bluuebunny/crossref_metadata_2025_split huggingface dataset:
GM-1, a Clone of the Monoblastic Phagocyte U937 That Expresses a Large Respiratory Burst Capacity Upon Activation With Interferon-γ
Authors: Garotta Gianni , Thelen Marcus , Delia Domenico , Kamber Markus , Baggiolini Marco 
Published: January 2018

Abstract
The human cell line U937 was cloned and screened for the responsiveness to interferon-γ (INF-γ). The selected subclone, named GM-1, expressed a high density of IFN-γ receptors and showed HLA typing similar to that of the parental line but was devoid of the Y chromosome. GM-1 cells display a promyeloid phenotype as revealed by flow cytometry using a panel of murine antibodies. Following treatment with IFN-γ GM-1 cells differentiated to a more mature monocyte stage and acquired the capacity to mount a respiratory burst. After treatment with differentiation promoters, such as phorbol 12-myristate 13-acetate (PMA), dimethyl sulfoxide (DMSO), and retinoic acid, GM-1 showed a more limited respiratory burst capacity. Superoxide release in IFN-γ-activated cells was stimulated with f-Met-Leu-Phe, C5a, or PMA. The development of the respiratory burst capacity was accompanied with the expression of cytochrome b558, a component of the phagocyte NADPH-oxidase. GM-1 cells are useful for the study of the effects of IFN-γ on the respiratory burst. They are more sensitive and yield a more homogenous response to IFN-γ than U937 cells. The phenotype of GM-1 cells was stable for more than 5 years.
Recombinant Interleukin-4 Enhances the Chemiluminescent Oxidative Burst of Murine Peritoneal Macrophages
Authors: Tan Henkie P , Nehlsen-Cannarella Sandra L , Garberoglio Carlos A , Tosk Jeffrey M 
Published: January 2018

Abstract
We evaluated the effects of murine recombinant interleukin-4 (rIL-4) on murine peritoneal macrophages. We showed a marked, dose-dependent stimulation of respiratory oxidative burst by IL-4 in peptone-elicited murine peritoneal macrophages. This effect was abolished by a neutralizing monoclonal antibody (mAb) to rlL-4 confirming that the enhanced chemiluminescence was due to IL-4. In contrast, rlL-4 depressed the respiratory oxidative burst of a transformed murine macrophage cell line, J774, in a dose-dependent mAb-reversible manner.
Alterations in Tyrosine Protein Kinase Activities Upon Activation of Human Neutrophils
Authors: Berkow Roger L , Dodson Robert W 
Published: January 2018

Abstract
Human neutrophils are phagocytic cells that can be activated by a variety of agonists to undergo a group of physiologic responses. This “stimulus-response” coupling is thought to be dependent on the phosphorylation of specific proteins. We have previously shown that, in addition to the widely distributed serine and threonine protein kinases, neutrophils contain tryosine protein kinase activity in the cell cytosol and particulate fractions. When neutrophils are treated with a variety of agents, phosphorylation of both cytosolic and particulate proteins on tyrosine residues occurs. Increases in tyrosine phosphorylation may be a result of increases in the activity of tyrosine kinases or a decrease in the activity of phosphotyrosine phosphatases. In this study, we have used a novel nondenaturing polyacrylamide gel electrophoretic method to demonstrate that treatment of human neutrophils with the chemotactic peptide FMLP or the phorbol ester phorbol myristate acetate induces a time- and concentration-dependent increase in the tyrosine protein kinase activity found in the cell cytosol and cell particulate fraction. The time course and concentration range over which these changes occur are similar to those seen for activation of the neutrophil oxidative burst and phosphorylation of proteins on tyrosine residues, suggesting that these events may be related.
Expression and Capping of a Proliferation-Associated Surface Membrane p34 kDa Antigen on Different Human Hematopoietic Cell Lines
Authors: Streck Richard J , Hurley Edward L , Pauly John L 
Published: January 2018

