bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemokines and serpentines: the molecular biology of chemokine receptors
Authors: Kelvin David J , Michiel Dennis F , Johnston James A , Lloyd Andrew R , Sprenger Hans , Oppenheim Joost J , Wang Ji-Ming 
Published: January 2018

Abstract
Chemokines are pro-inflammatory molecules with a diverse array of biological and biochemical functions. These molecules induce the migration of a number of leukocyte subsets including monocytes, neutrophils, and T-cells. The recent cloning of the IL-8, GRO, and MIP-lα chemokine receptors revealed that these glycoproteins belong to the serpentine family of seven transmembrane G-protein-coupled receptors. Other members of this family include die chemotactic receptors for fMLP and C5a, indicating that a common pathway for eliciting the directional migration of leukocytes is probably transduced via G proteins. Ligand binding to chemokine receptors is complex, featured by multiple chemokines binding to a single receptor and multiple receptors binding a specific ligand. Future directions in this field appear to be focused on the cloning of novel receptors and the identification of ligands for orphaned receptors.
Transendothelial migration of neonatal and adult bovine neutrophils in vitro
Authors: Bochsler Philip N , Neilsen Nancy R , Slauson David O 
Published: January 2018

Abstract
We have compared and quantitated transen-dothelial migration of neonatal neutrophils (N-PMNs) and adult bovine peripheral-blood PMNs (A-PMNs) in vitro using monolayers of endothelium and a two-chamber apparatus. Bovine aortic endothelial cells were cultured to confluence on polycarbonate filters perforated with 3.0-μm-diameter pores. 51Cr-labeled PMNs were added to the upper chamber, with or without an anti-CD18 antibody (monoclonal antibody 60.3). Chemotactic stimuli in the lower chambers included recombinant human interleukin-8 (rhIL-8; 75 ng/ml), rhC5a (10-7 M), and zymosan-activated bovine serum (ZAS; 10%). At 60 min incubation with rhIL-8, greater numbers (P &lt; .01) of N-PMNs (24.70 ± 5.95%) than of A-PMNs (15.77 ± 3.66%) had migrated across the endothelial barrier, and a similar difference was present at 90 min. Migration rates of N-PMNs and A-PMNs were similar (P &gt; .05) at all time points when using rhC5a and ZAS as stimuli. Anti-CD18 monoclonal antibody significantly decreased migration (P &lt; .01) of both N-PMNs and A-PMNs to low levels when IL-8 and ZAS were used as stimuli. Because leukocyte integrin expression on PMNs affects transendothelial migration, we also compared surface expression of CD18, CD11a, and CD11c on PMNs from the two age groups. We found no significant quantitative differences in integrin expression between PMNs from the two age groups, regardless of whether the PMNs were incubated with buffer alone or with chemotaxins (rhIL-8, rhC5a, ZAS). J. Leukoc. Biol. 55: 43–49; 1994.
Determination of leukotriene effects on human neutrophil chemotaxis in vitro by differential assessment of cell motility and polarity
Authors: Krauss A H -P , Nieves A L , Spada C S , Woodward D F 
Published: January 2018

Abstract
The effects of leukotriene (LT) B4 and D4 on the motility of human peripheral blood neutrophils were investigated employing a novel analytical method. Using the under-agarose technique, migration distance and vectorial orientation of neutrophils in response to selected LT concentrations were determined with the aid of digital image processing. Neutrophil polarization induced by a chemotactic gradient was very apparent even at fields taken adjacent to the cell seeding well where little directional cell motility had occurred. Thus, cell polarization appeared to be the earliest response to chemoattractive LTs. Cell motility occurred in a dose-dependent manner to LTB4 according to determination of the leading edge. LTD4 produced similar effects on neutrophil polarization and motility, but these occurred only at very high concentrations. These data support the view that vectorial orientation is a prerequisite for directional migration of cells and it is also feasible that these are separately regulated events. Furthermore, our studies confirm that LTB4 and, to a much lesser extent, LTD4 are chemotactic for human peripheral blood neutrophils. J. Leukoc. Biol. 55: 201–208; 1994.
Mechanism of suppression of nitric oxide synthase expression by interleukin-4 in primary mouse macrophages
Authors: Bogdan Christian , Vodovotz Yoram , Paik John , Xie Qiao-wen , Nathan Carl 
Published: January 2018

