bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differentiation of Rat Bone Marrow Cells Into Macrophages Under the Influence of Mouse L929 Cell Supernatant
Authors: Boltz-Nitulescu George , Wiltschke Christoph , Holzinger Christoph , Fellinger Alois , Scheiner Otto , Gessl Alois , Förster Othmar 
Published: January 2018

Abstract
Bone marrow cells (BMC) flushed from femora of Lewis rats were cultured in Dulbecco's modification of Eagle's medium supplemented with mouse L929 cell supernatant as a source of colony-stimulating factor (CSF). Differentiation of macrophage progenitor cells into macrophages (Mø) and expression of various markers were kinetically assessed. The proportion of Mø increases from approximately 4% in freshly isolated BMC to 100% after 7-8 days of cell culture. These cells, termed bone marrow cell-derived macrophages (BMDMø), adhere to and spread on plastic surface; exhibit Mø morphology; stain intensely for nonspecific esterase; are able to phagocytose latex particles, IgG-sensitized erythrocytes, and C3-coated red cells; and express receptors for IgG and C3. A subpopulation of BMDMø expresses MHC class II antigens as demonstrated by immunofluorescence using MRC OX6 and MRC OX17 monoclonal antibodies which recognize antigens coded in the I-A or I-E subregion of the MHC, respectively.
Collectively, our results show that supernatant from mouse L929 cells supports and is continuously required for proliferation and differentiation of rat BMC into typical Mø, and suggest that mouse CSF cross-reacts with the putative receptor on rat Mø.
Inhibition of Human Neutrophil Activation by the Allergic Mediator Release Inhibitor, CI-922: Differential Inhibition of Responses to a Variety of Stimuli
Authors: Wright Clifford D , Hoffman Michael D , Thueson David O , Conroy Mary Carol 
Published: January 2018

Abstract
The allergic mediator release inhibitor 3,7-dimethoxy-4-phenyl-N-1H-tetrazol-5-yl-4H-furo[3,2-b]indole-2-carboxamide, L-arginate (CI-922) is a potent inhibitor of human neutrophil functions in vitro. Over a concentration range from 1 to 100 μmol CI-922 inhibits the chemotactic response of neutrophils to the synthetic chemotaxin N-formyl-methionyl-leucyl-phenylalanine (FMLP). CI-922 also inhibits respiratory and secretory responses of neutrophils in response to agents that stimulate phospholipase C-dependent phosphoinositide hydrolysis to generate the second messengers inositol 1,4,5, trisphos-phate and 1,2 diacylglycerol, including: the plasma membrane receptor-specific ligands FMLP and C5a; serum-opsonized zymosan; concanavalin A; and the guanine nucleotide regulatory protein-specific stimulus guanosine-5′-0-(3-thiotriphosphate) (GTPγS). CI-922 also inhibits neutrophil functions stimulated by the calcium ionophore A23187. In contrast, CI-922 does not inhibit neutrophil responses to protein kinase C-specific stimuli such as phorbol 12-myristate 13-acetate (PMA) or L-α-1,2 dioctanoylglycerol (DiC8). CI-922 also fails to inhibit the synergistic activation of the respiratory burst by suboptimal concentrations of PMA and calcium ionophore A23187. The observation that CI-922 inhibits neutrophil responses to a variety of soluble and particulate stimuli, excluding protein kinase C-specific stimuli, allows us to postulate the site of action of the compound. We propose that CI-922 inhibits neutrophil activation at a site distal to signal transduction through the guanine nucleotide regulatory protein required for second messenger generation but proximal to phosphorylation reactions mediated by protein kinase C and calmodulin-dependent protein kinases.
Regulation of Macrophage-Derived Fibroblast Growth Factor Release by Arachidonate Metabolites
Authors: Phan Sem H , McGarry Bridget M , Loeffler Kathryn M , Kunkel Steven L 
Published: January 2018

