells but that this cytokine had an essential role in the induction of the augmented killing by α-l-fucose.
Macrophage inflammatory proteins MIP-1 and MIP-2 are involved in T cell–mediated neutrophil recruitment
Authors: Appelberg Rui 
Published: January 2018

Abstract
Mice intraperitoneally (i.p.) infected with Mycobacterium bovis bacille Calmette-Guérin (BCG) respond to an i.p. challenge with mycobacterial antigen with an acute and extensive accumulation of neutrophils. This influx was not mimicked by the inoculation of recombinant interferon-γ (IFN-γ) or tumor necrosis factor α (TNF-α). The antigen-induced recruitment of neutrophils was not affected by coinoculation of anti–IFN-γ antibodies, was enhanced by anti–TNF-α antisera, and was significantly reduced by antisera against macrophage inflammatory proteins MIP-1 and MIP-2. The latter two sera had no additive effects. We hypothesize that mycobacteria-specific T cells are triggered by antigen to secrete MIP-1 and MIP-2, which directly mediate, at least partly, the influx of neutrophils that takes place in this model.
Polyamine involvement in functional activation of human macrophages
Authors: Messina Luigi , Spampanato Giuseppina , Arcidiacono Antonio , Maiaguarnera Lucia , Pagano Maria , Kaminska Bozena , Kaczmarek Leszek , Messina Angelo 
Published: January 2018

Abstract
Polyamines naturally occur in all living beings and play an important role in the regulation of cell proliferation, differentiation, and functional stimulation of terminally differentiated cells. Our studies, using specific inhibitors of polyamine biosynthesis such as α-difluoro- methylornithine and methylglyoxal-bis[guanylhydrazone] to prevent polyamine accumulation, have indicated that polyamines are associated with functional activation of human macrophages. Both inhibitors diminished the respiratory burst activity of macrophages induced by lipopolysaccharide and interferon gamma. The methyl- glyoxal-bis[guanylhydrazone] inhibitory effect was concentration-dependent and could be reversed by spermine, which is the final product of polyamine biosynthesis.
Syn-capping of human T lymphocyte adhesion/activation molecules and their redistribution during interaction with endothelial cells
Authors: Rosenman Stephen J , Ganji Amir A , Tedder Thomas F , Gallatin W Michael 
Published: January 2018

Abstract
Lymphocyte-endothelial cell interactions are mediated in part by multiple lymphocyte surface adhesion/activation molecules and their cognate ligands. We investigated the surface localization of several of these molecules implicated in T cell adhesion and transen- dothelial migration mechanisms to determine if spatial regulation of their distribution contributes to these processes. T lymphocyte suspensions were stained to define distribution, ability to be aggregated into energy- dependent caps, and potential cocapping of several adhesion structures. CD2, CD44, L-selectin (LAM-1, LECCAM-1), and CDlla/CD18 (LFA-1) exhibited uniform distribution on the T cell surface by direct immunofluorescence but formed caps in an energy- dependent, and therefore cytoskeletally driven, manner when examined by indirect immunofluorescence. CD2 was shown to syn-cap (unidirectionally cocap) with GD44 and CDlla/CD18 (LFA-1), an observation potentially related to functional cooperation among these molecules in T cell activation. T cells were also added to endothelial cell monolayers to assess, in a physiologically relevant context, potential surface molecule reorganization. Lymphocytes co-cultured with human umbilical vein endothelial cells (HUVEC) underwent a profound shape change, from essentially round cells to polarized cells bearing pseudopodia. Immunofluorescent localization of T cell adhesion/activation molecules using confocal microscopy revealed the redistribution of CD2, CD44, and L-selectin to the pseudopod. In contrast, CDlla/CD18 remained globally distributed on the cell surface, even in severely deformed cells. Both lymphocyte shape change and membrane molecule redistribution appear to be cell-cell contact-dependent phenomena requiring intact, viable endothelial cells. Mechanisms that control these events may be critical to lymphocyte recirculation and inflammation. J. Leukoc. Biol. 53: 1–10; 1993.
Immunotherapy of tularemia: characterization of a monoclonal antibody reactive with Francisella tularensis
Authors: Narayanan RB , Drabick Joseph J , Williams Jim C , Fortier Anne H , Meltzer Monte S , Sadoff Jerald C , Bolt Christopher R , Nacy Carol A 
Published: January 2018