Abstract
Nitric oxide (NO) contributes to the anti-tumor, antimicrobial, and immunosuppressive activity of macrophages. An inducible form of NO synthase (iNOS) is responsible for high output generation of nitric oxide by macrophages after stimulation with cytokines and/or lipopolysaccharide (LPS). In the present study, we demonstrate that interleukin 4 (IL-4) suppressed production of NO by primary mouse peritoneal macrophages exposed to IFN-γ with or without LPS, even while synergizing with IFN-γ to increase the secretion of TNF-α. Suppression of NO production was paralleled by decreases in iNOS enzyme activity and iNOS antigen. IL-4 did not inhibit induction of iNOS mRNA 4–6 h after exposure to IFN-γ, but strongly reduced iNOS mRNA at later times of stimulation (24–72 h), without increasing its turnover. The conditions for maximal suppression of iNOS expression by IL-4 and the mechanisms of suppression differed from those determined in parallel for transforming growth-factor-β as described elsewhere. These results illustrate the diversity of phenotypes of macrophages deactivated by different cytokines, and demonstrate that IL-4 has the potential to reduce one component of the anti-tumor, antimicrobial, and immunosuppressive activities of macrophages. J. Leukoc. Biol. 55: 227–233; 1994.
Human monocyte chemotaxis to complement-derived chemotaxins is enhanced by Gc-globulin
Authors: Piquette C A , Robinson-Hill R , Webster R O 
Published: January 2018

Abstract
Gc-globulin has been found in bronchoalveolar lavage fluid in patients with chronic obstructive pulmonary disease (COPD) and adult respiratory distress syndrome (ARDS) and has been shown to enhance neutrophil chemotaxis to C5-derived peptides in vitro. We proposed that Gc-globulin may enhance the inflammatory response in lungs by influencing monocyte chemotaxis to C5-derived peptides as it does with neutrophils. Monocyte chemotaxis was measured in blind well chambers by a leading-front technique. Purified human Gc-globulin had no intrinsic chemotactic activity for monocytes at concentrations ranging from 1 fM to 1 μM. However, Gc-globulin, at concentrations as low as 10 pM, increased monocyte chemotaxis over 10-fold in a concentration-dependent fashion when added to non-chemotactic doses of C5a (0.1 nM) and C5a des Arg (0.5 nM). The chemotaxis-enhancing effect of Gc-globulin was specific for C5-derived peptides, as Gc-globulin did not enhance monocyte chemotaxis to other chemoattractants such as leukotriene B4 or formyl-Met-Leu-Phe. The enhancement of monocyte chemotaxis to C5-derived peptides by Gc-globulin was not a nonspecific effect of anionic proteins, as other serum proteins of similar size and charge did not enhance monocyte chemotaxis to C5a des Arg. These results indicate that Gc-globulin enhances the monocyte response to C5-derived peptides and, together with previous work, indicates that its presence in the airways of patients with COPD and ARDS may up-regulate the monocyte inflammatory response in the lungs. J. Leukoc. Biol. 55: 349–354; 1994.
Metastatic competence of BW5147 T-lymphoma cell lines is correlated with in vitro invasiveness, motility and F-actin content
Authors: Verschueren Hendrik , Van der Taelen Imme , Dewit Joëlle , De Braekeleer Jos , De Baetselier Patrick 
Published: January 2018

Abstract
The aim of our study was to investigate whether the level of actin polymerization plays a role in the motile and tissue infiltrating behavior of malignant lymphoma cells. For a panel of cell lines derived from the murine BW5147 T-cell lymphoma, we had previously shown a correlation between experimental metastasis formation and in vitro monolayer invasion. We have analyzed the motility and the F-actin content of six non-metastatic, noninvasive (meta-inv-) and five metastatic, invasive (meta+inv+) variants of BW5147. Fourier analysis of cell contours was used to quantify shape changes of cells. All meta+inv+ lines rapidly protruded and retracted pseudopodia, whereas only one of the six meta-inv- lines showed this type of motility. Flow cytometry of cells stained with fluorescein-labeled phalloidin showed that the motile meta+inv+ cell lines have a higher F-actin content than their nonmotile meta-inv- counterparts. The results indicate that in lymphoma cells a high level of actin polymerization is a prerequisite for the formation of pseudopodia, which in turn are necessary for infiltration of the cells into tissues, and eventually for efficient metastasis formation. A corollary of this conclusion is that regulation of actin polymerization is a possible target for intervention aimed at moderating the spread of malignant lymphoma. J. Leukoc. Biol. 55: 552–556; 1994.
Induction of mycobacterial proteins during phagocytosis and heat shock: a time interval analysis
Authors: Alavi Mohammad R , Affronti Lewis F 
Published: January 2018