Abstract
The macrophage is a source of many mediators with direct and indirect fibrogenic potential. In this study, release of macrophage-derived fibroblast growth factor (MDGF) activity by murine peritoneal macrophages is examined with regard to its regulation by arachidonate metabolites. Upon stimulation with 10 μg/ml lipopolysaccharide (LPS), resident peritoneal macrophages from CBA/J mice released MDGF activity into media rapidly, reaching maximal levels in approximately 1 h. Lysates of these stimulated cells also revealed significantly increased cell-associated MDGF activity, composing 45% of the total assayable activity. This activity, as assayed by radioactive thymidine incorporation by primary cultures of rat lung fibroblasts, was separable from interleukin-1 (IL-1) activity by reverse phase high performance liquid chromatography (HPLC). Furthermore, purified murine IL-1 had no MDGF activity in this assay system. This stimulated MDGF release was enhanced by the cylooxygenase inhibitors indomethacin, Ibuprofen, and aspirin at micromolar concentrations, but inhibited in a dose-dependent manner by prostaglandin E2 (PGE2). On the other hand, nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor was inhibitory at 0.1 and 0.4 μM but not at 2.5 μM. Zymosan-stimulated macrophages also markedly increased MDGF release, albeit with a different time course which was characterized by a delay of approximately 7 h before peak levels were attained. Such stimulation, which is known to cause increased lipoxygenase activity, was also inhibited by 0.5 μM NDGA. In contrast, the lipoxygenase pathway products leukotrienes B4 (LTB4) and C4 (LTC4) stimulated MDGF release in a dose-dependent (10-10-10-8 M) manner, with LTC4 being more potent on a per unit dose basis. Stimulation by LTC4 was inhibited by the putative leukotriene receptor antagonist, FPL55712, while LTD4 and LTE4 did not stimulate MDGF release, thus suggesting the mediation of this effect by specific LTC4 receptors. These data suggest also that products of the cyclooxygenase and lipoxygenase pathways are potentially important both as exogenous (ie, derived from cells other than the macrophage itself) and auto- or self-regulators of macrophage MDGF release. This, in turn, implies that cyclooxygenase products are antifibrogenic and important in maintaining or returning to the quiescent or normal state, whereas the lipoxygenase products are profibrogenic and important in induction of fibrosis or wound-healing and tissue repair. Any alteration in the balance between these two pathways may result in either a desirable or a harmful outcome.
Effect of Mitogens on the Cell Cycle Progression and the Quantification of T-Lymphocyte Surface Markers in Acquired Immune Deficiency Syndrome
Authors: Hornicek F J , Malinin G I , Thornthwaite J T , Whiteside M E , MacLeod C L , Malinin T I 
Published: January 2018

Abstract
The cell cycle progression and viability of stimulated and intact lymphocytes from 20 subjects with acquired immune deficiency syndrome (AIDS) was determined by flow cytometry. As compared to controls, 62% less AIDS lymphocytes, cultured for 72 hr in the presence of lectins (Con-A, PHA, PWM), had entered the proliferative phases of the cell cycle, while the respective value for periodic-acid (H5lO6)-stimulated cells was 34%. The helper-suppressor ratios and natural kill cell percentages of the unstimulated and PHA-activated AIDS lymphocytes increased approximately 3-fold after 72 hr in culture. The natural killer (NK) cell fraction of the PHA-stimulated and unstimulated AIDS cultures comprised approximately 20% as compared to 10% in controls. However, no changes in the percentages of T-lymphocytes were detected in the AIDS cell cultures. Throughout the culture period, viability of the unstimulated AIDS lymphocytes exceeded 90%, whereas in stimulated cultures it fluctuated within the 65-90% range. It is concluded that the liability of AIDS lymphocytes to mitogens is probably a direct consequence of the human immunodeficiency virus (HIV) infection.
C3-Mediated Release of Prostaglandin From Human Monocytes: Evidence for Independent Regulation of Thromboxane and Prostaglandin Synthesis
Authors: Rutherford R Bruce 
Published: January 2018

Abstract
Human mononuclear phagocytes (HMP) lose the capacity to respond to C3b, exogenous arachidonic acid (AA), and other stimuli of arachidonic acid (AA) metabolism when precultured for 24 hours prior to the addition of stimulus. Data presented in this report suggest that this reduced capacity is not due to loss of the cyclooxygenase enzyme, to autoinactivation of cyclooxygenase, or to release by the cells of inhibitors of PGE and TxB2 production. Additional metabolism of PGE or a shift of AA metabolism from the cyclooxygenase pathway to the lipoxygenase pathways does not occur and hence cannot account for the observation. HMP precultured for 24 hours with gamma interferon (IFN-γ) retain the capacity to metabolize AA in response to subsequent exposure to C3b and LPS. HMP precultured with LPS or C3b respond to exogenous AA, but not to restimulation with LPS or C3b, by releasing PGE and to a lesser extent TxB2. The amounts of PGE and TxB2 produced under these conditions are reversed when compared to HMP treated with IFN-γ LPS, or C3b at the initiation of culture. These data suggest that the producton of TxB2 and PGE may be independently regulated in HMP and that IFN-γ affects HMP AA metabolism by different mechanisms than LPS or C3b.
Influence of Heparin and a Low Molecular Weight Heparin Fraction of the Leukocytes in an Experimental Venous Thrombosis Model
Authors: Doutremepuich C , Toulemonde F , de Seze O , Pereira F , Anne M C , Doutremepuich F 
Published: January 2018