Abstract
An IgM monoclonal antibody (mAb) recognized surface antigens specific to Francisella tularensis wild-type (Schu4) and live vaccine strain (LVS), and reacted with both in ELISA and slide agglutination tests. This mAb also reacted with LVS microorganisms in tissues of infected mice as assessed by an indirect fluorescence technique. Western blot analysis showed the mAb to react with antigens associated with F. tularensis LPS. J. Leukoc. Biol. 53: 112–116; 1993.
Effects of modulators of cytosolic Ca2+ on phytohemagglutin-dependent Ca2+ response and interleukin-2 production in Jurkat cells
Authors: Dupuis Gilles , Aoudjit Fawzi , Ricard Isabelle , Payet Marcel D 
Published: January 2018

Abstract
We have previously reported the presence, in Jurkat T cells, of outward K+ currents and inward currents that have been attributed to Ca2+ channels. Here, we have studied the effects of dimethyl 1,4-dihydro- 2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridine-dicarboxylate (nifedipine) and 4-(2,l,3-benzoxadiazol-4-yl)-l,4-dihydro- 2,6-dimethyl-5-methoxy-carbonylpyridine-3-carboxylate (PN200-110), two dihydropyridines (DHPs) known to inhibit voltage-dependent Ca2+ channel activity in different types of cells, and two inhibitors of internal Ca2+ release (muscle cells), ryanodine and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), on the Phaseo- lus vulgaris phytohemagglutinin (PHA)-dependent responses in Jurkat T lymphocytes. Our results show that nifedipine and PN200-110 inhibit the PHA-dependent production of interleukin-2 except when 12-0- tetradecanoyl-13-O-acetyl phorbol is added to the cultures. Ryanodine and TMB-8 are not inhibitors. The PHA-dependent Ca2+ response is significantly reduced when the cells are preincubated in the presence of the DHPs. Under these conditions, ryanodine has only a small inhibitory effect and TMB-8 has no effect. In contrast, only ryanodine (50 μM) decreases the PHA- dependent cytosolic release of Ca2+ when the cells are bathed in a medium containing a low concentration of Ca2+ (60 nM). The inhibitory effects of nifedipine and PN200-110 may result from the binding of these DHPs to specific receptor sites as revealed by studies using [3H]PN200-110 (KD - 8.5 ± 3.1 nM; 2300 ± 500 apparent binding sites/cell). Photoaffinity labeling studies using [3H]azidopine as a probe showed specific incorporation of label into three glycoproteins of molecular mass (± SD) 170 ± 13, 110 ± 25, and 60 ± 17 kd as analyzed by electrophoresis under reducing conditions. J. Leukoc. Biol. 53: 66–72; 1993.
Effect of acute oral administration of alcohol on superoxide anion production from mouse alveolar macrophages
Authors: Libon C , Forestier F , Cotte-Laffitte J , Labarre C , Quero AM 
Published: January 2018

Abstract
The production of superoxide anions (superoxide) from alveolar macrophages stimulated or not with opsonized zymosan was investigated in the mouse after acute oral administration of alcohol (6.5 g/kg). Superoxide production was assayed using a nitroblue tetrazolium (NBT) reduction and chemiluminescence assay. In the absence of opsonized zymosan, superoxide concentration was not affected 1 h after ethanol treatment but was significantly increased 15 and 24 h after treatment. In the presence of opsonized zymosan, a biphasic response was observed. Superoxide production was significantly reduced 1 and 3 h after administration but was increased 15 and 24 h after treatment. One hour after treatment, the percentage of cells that phagocytized opsonized zymosan and reduced NBT was significantly decreased, whereas 24 h after alcohol treatment, phagocytosis was normal and the percentage of cells reducing NBT was significantly increased. The activity of cytosolic superoxide dismutase from alveolar macrophages was not altered 1 h after administration but was significantly reduced 24 h later. Considering the functions of alveolar macrophages in the defense of the lung, these alterations in the production of reactive oxygen species after ingestion of alcohol could explain why alcoholics are more sensitive to pulmonary infections. J. Leukoc. Biol. 53: 93–98; 1993.
Endogenous nitric oxide inhibits the synthesis of cyclooxygenase products and interleukin-6 by rat Kupffer cells
Authors: Stadler Josef , Harbrecht Brian G , Di Silvio Mauricio , Curran Ronald D , Jordan Mark L , Simmons Richard L , Billiar Timothy R 
Published: January 2018