Abstract
Mycobacterium tuberculosis survives macrophage bactericidal activities by mechanisms that may include induction of stress proteins. We sought to determine whether the synthesis of any mycobacterial proteins is increased during phagocytosis and whether any of these proteins are also up-regulated during heat shock. Protein synthesis by M. tuberculosis H37Ra during phagocytosis by the mouse macrophage cell line IC-21, and during heat shock at 45 and 48 °, was monitored at various time intervals using 35S-labeled methionine/cysteine and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Our data suggest the existence of certain common elements in the stress response of mycobacteria to the three stress stimuli. This apparent similarity was best characterized by the up-regulation of a 25-kDa protein after exposure to each of the stress conditions. Furthermore, this 25-kDa protein and a 37-kDa protein that was also synthesized during phagocytosis appeared to be extracellular because they were preferentially solubilized when infected macrophages were lysed with 0.5% NP-40. J. Leukoc. Biol. 55: 633–641; 1994.
Interferon-γ inhibits tumor antigen presentation by epidermal antigen-presenting cells
Authors: Grabbe Stephan , Bruvers Sandra , Beissert Stefan , Granstein Richard D 
Published: January 2018

Abstract
Murine I-A+ epidermal antigen-presenting cells (APGs) have been shown to be capable of presenting soluble tumor fragments (TFs), as a source of tumor-associated antigens (TAAs), for primary and secondary tumor immune responses. In this study we investigated whether incubation of epidermal APCs in interferon-7 (IFN-γ) modulates their ability to present TAA and whether the effects of IFN-γ on the presentation of tumor antigen correspond to its effects on alloantigen presentation in both primed and unprimed systems. Our results show that three weekly subcutaneous injections of naive mice with GM-CSF-cultured but not with fresh TAA-pulsed epidermal APCs induce protective tumor immunity in naive mice and that the immunostimulatory effect of GM-CSF in this system is abrogated by coculture of epidermal cells in IFN–γ. Furthermore, epidermal APCs are able to present TAA to primed, tumor-immune mice, as assessed by the elicitation of tumor-specific delayed-type hypersensitivity after injection of TAA-pulsed epidermal APCs. IFN–γ was found to inhibit tumor antigen presentation by freshly prepared epidermal APCs in this system. The effects of IFN–γ on the presentation of tumor antigen correlated well with its effects on the primary and secondary mixed epidermal cell-lymphocyte reaction, indicating that IFN–γ differentially modulates the function of epidermal APCs with regard to induction versus elicitation of immunity. J. Lcukoc. Biol. 55: 695–701; 1994.
Blockade of liver macrophages by gadolinium chloride reduces lethality in endotoxemic rats—analysis of mechanisms of lethality in endotoxemia
Authors: Iimuro Yuji , Yamamoto Masayuki , Kohno Hiroshi , Itakura Jun , Fujii Hideki , Matsumoto Yoshiro 
Published: January 2018

Abstract
We investigated the effects of gadolinium chloride (GdCl3 · 6H2O), which blocks phagocytosis by liver macrophages, on the mortality, blood tumor necrosis factor (TNF) levels, and hepatotoxicity in a lethal endotoxic shock rat model system [10 mg/kg body weight lipopolysaccharide (LPS) intravenously]. With administration of GdCl3, twice at 0.5 or 5 mg/kg, the survival rate 24 h after LPS injection was 56% and 100%, respectively, whereas the level of TNF in blood was not affected. Microscopic investigation of the liver revealed that the focal necrosis of hepatocytes under endotoxemia was completely protected by the administration of GdCl3 at 5 mg/kg. We then investigated the effects of GdCl3 on superoxide (O2) production by isolated liver macrophages in vitro. The O2- production by liver macrophages isolated from control rats was suppressed by GdCl3 in a dose-dependent manner. GdCl3 also had a cytotoxic effect on these macrophages. The enhanced O2- production by liver macrophages isolated from sublethal endotoxemic (1 mg/kg) rats was suppressed by pretreatment with GdCl3 (5 mg/kg). It was suggested that lethality in endotoxemia cannot be explained only by the degree of increase in blood TNF levels and that the mechanism by which GdCl3 reduces mortality and hepatotoxicity in endotoxemia possibly includes suppression of superoxide production by liver macrophages. J. Leukoc. Biol. 55: 723–728; 1994.
Macrophage precursor cells produce perforin and perform Yac-1 lytic activity in response to stimulation with interleukin-2
Authors: Li Hao , Pohler Uwe , Strehlow Inga , Hertig Sylvie , Baccarini Manuela , Emmendörffer Andreas , Tschopp Jürg , Lohmann-Matthes Marie-Luise 
Published: January 2018