Abstract
A randomized study was performed to observe the effects induced by heparin and a low molecular weight heparin fraction (at different dosages) on the leukocytes of rats in the presence of experimental venous thrombosis. The experimentation was carried out on two series of animals: the first with a ligature of the inferior vena cava inducing the formation of a thrombus, the second without any ligature. The results show that the induction of thrombosis involves: in the blood, an increase of the number leukocytes, principally polymorphonuclear cells; in the thrombi, a significant rise in the total count of leukocytes, here mononuclear cells; the latter number increases with the dosages of the administered drugs.
Expression of Ia Antigen in Colonies of Bone Marrow-Derived Macrophages
Authors: Yen Shing-Erh , Beelen Robert H J , Walker William S 
Published: January 2018

Abstract
Cells in colonies of culture-derived mouse and rat bone marrow macrophages were examined for membrane la antigen to determine if the steady-state expression of the antigen was restricted to macrophages derived from a distinct population of progenitor cells. Multiple subcultures of macrophages derived from single soft-agar colonies were tested for 1a + cells on three different days of culture. About one-half of the colonies gave rise to subcultures that never contained 1a + cells, about 40% yielded subcultures that contained some la+ cells on at least 2 of the 3 assay days, and about 10% of the colonies produced subcultures that contained 1a-bearing cells on all 3 assay days. Thus, when cultures were assayed at any one time for their content of 1a-bearing cells, the results raised the possibility of phenotypically distinct subpopulations of progenitors. However, sequential analyses of the subcultures revealed the variable expression of la on cells from at least one-half of the colonies. We conclude that, under steady-state conditions, the presence of la antigen on bone marrow-derived macrophages is not clonally restricted. That a T-cell-derived lymphokine induced la antigen on essentially all the cells in most of the colonies of macrophages confirms their potential to express the antigen.
Restoration of the Lipopolysaccharide-Responsive Phenotype in C3H/HeJ Peritoneal Macrophage-P388D1 Cell Hybrids
Authors: Zuckerman Steven H , Surprenant Yvonne M , Carlson Donald G , Beutler Bruce 
Published: January 2018

Abstract
The fusion of thioglycollate-elicited peritoneal macrophages from the lipopolysaccharide (LPS)-nonresponsive C3H/HeJ mouse strain to a hypoxanthine phosphoribosyltransferase (HPRT)-negative variant of the murine macrophage cell line P388D1 has resulted in the derivation of eight hybrid clones following HAT selection. Propidiumiodide staining followed by flow cytometry has demonstrated that the DNA content of the hybrids represents the sum of the parents. Codominant expression of class I antigens from both parental haplotypes is observed in the hybrids. While class II antigens are inducible following a 72-hr induction with gamma interferon-containing supernatants, the amount of each haplotype varies between clones. These hybrids demonstrate Fc-mediated crythrophagocytosis in contrast to P388D1. In distinction to the C3H/HeJ primary peritoneal-macrophage parent, LPS treatment of the hybrids results in the Increased release of both interieukin-1 (IL-1) and cachectin/tumor necrosis factor (TNF) into culture supernatants. Therefore, cell fusion has resulted in the stable restoration of the LPS-responsive phenotype in C3H/HeJ macrophage hybrids. These macrophage hybrids should serve as useful models In understanding the regulation of macrophage effector functions in response to environmental stimuli.
Tumor Cell Killing and Cytostasis by C3H/HeJ Macrophages Activated In Vitro by Lipid A-Associated Protein and Interferon Gamma
Authors: Chapes Stephen K , Killion James W , Morrison David C 
Published: January 2018

Abstract
Experiments have been carried out to assess the ability of purified protein-free lipopolysaccharide (LPS) and lipid A-associated protein (LAP) containing LPS to activate macrophages from C3H/HeJ endotoxin-unresponsive mice. Assays for in vitro activation have included cytotoxic and cytostatic effects on a simian virus 40 (SV40)- transformed fibroblast cell line. While neither preparation of LPS would effect C3H/HeJ macrophage activation for either cytostasis or cytolysis, the addition of murine interferon gamma to cultures of LAP-LPS stimulated C3H/HeJ macrophages resulted in cells which were both cytotoxic and cytostatic. These results suggest that LAP can provide one component of the triggering mechanism but, of itself, is insufficient to effect full activation. A second signal, which can be provided by murine interferon gamma, appears also to be required.
Human Natural Killer Cells Enhance a Mixed Leukocyte Reaction
Authors: Weissler Jonathan C , Yarbrough William C , Toews Galen B , Nicod Laurent P 
Published: January 2018