Abstract
Macrophage production of nitric oxide (•N=O) leads to considerable alterations of vital metabolic pathways in various target cells. The present study tested whether •N=O synthesis by Kupffer cells (KCs), the resident macrophages of the liver, interferes with the secretory function of these cells. As in other macrophage- type cells, the combination of lipopolysaccharide (LPS) and interferon-γ (IFN-γ) was a potent stimulus of •N=O synthesis by KC. Treatment with LPS and IFN-γ also induced significant production of prostaglandin E2 (PGE2), thromboxane B2 (TBX2), tumor necrosis factor α (TNF- α), interleukin-1 (IL-1), and IL-6. Inhibition of •N=O synthesis by the L-arginine analogue NG-monomethyl-L-ar- ginine (NMA) resulted in a further increase of PGE2, TXB2, and IL-6 but not IL-1 and TNF-α production, indicating specific inhibitory effects of endogenous •N=O synthesis on the secretory activity of KCs. PGE2 production was most sensitive to the suppressive effect of •N=O and increased 24 h after stimulation with LPS and IFN-γ from 16.3 ± 4.9 ng/106 KCs without NMA to 94.3 ± 17.9 ng/106 KCs with NMA. This effect of NMA was reversed by a 10-fold increase of the L-arginine concentration. No recovery of PGE2 production was seen when •N=O synthesis was blocked after 24 h. NMA treatment increased cyclooxygenase activity more than threefold, suggesting that •N=O inhibits PGE2 and TXB2 production through diminished PGH2 availability. •N=O synthesis did not significantly affect total protein synthesis or viability of the KCs. These results show that •N=O influences the production of specific inflammatory mediators by KCs. J. Leukoc. Biol. 53: 165–172; 1993.
Macrophage phenotype regulation by colony-stimulating factors at bone marrow level
Authors: Wijffels JFAM , de Rover Z , Kraal G , Beelen RHJ 
Published: January 2018

Abstract
Macrophages (mφs) can be divided into several subpopulations, which differ in phenotype, function, and localization patterns. However, little is known about the mechanisms that regulate this heterogeneity. We investigated whether mφ heterogeneity is regulated by colony-stimulating factors (CSFs) at the bone marrow level. By clonal expansion of bone marrow-derived precursor cells in die presence of CSF-1, granulocyte-macrophage CSF or multi-CSF (interleukin-3), phenotypic heterogeneity was observed between mφ colonies. Heterogeneity was found especially when different CSF culture conditions were used but also between mφ colonies derived under the same CSF culture condition. Our results illustrate that CSFs from the bone marrow hemopoietic microenvironment are important for the induction of phenotypic heterogeneity within the progeny of cloned mφ precursor cells during maturation and differentiation in vitro. J. Leukoc. Biol. 53: 249–255; 1993.
Distinct populations of antigen-presenting macrophages are required for induction of effector and regulatory cells in contac sensitivity response in mice
Authors: Szczepanik M , Bryniarski K , Pryjma J , Ptak W 
Published: January 2018

Abstract
Macrophages (Mf) and other antigen-presenting cells (APCs) are able to induce both immune and regulatory T cells. We compared the antigen-presenting activities of different subpopulations of thioglycolate-in- duced peritoneal macrophages from mice that were or were not treated with cyclophosphamide (CY) by several functional (adherence and phagocytosis) and morphologic (phenotypic) markers (FcR, Ia). Different subpopulations of macrophages were derivatized with trinitrophenyl and injected intravenously into recipients, which were tested directly for a contact sensitivity (CS) reaction or for the presence of efferent suppressor T (Ts) cells in passive transfer experiments. Our results demonstrate that peritoneal macrophages are both morphologically and functionally heterogeneous. Macrophages that induce immune cells that mediate CS have characteristics different from those that induce Ts cells. They accumulate in the low-density cell fraction on a discontinuous Ficoll gradient, are insensitive to treatment in vivo with low doses of CY, phagocytose poorly and adhere to plastic, and perhaps have low expression of FcRI and FcRII. Both macrophage fractions seem not to differ in expression of la, Mac-1, and Mac-3 antigens. It is argued that low doses of CY abrogate suppression in vivo by selective action on Ts cells. Our results confirm that at least a portion of the action of CY may be due to its influence on certain subpopulations of APCs. J. Leukoc. Biol. 53: 320–326; 1993.
Inflammation, immunoregulation, and inducible nitric oxide synthase
Authors: Nussler Andreas K , Billiar Timothy R 
Published: January 2018

Abstract
Nitric oxide (NO), the molecule of the year 1992, is gaining recognition as an important biological mediator. Its multitude of physiologic and pathophysiologic functions result from both a wide distribution of synthesis and diverse mechanisms of action. Besides its functions as a potent vasodilator and neurotransmitter, NO is important in inflammation and immunity. Both beneficial and detrimental consequences of induced synthesis have been discovered. Information is now accumulating on the regulation and function of induced NO. The recent cloning of human inducible NO cDNA should assist in defining the role of inducible NO in human physiology and pathophysiology.