Abstract
Macrophage precursor cells, derived from mouse bone marrow culture with granulocyte-macrophage colony-stimulating factor or colony-stimulating factor 1 (CSF-1) as growth factor and interleukin-2 (IL-2) as stimulating factor, were activated by IL-2 to exert strong cytolytic activity against Yac-1 cells. In response to IL-2 stimulation these bone marrow macrophage precursor cells produced perforin as lytic molecules. The purity of the precursor cells for the study was proved as homogeneous positivity for Mac-1, NK-1.1 and negativity for Lyt 1 and 2. The cells express CSF-1 receptors on their surface, are able to proliferate and differentiate into typical macrophages when stimulated with CSF-1, and are therefore members of the macrophage lineage. Perforin transcripts were identified by Northern blot analysis of IL-2–treated macrophage precursor cells, and the presence of perforin protein in the cytoplasmic granules was demonstrated by immunhistochemical staining using a monoclonal antiperforin antibody. In addition, the biological activity of the perforin contained in the macrophage precursor’s granules could be documented as calcium-dependent lytic activity using Yac-1 and sheep red blood cells as targets. The results presented in this paper imply the existence of a bipotent precursor cell, which can mature into a typical macrophage if CSF-1 or phorbol 12-myristate 13-acetate is supplied as differentiation stimulating factor but develops into an NK/LAK cell when early activation with IL-2 is provided. J. Leukoc. Biol. 56: 117–123; 1994.
Analysis of human cytomegalovirus-infected peripheral blood mononuclear cells from infants with liver dysfunction by flow cytometry and the polymerase chain reaction
Authors: Numazaki Kei , Asanuma Hideomi , Nagata Nobuo , Chiba Shunzo 
Published: January 2018

Abstract
Perinatal human cytomegalovirus (HCMV) infection often involves the hepatobiliary tract, but infected individuals usually remain asymptomatic. We investigated the role of CD8+ lymphocytes in 13 infants with liver dysfunction associated with perinatal HCMV infection. In three patients more than 40% of CD8+ cells were positive for HCMV immediate early antigen (IEA) and late antigen (LA) by flow cytometry after selection of T lymphocytes subpopulations. In the other 10 infants, 20% to 30% of CD8+ cells were positive for HCMV IE A and LA. HCMV IE DNA was detected in CD8+ cells from one infant, in CD4+ cells from one infant, and in both CD4+ and CD8+ cells from three infants. HCMV infection of CD8+ cells may play an important role in the process of perinatal primary infection. J. Leukoc. Biol. 56: 187–191; 1994.
Tropism for primary monocytes and for monocytoid cell lines are separate features of HIV-1 variants
Authors: Valentin Antonio , Nilsson Kenneth , åsjö Birgitta 
Published: January 2018

Abstract
We have analyzed the phenotype of five human monocytoid cell lines (U-937, THP-1, RC.2A, Mono Mac 6, and DD) and their capacity to support replication of HIV-1 strains with known tropism for T lymphocytes and mononuclear phagocytes. HIV-1Ba-L, a prototype monocytotropic HIV-1 strain, was unable to establish continuous replication in any of the cell lines used. In contrast, the lymphotropic strain IIIB could replicate in all CD4-positive cell lines. We conclude that the capacity of HIV-1 isolates to replicate in established human monocytoid malignant cells does not correlate with the tropism of the virus for primary mononuclear phagocytes. Since monocytoid cell lines do not distinguish HIV-1 variants tropic for mononuclear phagocytes, we suggest the use of primary cells for studies of HIV-1 tropism. J. Lcukoc. Biol. 56: 225–229; 1994.
Endotoxin stimulates the expression of glucose-6-phosphate dehydrogenase in Kupffer and hepatic endothelial cells
Authors: Spolarics Zoltán , Navarro Lan 
Published: January 2018