Abstract
A novel surface membrane nonglycosylated acidic polypeptide (34 kDa), encoded by a structural gene on chromosome 11, has been identified using murine monoclonal antibody (MoAb) 53.6 (lgG2a). MoAb 53.6, raised against uninduced cells of a human erythroleukemia line (HEL), recognizes a surface membrane antigen that is displayed on proliferating (cell cycle phase G., S, and M + G2 phase) human leukocytes. The expression and redistribution (i.e., patching and capping) of the p34 kDa antigen on 27 different long-term human hematopoietic cell (HHC) lines was defined by fluorescence microscopy. These lines had been established from patients with leukemia or healthy donors and included phenotypically defined populations of T cells, B cells, and myelomonocytic cells. Almost all (&gt;95%) of the leukocytes of the 27 lines reacted strongly with MoAb 53.6. The majority of the leukocytes displayed p34 kDa antigen patching (26/27 lines; patched cells, 96–100%); moreover, 20 of 27 lines exhibited p34 kDa antigen capping (capped cells, 8–96%). Presentation of the p34 kDa antigen on surface membrane ultrastructures, imaged with immunogold using an indirect antibody labeling procedure, was illustrated by scanning electron microscopy, and endocytosis of the gold-tagged antigen-antibody complex was studied by transmission electron microscopy. The HHC lines are thought to represent immortalized populations of different human leukocyte subsets that are in different stages of maturation and/or differentiation; thus these lines should prove useful as models for further characterizing this unique p34 kDa proliferation-associated antigen and for defining the mechanisms and significance of surface membrane antigen redistribution and modulation that has been associated with leukocyte activation and propagation.
[Ca2+]i Changes and Respiratory Burst in Human Neutrophils and Monocytes Induced by NAP-1/Interleukin-8, NAP-2, and gro/MGSA
Authors: Walz Alfred , Meloni Federica , Clark-Lewis Ian , von Tscharner Vinzenz , Baggiolini Marco 
Published: January 2018

Abstract
The stimulatory effects of neutrophil-activating peptide 1 (NAP-1), also termed interleukin 8 (IL-8), neutrophil-activating peptide 2 (NAP-2), and melanoma growth-stimulatory activity (gro/MGSA) on human neutrophils and monocytes were compared on the basis of two responses that can be assessed in real time, the changes in cytosolic free calcium and the respiratory burst. All three peptides induced a rapid and transient rise of cytosolic-free calcium and the respiratory burst in neutrophils. Both responses were also obtained in monocytes on stimulation with NAP-1/IL-8 and gro/MGSA, but not with NAP-2, which appeared to be more selective for neutrophils. Pretreatment with concanavalin A (ConA) enhanced several fold the rate and duration of the respiratory burst of neutrophils stimulated with all three peptides and of monocytes stimulated with NAP-1/IL-8 and gro/MGSA, but not with NAP-2. Sequential stimulation showed mutual cross desensitization by NAP-2 and gro/MGSA in neutrophils. In addition, desensitization of neutrophils toward NAP-2 and gro/MGSA, and of monocytes toward gro/MGSA, was obtained by prestimulation with NAP-1/IL-8. Prestimulation with either NAP-2 or gro/MGSA, however, did not desensitize the cells for NAP-1/IL-8.
These results suggest that under conditions where multiple stimulatory agents are produced, neutrophil-activating peptides may contribute to the formation of substantial amounts of oxygen-derived radicals. In addition, the study shows that NAP-1/IL-8 and gro/MGSA, but not NAP-2, have some stimulatory effects on monocytes as well.
Reactivity of antineutrophil cytoplasmic autoantibodies with mononuclear phagocytes
Authors: Charles Linda A , Falk Ronald J , Jennette J Charles 
Published: January 2018

Abstract
Antineutrophil cytoplasmic autoantibodies (ANCA) react with proteins found in the granules of neutrophils and the peroxidase-positive lysosomes of monocytes, including myeloperoxidase (MPO), proteinase 3 (PR-3), and elastase. ANGA-associated diseases, such as Wegener's granulomatosis and polyarteritis nodosa, are characterized by necrotizing vascular inflammation. The inflammatory lesions typically contain both neutrophils and mononuclear phagocytes, with the latter sometimes predominating, for example, in the granulomatous lesions of Wegener's granulomatosis. We investigated the presence of the ANCA target antigens PR3, MPO, and elastase in mononuclear phagocyte cytoplasm during the course of differentiation in vitro and in alveolar and peritoneal macrophages. We observed that ANCA antigens were down-regulated during mononuclear phagocyte differentiation, with the loss corresponding to that of peroxidase-positive granules. This suggests that ANCA can directly interact only with monocytes and early exudative macrophages and not with mature macrophages.
Heterogeneity in the mobilization of cytoplasmic calcium by human polymorphonuclear leukocytes in response to fMLP, C5a and IL-8/NAP-1
Authors: Eisner Jörn , Kaever Volkhard , Emmendörffer Andreas , Breidenbach Thomas , Lohmann-Matthes Marie-Luise , Roesler Joachim 
Published: January 2018

