bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expansion of the liver-associated macrophage system in systemic lupus erythematosus-prone NZB/W mice
Authors: Emmendörffer Andreas , Müller Meike , Wedekind Dirk , Hartung Klaus , Lohmann-Matthes Marie-Luise 
Published: January 2018

Abstract
Systemic lupus erythematosus is characterized by profound changes of the immune system. We report on alterations of the macrophage system in the murine NZB/W model of this disease. A greatly increased number of mature macrophages was isolated from the liver of NZB/W mice as compared to BALB/c mice and several other inbred strains used as healthy controls. In addition, the macrophage precursor compartment in the liver of NZB/W mice was expanded severalfold as measured by proliferation of light-fraction nonadherent nonparen-chymal cells (NPCs) in response to colony-stimulating factors. Functional properties of the macrophages isolated from various anatomic sites of the lupus-prone mice were tested. Production of monokines by macrophages from liver, spleen, and peritoneal cavity, calculated on a per cell basis, was in the same range as in several healthy control strains tested. Yet the overall production of these immunregulatory molecules by the increased liver macrophage system, the body’s largest compartment of macrophages, is likely to result in increased levels of circulating monokines in the plasma of lupus-prone NZB/W mice. Indeed, significantly elevated levels of interleuldn-6, in-terleukin-1, and colony-stimulating activity could be demonstrated in the plasma of these mice both spontaneously and after stimulation with lipopolysaccharide. A possible contribution of the expansion of the macrophage system to the development of the disease is discussed. J. Leukoc. Biol. 53: 294–300; 1993.
Location of the domains of ICAM-1 by immunolabeling and single-molecule electron microscopy
Authors: Kirchhausen Tomas , Staunton Donald E , Springert Timothy A 
Published: January 2018

Abstract
Intercellular adhesion molecule 1 (ICAM-1), a member of the immunoglobulin gene superfamily, is a cell surface glycoprotein with an extracellular domain comprising five immunoglobulin-like domains. Soluble ICAM-1, a recombinant protein truncated at the transmembrane domain, has a rod-like shape, 19 nm long overall, with a characteristic bend 7.6 nm from one end of the molecule. Because the link between domain D2 and domain D3 is proline rich, it has been proposed that the short arm contains domains D1 and D2 and the long arm contains domains D3-D5. We used single-molecule electron microscopy of soluble ICAM-1 decorated with monoclonal antibodies specific for domains D1 and D4 to show that the bend instead lies between domains D3 and D4. Therefore, the short arm lies closer to the plasma membrane, whereas the long arm, containing all the known ligand binding sites on ICAM-1, is positioned toward the target cell surface. J. Leukoc. Biol. 53: 342–346; 1993.
Characterization of a human monocyte antigen, B148.4, regulated during cell differentiation and activation
Authors: Anegón Ignacio , Blottier Hervé , Cuturi Maria Cristina , Lenne Wonne , Trinchieri Giorgio , Faust Jeffrey , Perussia Bice 
Published: January 2018

Abstract
We analyzed the phenotypic changes associated with monocyte activation and differentiation using a newly developed monoclonal antibody (B148.4). Among peripheral blood leukocytes, the antigen recognized by this antibody is expressed on monocytes and granulocytes at high and low density, respectively. Antigen expression is lost during in vitro differentiation of monocytes and is absent on tissue macrophages, indicating that expression of this antigen is related to monocyte differentiation. Only la, 25-dihydroxyvitamin D3 and phorbol diesters, of several inducers tested, up-regulate B48.4 antigen expression on cells (monocytes and certain myeloid cell lines) that constitutively bear the antigen, without, however, allowing its maintenance during monocytic differentiation or inducing it on negative cells. By im- munoprecipitation from B148.4* U937 cells, the antigen is a complex of a major 116-kd and two minor 38- and 46-kd molecules. Analysis of eight different tissues reveals that the antigen is shared with endothelial cells. Biochemical characteristics, cellular distribution, and expression pattern on monocytes, myeloid cell lines, and AML cells upon culture with different stimuli indicate that B148.4 is a novel monocyte differentiation antigen. J. Leukoc. Biol. 53: 390–398; 1993.
Diminished transcription of interleukin-8 by monocytes from preterm neonates
Authors: Schibler Kurt R , Trautman Michael S , Liechty Kenneth W , White William L , Rothstein Gerald , Christensen Robert D 
Published: January 2018