Abstract
The aim of the study was to elucidate the effect of lipopolysaccharide (LPS) administration in vivo (Escherichia coli endotoxin, 1 mg/kg body weight) on the expression and cellular activity of glucose-6-phosphate dehydrogenase (G6PDH, EC 1.1.1.49), the rate-limiting enzyme of the hexose monophosphate shunt in hepatic cells. Under basal conditions, Kupffer cells displayed higher activity of G6PDH than endothelial or parenchymal cells. In vivo LPS treatments for 7 and 22 h resulted in 40 and 60% increases, respectively, in the cellular activity of G6PDH in Kupffer cells. G6PDH activity was increased by 140 and 90% after 7- and 22-h LPS treatments in endothelial cells. G6PDH activity in parenchymal cells prepared from animals after 22 h of LPS treatment was decreased by approximately 60% compared with that in cells from saline-injected animals. Total cellular RNA or protein extracts from these cells were analyzed by Northern or Western blots. Under basal conditions, G6PDH mRNA levels relative to total cellular RNA were higher in Kupffer than in endothelial cells and were not detectable in parenchymal cells. LPS injection caused a time-dependent increase in G6PDH mRNA expression in Kupffer and endothelial cells. Western blot analysis of Kupffer cell extracts also showed that LPS treatments cause markedly elevated expression of protein in these cells. These results show that endotoxemia results in marked induction of G6PDH in Kupffer and hepatic endothelial cells but has no such effect in the parenchymal cells. These findings also suggest that the elevated cellular expression of G6PDH is an important regulatory event in the adaptive responses of hepatic nonparenchymal cells to infections. The elevated expression of G6PDH may be important for support of the upregulated NADPH-dependent pathways, such as superoxide anion and nitric oxide production, macromolecular synthesis, or the maintenance of cellular glutathione status. J. Leukoc. Biol. 56: 453–457; 1994.
Costimulatory receptors for the superantigen staphylococcal enterotoxin B on human vascular endothelial cells and T cells
Authors: Krakauer Teresa 
Published: January 2018

Abstract
Cell-surface molecules on human vascular endothelial cells (ECs) and T lymphocytes that mediate staphylococcal enterotoxin B (SEB)-induced T cell proliferation and cytokine production were investigated. Expression of HLA-DR and intercellular adhesion molecule 1 (ICAM-1) on EC was induced by interferon-7 (IFN-γ). IFN-γ-treated ECs bound SEB effectively and stimulated T cells to proliferate and secrete tumor necrosis factor α (TNF-α) and IFN-γ. SEB-induced T cell proliferation was inhibited by monoclonal antibodies to CD2, CD11a, CD28, ICAM-1, and endothelial leukocyte adhesion molecule (ELAM). These antibodies also blocked production of the proinflammatory mediators, TNF-α and IFN-γ, in SEB-stimulated T cell-EC cocultures. These results suggest that the surface molecules, CD11a:CD18/ICAM-1, CD2, CD28, and ELAM, are all important costimulatory receptors for T cell activation by superantigens with the EC as the antigen-presenting cell. Thus, like conventional antigens, multiple stimulatory signals from the interactions of these receptors are required for superantigen-induced immune responses with ECs and T cells. Reducing proinflammatory mediators such as TNF-α and IFN-γ by these antibodies in SEB-induced T cell responses may be a useful therapeutic strategy for circumventing SEB toxicity and pathogenesis. J. Leukoc. Biol. 56: 458–463; 1994.
Pulmonary surfactant lipids inhibit prostanoid production of guinea pig alveolar macrophages
Authors: Földes-Filep éva , Sirois Pierre , Filep János G 
Published: January 2018

Abstract
Changes in the amount and composition of pulmonary surfactant are important features of the adult respiratory distress syndrome. The goal of the present study was to investigate the effects of natural surfactant material and several of its lipid components on prostanoid production and superoxide generation by guinea pig alveolar macrophages. Natural surfactant (10–500 μg/ml) inhibited (up to 65%) prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) production elicited by platelet-activating factor (PAF, 10-6 M) and arachidonic acid (5 10-6 M) but not fMet-Leu-Phe (10-7 M). Dioleyl-phosphatidylglycerol (diOPG, 1–100 μg/ml) and dioleyl-phosphatidylcholine (diOPC, 1–100 μg/ml) prevented fMet-Leu-Phe- and PAF-stimulated prostanoid release in a concentration-dependent fashion with a maximal inhibition of 94%. DiOPC (100 μg/ml) also inhibited arachidonic acid induced PGE2 production by 67%. Phosphatidylcholine (100 μg/ml) and sphingomyelin (10–100 μg/ml) significantly attenuated TxB2 production elicited by arachidonic acid. Neither PAF- nor fMet-Leu-Phe-stimulated superoxide production was affected significantly by natural surfactant and its lipid components with the exception of phosphatidylcholine. At a concentration of 100 μg/ml, phosphatidylcholine decreased superoxide production by about 57% in response to PAF. These results show that diOPC and diOPG are capable of inhibiting prostanoid production of guinea pig alveolar macrophages in response to inflammatory stimuli and suggest that a decrease in the diOPG and diOPC content of surfactant would lead to enhanced intrapulmonary formation of prostanoids and consequently to the deterioration of pulmonary function in the adult respiratory distress syndrome. J. Leukoc. Biol. 56: 475–480; 1994.