Abstract
The visible excitation and emission wavelengths of the recently developed fluorescent Ca2+ indicator fluo-3 permit analysis of the intracellular Ca2+ concentration, [Ca2+]i, in flow cytometry with a 488-nm argon laser. The role of [Ca2+]i in human polymorphonuclear leukocyte heterogeneity was investigated in response to formyl-methionyl-leucyl-phenylalanine (fMLP), C5a, and interleukin 8/neutrophil attractant/activation protein 1 (IL-8/NAP-1) by flow cytometry. The [Ca2+]i changes in different subpopulations within a heterogeneous cell suspension were resolved upon stimulation with fMLP. Using an anti-CD16 phycoerythrin-conjugated antibody and fluo-3 simultaneously, neutrophils affected and nonaffected in Ca2+ mobilization were distinguished in two patients suffering from glycogen storage disease type lb. In normal neutrophils, a different time course of Ca2+ mobilization of neutrophil subpopulations immediately after stimulation with fMLP was detected. In addition, after stimulation with a low concentration of IL-8/NAP-1 (10-10 M) two subsets of neutrophils appeared; one of them showed an increase in [Ca2+]i, while the other did not. These results indicate heterogeneity in the neutrophil signal transduction process involved in Ca2+ mobilization. Therefore, flow cytometric analyses can resolve changes in single-cell [Ca2+]i distribution patterns, which is important for the understanding of [Ca2+]i in neutrophil heterogeneous activation processes.
Differential production of granulocyte-macrophage colonystimulating factor by macrophages from mice susceptible and resistant to Leishmania mexicana amazonensis
Authors: Soares Luis Roberto B , Barcinski Marcello A 
Published: January 2018

Abstract
The present results demonstrate that macrophages from mice susceptible to infection with Leishmania mexicana amazonensis sustain a higher production of granulocyte-macrophage colony-stimulating factor (GM-GSF) throughout the in vitro infection than macrophages from a resistant strain. Resident macrophages from BALB/c and C57B1/10 mice were infected with promastigotes of L. mexicana amazonensis and the amount of biologically active GM-CSF was measured in the supernatants collected at different times of infection. Measurements were made by bone marrow and GM-CSF/interleukin-3 addicted cell proliferation. Because GM-GSF is a disease-exacerbating cytokine, its differential production by infected macrophages may be one of the mechanisms defining resistance or susceptibility to a leishmanial infection.
Synthetic hexapeptides derived from the transmembrane envelope proteins of retroviruses suppress N-formylpeptide–induced monocyte polarization
Authors: Oostendorp Robert AJ , Schaaper Wim M M , Post Jacob , Meloen Rob H , Scheper Rik J 
Published: January 2018

Abstract
Retroviral infections are frequently associated with immunosuppression. Retroviral transmembrane envelope proteins (TM proteins) play an important role in this phenomenon. CKS-17, a synthetic heptadecapeptide, represents the immunosuppressive site of these retroviral TM proteins. Here we report on the further delineation of this immunosuppressive site using CKS-17-derived hexapeptides. The N-formyl-methionyl-leucyl-phenylalanine-induced monocyte polarization assay was used throughout this study because this monocyte function has been shown to be highly sensitive to TM protein p15E-related immunosuppression. We found that in addition to CKS-17 one CKS-17-derived hexapeptide, LDLLFL, reversibly inhibited monocyte polarization, with 50% inhibitory concentrations of 20 and 2 μM respectively. LDLLFL-mediated inhibition was sequence specific because the reverse peptide LFLLDL and scrambled peptides were not inhibitory. Hexapeptides corresponding to LDLLFL, but derived from various retroviruses other than murine leukemia virus, also inhibited monocyte polarization. Peptides most homologous to LDLLFL –- LDILFL (feline leukemia virus) and LDLLFW (human T lymphotropic virus types I and II)–-were the most potent inhibitors. Peptides homologous to primate and human endogenous proviruses were not suppressive. LDLLFL and some of its homologues also inhibited polarization of neutrophilic granulocytes. These findings lend further support to the view that conserved retroviral TM protein–related peptides can play an important role in suppression of inflammatory cell function as encountered in retrovirus-associated immunosuppression.
In vivo metabolic response of hepatic nonparenchymal cells and leukocytes to granulocyte-macrophage colony-stimulating factor
Authors: Spolarics Zoltan , Schuler Agnes , Bagby Gregory J , Lang Charles H , Nelson Steve , Spitzer John J 
Published: January 2018