Abstract
Natural killer cells (NK) have been reported to down-regulate the initiation of T cell responses in animal models. In the current study, highly purified CD16 + human NK cells were obtained by cell sorting and their effect on the stimulation of allogeneic T cells (MLR) determined. NK cells did not directly stimulate T cell proliferation. However, when added to a population of loosely adherent mononuclear cells (LAM), NK enhanced the ability of these accessory cells to stimulate T proliferation. This effect was not reproduced by the addition of sorted CD5 + T cells, sorted CD16 – cells, or control lymphocytes to the MLR. The effect of NK on the MLR was not restricted by class II antigens and was similar to the effect of adding IL-1 to MLR cultures. These results demonstrate that human NK cells are capable of enhancing a T cell response.
Human Mononuclear Cells Which Produce Interferon-Alpha During NK(HSV-FS) Assays Are HLA-DR Positive Cells Distinct From Cytolytic Natural Killer Effectors
Authors: Fitzgerald-Bocarsly Patricia , Feldman Michael , Mendelsohn Monica , Curl Shelley , Lopez Carlos 
Published: January 2018

Abstract
Human mononuclear cells were previously shown to produce interferon-alpha (IFN) during 14 hr assays using herpes simplex virus type-1 infected fibroblasts [NK(HSV-FS)]. In this study, we have compared the effectors responsible for mediating NK(HSV-FS) cytolytic activity to those which produce IFN-alpha. Both activities were found to reside in non-adherent fractions, negative for non-specific esterase-staining cells. Like cells mediating NK cytolytic activity, IFN-alpha producing cells were found in light density Percoll gradient fractions. However, although NK(HSV-FS) and IFN production were largely overlapping, peak IFN production was consistently found in fractions slightly less dense than peak NK(HSV-FS) activity. IFN production was greatly augmented in fractions enriched for dendritic cells on hypertonic metrizamide gradients. The cells which produce IFN-alpha were phenotypically distinct from cytolytic NK effector cells: they lacked the Leu-11, Leu-7 and NKH1 cell surface markers shown to be present on both NK(HSV-FS) and NK(K562) effector cells. In addition, the IFN-alpha producing cells were found to be negative for a number of other markers characteristic of T cells, B cells or macrophages but were positive for Ia and HLA. The cells which produced IFN in response to UV-inactivated HSV antigen and to HSV-infected Raji cells were also found to be Leu-11 negative, and Ia positive. We conclude that the cells which produce IFN in response to HSV are a light density, Ia positive population which are distinct from NK cytolytic effector cells and co-purify with cells bearing a dendritic morphology. These results support our earlier findings that NK(HSV-FS) activity and IFN production are independent of one another and can segregate independently in vivo.
Characteristics of Binding of a Potent Chemotactic Formyl Tetrapeptide, Formylmethionyl-Leucyl-Phenylalanyl-Phenylalanine, to the Receptors on Rabbit Neutrophils
Authors: Kermode John C , Muthukumaraswamy Natesa , Freer Richard J 
Published: January 2018

Abstract
Binding of a potent chemotactic formyl tetrapeptide, formylmethionyl-leucyl-phenyl-alanyl-phenylalanine (fMet-Leu-Phe-Phe), to the formyl peptide receptors on the rabbit neutrophil was assessed by two approaches. A tritiated preparation of fMet-Leu-Phe-Phe was used for direct binding studies, whereas indirect studies comprised an assessment of the ability of the formyl tetrapeptide to competitively inhibit the binding of 35S-labeled formylmethionyl-leucyl-phenylalanine. These two approaches yielded analogous results. The formyl tetrapeptide fMet-Leu-Phe-Phe showed rapid and saturable binding to the same chemotactic receptors as the less potent formyl tripeptides with which it was compared. Its equilibrium-binding pattern, however, was different: fMet-Leu-Phe-Phe showed a homogeneous binding pattern, in contrast to the heterogeneity seen with the less potent compounds. The relative potencies for high-affinity binding of the two standard formyl tripeptides and fMet-Leu-Phe-Phe correlated well with their relative potencies for stimulating the biological response of degranulation; the relative potencies for low-affinity binding correlated less well.
Generation of Neutrophil Chemotactic Activity by Phorbol Ester-Stimulated Calf Pulmonary Artery Endothelial Cells
Authors: Gudewicz Paul W , Odekon Lale E , Del Vecchio Peter J , Saba Thomas M 
Published: January 2018