Abstract
This study investigates the in vivo glucose utilization of various immune-competent cells after an intra-arterial injection of a nonlethal dose (30 μg/kg body weight) of murine recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF). Injection of GM-CSF resulted in a rapid but transient reduction in the number of circulating neutrophils. After 20 min the number of neutrophils returned to normal values, and by 4 h it was about 80% greater than in time-matched saline-injected controls. One hour after the treatment, neutrophils were accumulated in the livers of GM-CSF-injected animals but not in control livers. In vivo glucose utilization by circulating neutrophils and mononuclear cells and various liver cell types was investigated by combining the 2-deoxyglucose tracer technique with cell isolation procedures. GM-GSF increased the in vivo glucose utilization of circulating and infiltrating neutrophils by more than 200%. Glucose utilization by circulating mononuclear cells was also doubled. After GM-GSF injection, glucose utilization by Kupffer cells was increased by 130% and by hepatic endothelial cells was increased by 60%. Indomethacin pretreatment blunted the hyperglycemia caused by GM-CSF injection; however, it did not inhibit the increased glucose utilization by immune-competent cells. This suggests that the effect of GM-GSF on glucose utilization by these cells is not mediated by prostanoids and is at least partially independent of the mass action of elevated glucose concentration. These findings indicate that GM-CSF may be an important member of the cytokine cascade that mediates the acute in vivo metabolic response of immune-competent cells in sepsis or endotoxemia.
In vitro adhesion of human epidermal Langerhans cells to laminin and fibronectin occurs through β1 integrin receptors
Authors: Le Varlet B , Staquet M J , Dezutter-Dambuyant C , Delorme P , Schmitt D 
Published: January 2018

Abstract
Human epidermal Langerhans cells are dendritic cells that can capture, process, and present antigens to T cells. It was previously shown that these Langerhans cells express the very late activation antigen (VLA) protein family of β1 integrins. β1 integrins mainly mediate the adhesion of cells to a number of extracellular components, such as laminin, fibronectin, and collagen, which are present in the skin. In this report, we demonstrate that a large percentage of the Langerhans cell population was able in vitro to attach to laminin and fibronectin but not to collagen. An ultrastructural study of adherent Langerhans cells showed that they were spread largely on laminin, with a loss of their round shape, and partially on fibronectin. Langerhans cell binding to laminin or fibronectin induced a decrease of the Birbeck granule number. Specific inhibitions of cell adhesion were performed, and it was demonstrated that VLA-6 was the major receptor involved in Langerhans cell adhesion to laminin. This adhesion was not RGD dependent and was slightly enhanced by Mn2+. VLA-3 and especially VLA-5 mediated Langerhans cell binding to fibronectin through the RGDS sequence of the protein. Mn2+ sharply increased the Langerhans cell adhesion to fibronectin. VLA-6 mediated in vitro Langerhans cell adhesion to laminin, which suggests that in vivo VLA-6 could permit Langerhans cells to attach and migrate through the basement membrane. Moreover, VLA-5 and VLA-3 take part in the in vitro Langerhans cell binding to fibronectin, suggesting that in vivo these fibronectin receptors could facilitate Langerhans cell passage throughout the fibronectin network of the dermis before migration to lymph nodes.
Formation of LTB4 by fMLP-stimulated alveolar macrophages accounts for eosinophil migration in vitro
Authors: Hidi Rabiâ , Coëffier Eliane , Vargaftig B Boris 
Published: January 2018

Abstract
Guinea pig alveolar macrophages obtained by bronchoalveolar lavage were isolated by adherence for 2 h and stimulated with 1 μM of N-formyl-l-methionyl-l-leucyl-l-phenylalanine (fMLP) for different time intervals. The supernatants then were tested for their chemotactic effect on guinea pig peritoneal normodense eosinophils and for release of thromboxane B2, leukotriene B4 (LTB4), and platelet activating factor (PAF). The supernatant from fMLP-stimulated alveolar macrophages induced a significant eosinophil attraction (96.0 ± 11.9, number of migrating eosinophils [mean ± SEM], n = 17) as compared to unstimulated macrophages (4.8 ± 1.4, n = 15). This effect was not accounted for by fMLP carry-over to the macrophages because, in contrast to human eosinophils, fMLP has no chemotactic effect on guinea pig eosinophils. Pretreatment of eosinophils with BN 52021 (100 μM), a specific PAF antagonist, and with indomethacin (10 μM), a cyclooxygenase inhibitor, failed to inhibit migration of eosinophils induced by supernatants from either stimulated or unstimulated alveolar macrophages. In contrast, inhibition of the 5-lipoxygenase enzyme with N-(3-phenoxycinamyl)-acetohydroxamic acid (1 μM) suppressed eosinophil migration by alveolar macrophage supernatants (94.1 ± 2.6% of inhibition, n = 6). Desensitization of eosinophils by and to LTB4 (10 nM) inhibited migration induced by supernatants from stimulated alveolar macrophages (87.5 ± 5.4% of desensitization toward LTB4 and 83.1 ± 5.4% of desensitization toward supernatants, n = 5). Under the present experimental conditions, LTB4 is the only agent implicated in eosinophil migration induced by supernatants from fMLP-stimulated alveolar macrophages.
Inhibition of some human neutrophil functions by the cyclooxygenase inhibitor ketorolac tromethamine
Authors: Hyers Thomas M , Tricomi Sally M , Liao Jeng-Jong 
Published: January 2018

Abstract
Ketorolac tromethamine, a new nonsteroidal anti-inflammatory agent of the pyrrolo-pyrrole group, was assayed for inhibitory effects on polymorphonuclear leukocytes (PMN) in a variety of systems. Ketorolac inhibited PMN superoxide anion generation, lysozyme release, myeloperoxidase release, adherence to plastic surfaces, and chemotaxis in response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) in a dose-dependent manner. Ketorolac also inhibited phorbol myristate acetate-stimulated adherence of PMN to bovine pulmonary artery endothelial cells. The drug inhibited lysozyme and myeloperoxidase release by PMN in response to C5a but failed to inhibit C5a stimulation of PMN in any of the other assays. Levels of ketorolac required to inhibit PMN function in most systems were in the range of 0.2 to 1.0 mg/ml, but chemotaxis to fMLP was inhibited by concentrations of ketorolac as low as 1 μg/ml. Ketorolac, currently the only nonsteroidal anti-inflammatory drug available in a parenteral form may have therapeutic usefulness in a variety of conditions thought to be mediated in part by PMN, including sepsis.
Tumor necrosis factor α and interleukin 1 α enhance lipopolysaccharide-mediated bovine endothelial cell injury
Authors: Sharma Smita A , Olchowy Timothy WJ , Yang Zhengang , Breider Mike A 
Published: January 2018

Abstract
Alveolar macrophages (AMs) are important in the host response to aerogenous pulmonary bacterial infections, such as Pasteurella haemolytica–induced pneumonia in cattle. Previous work has shown that AMs enhance P. haemolytica–mediated pulmonary endothelial cell (EC) damage in vitro. The purpose of this study was to determine the mechanism of AM-enhanced EC damage using an in vitro AM-EC coculture system consisting of AMs cultured on culture plate insert membranes and ECs in the underlying chamber. The addition of lipopolysaccharide (LPS) to the culture plate insert chamber resulted in EC damage indicated by 51Cr release, which was enhanced in the presence of AMs. To determine the role of AM-secreted cytokines, recombinant human interleukin 1 α (IL-1) or tumor necrosis factor α (TNF) was added to ECs simultaneously with varying concentrations of LPS. Although TNF and IL-1 alone had only marginal toxic effects on ECs, the simultaneous treatment of TNF or IL-1 with LPS greatly increased the LPS cytotoxic effect on ECs. In addition, IL-1 receptor antagonist eliminated the IL-1 enhancement of LPS-mediated EC toxicity. These results suggest that macrophage-secreted cytokines synergistically enhance LPS-mediated pulmonary EC damage.
Effect of divalent cations on adhesion of polymorphonuclear leukocytes to matrix molecules in vitro
Authors: Lundgren-Åkerlund Evy , Berger Elaine , Arfors Karl-E 
Published: January 2018

Abstract
Adhesion of N-formyl-methionyl-leucyl-phenylalanine-stimulated human polymorphonuclear leukocytes (PMNs) to dishes coated with laminin, fibronectin, or collagen types I and IV was dependent on the presence of magnesium (Mg2+) but not calcium (Ca2+). Addition of manganese (Mn2+) in combination with Ca2+ and Mg2+ further increased the number of PMNs adhering to the matrix proteins. Monoclonal antibody 60.3 (mAb 60.3) was equally effective at inhibiting adhesion of PMNs to all the matrix proteins. The presence of Mn2+ (50 μM), in addition to 1 mM Ca2+ and Mg2+, required higher concentrations of mAb 60.3 to inhibit adhesion of PMNs to collagens type I or IV, suggesting increased affinity of PMNs for these substrates. These findings suggest that the PMNs may regulate the affinity of CD11/CD18 (or multiple ligands by binding different divalent cations to the receptor.