Abstract
Chemotactic activity for human polymorphonuclear leukocytes (PMNL) was detected in serum-free conditioned media 1 to 4 hr after monolayers of calf pulmonary artery endothelial cells were pretreated with phorbol myristate acetate (PMA). Chemotactic activity was increased in conditioned media following pretreatment with either PMA or the less lipophilic active phorbol ester, 4-β-phorbol-12,13-dibutyrate (P(Bu)2) in a dose-dependent manner. Chemotactic activity of conditioned media from PMA-treated endothelial cells was confirmed by checkerboard analysis. The chemotactic activity in conditioned media from PMA-pretreated endothelial cells was completely inhibited by pretreating endothelial cells with either cycloheximide, actinomycin D, or the lipooxygenase inhibitor, diethylcarbamazine. Furthermore, the chemotactic activity was heat-stable, inhibited by trypsin treatment, and present in both aqueous and lipid phases after ether extraction. The data demonstrate that pulmonary artery endothelial cells exposed to active phorbol esters release potent chemotactic factor(s) for PMNL. These findings suggest a role for activators of protein kinase C in mediating endothelial cell release of chemotactic factor(s) that may be important in the directed migration of circulating leukocytes to sites of vascular injury.
Thymic Stroma-Derived T-Cell Growth Factor (TSTGF): II. Biochemical and Functional Characterization
Authors: Sato Soichiro , Ogata Masato , Sano Haruo , Mizushima Yumiko , Muramatsu Minoru , Doi Hideyuki , Itoh Tsunetoshi , Hamaoka Toshiyuki , Fujiwara Hiromi 
Published: January 2018

Abstract
The culture supernatant (SN) from a cloned line of thymic stroma-derived cells in fibroblastic form (TSCF) contained a factor capable of supporting the growth of the interleukln (IL) 2-dependent, antigen-specific helper T cell (Th) clone 9-16 without requiring IL2 and antigen. This active substance, designated as thymic stroma-derived T-cell growth factor (TSTGF), was partially purified through DEAE-Sephacel chromatography and PBE 94 chromatofocusing. The original SN did not contain IL1, IL2, IL3, IL4, or interferon activities; but an appreciable magnitude of colony-stimulating factor (CSF) activity in addition to TSTGF was present, whereas the partially purified preparation of TSTGF was depleted of any type of CSF activity. The elution profile of TSTGF activity on the chromatofocusing has revealed that TSTGF has an isoelectric point (pI) of about 6.0. When a purified TSTGF sample was applied to Sephacryl S-200 column chromatography and sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis, TSTGF activity was eluted in a single peak around an apparent molecular weight of about 25,000. The activity of TSTGF also was shown to be relatively stable with heat treatment and in the wide range of pH, but it was abolished by treatment with either trypsin or dithiothreitol. These results indicate that TSTGF, a novel T-cell growth factor, is the protein that has an apparent molecular weight of about 25,000 and a pI of 6.0, and in the intact molecule, it contains the disulfide bond(s) required to maintain and/or express its biologic activity.
Procoagulant Synthesis by Exudate and Bone Marrow-Derived Murine Macrophages
Authors: Shands Joseph W , Sunnenberg Thomas D , Lottenberg Richard 
Published: January 2018

Abstract
Murine exudate macrophages elicited by different stimuli and bone marrow-derived macrophages were studied for their capacity to synthesize factor VII and tissue factor in a basal state and on stimulation with endotoxin (LPS). Cells elicited by different stimuli varied in their production of both factors. Thioglycollate-elicited cells generally made more, but not significantly more, tissue factor in response to endotoxin than cells elicited with periodate or streptococci. Cells elicited with proteose-peptone, fetal calf serum (FCS), or LPS produced less or very little tissue factor. Thioglycollate-elicited cells and cells elicited with streptococci or proteose-peptone consistently made more factor VII than cells elicited with periodate, FCS, and LPS. Bone marrow-derived macrophages were responsive to LPS by the production of tissue factor by the fifth day of culture, and this rose to a maximum by day 10. The maximal production of factor VII occurred on day 5 of culture and declined with longer cultivation. Factor VII production was not enhanced by LPS, and prolonged cultivation in the presence of LPS turned off the synthesis of both tissue factor and factor VII. We conclude that exudate cells are heterogeneous in the production of coagulant factors and that the production of these factors varies with the maturity of the cells. In addition, the production of the tissue factor and the factor VII were not necessarily expressed in a coordinate fashion.