Abstract
Developmental delays, which impair antibacterial host defense, are present in the neutrophil system of human preterm neonates. We hypothesized that diminished production of interleukin-8 (IL-8), a neutrophil chemotactic peptide, might in part be responsible for these defects. To test this, monocytes from the blood of preterm neonates, term neonates, and adults were isolated immunologically by “negative panning” and subsequently stimulated with interleukin-1α (IL-lα), tumor necrosis factor a (TNF-α), or lipopolysaccharide (LPS), after which IL-8 levels in the supernatants were measured by ELISA. Total cellular RNA was extracted and IL-8 mRNA was assessed by Northern blotting and by competitive polymerase chain reaction (PCR) analyses. After stimulation with IL-lα, IL-8 accumulation was lowest in supernatants of monocytes from preterm neonates, intermediate in supernatants of monocytes from term neonates and greatest from monocytes of adults. Similarly, when stimulated with TNF-α or LPS, monocytes from preterm neonates produced less IL-8 than cells from term neonates and adults. These differences in IL-8 concentrations paralleled differences in IL-8 mRNA expression. J. Leukoc. Biol. 53: 399–403; 1993.
Human neutrophil adhesion to bovine aortic endothelium. Evidence for endothelial lipoxygenase activity
Authors: Damtew Belai , Goldsmith George , Tserng Koy-Yi , Spagnuolo Philip J 
Published: January 2018

Abstract
We examined the effect of phorbol myristate acetate on cultured bovine aortic endothelial cells to determine the role of endothelial cells in neutrophil-endothelial cell adhesive interactions. Confluent endothelial cells were preincubated with phorbol myristate acetate and other inflammatory signals including JV-formylmethionyl- leucyl-phenylalanine (f-Met-Leu-Phe), the ionophore A23187, and thrombin; washed extensively; and incubated with 51Cr-labeled neutrophils. Preincubation of endothelium with A23187, phorbol ester, or thrombin increased adherence of neutrophils by 3.1-, 5.7-, and 3.7-fold over baseline. In contrast, f-Met-Leu-Phe preincubation failed to increase adhesion over baseline. Supernatants from endothelium preincubated with phorbol failed to augment adherence of untreated endothelial cells. Preincubation of endothelium with lipoxygenase inhibitors nordihydroguaiaretic acid (50μM), 5,8,11,14-eicosatetraenoic acid (50 μM), and BW755C (50 μM) inhibited the effect of phorbol preincubation of endothelium significantly by 55, 27, and 22%, respectively. In contrast, inhibitors of cyclooxygenase and thromboxane synthase or thromboxane receptor antagonists had no effect on phorbol-induced adhesion. Specific desensitization of neutrophil adhesion to phorbol-treated endothelium could be demonstrated by prior exposure of neutrophils to low concentrations of leukotriene B4 (3.8 × 10−10 M). Endothelium preincubated with phorbol but not f-Met-Leu-Phe or thrombin produced several fatty acid peaks at 280 nm, one of which comigrated with authentic leukotriene B4 (LTB4). This peak, isolated and purified, increased endothelial cell adherence in a temporal fashion in the same way as LTB4 and was demonstrated to be LTB4 by ultraviolet spectroscopy, high- performance liquid chromatography, and mass spectroscopy. These data demonstrate that endothelial cell-derived lipoxygenase metabolites, in particular LTB4, are involved, in part, in the acute regulation of neutrophil adhesion to endothelium induced by inflammatory signals such as phorbol ester. J. Leukoc. Biol. 53: 619–629; 1993.
Failure to establish long-term marrow cultures from immunodeficient mice (MAIDS): effect of zidovudine in vitro
Authors: Tse Kam-Fai , Hughes Nedda K , Gallicchio Vincent S 
Published: January 2018

Abstract
We report here the results of studies examining the ability of zidovudine (AZT) to influence the establishment and maintenance of long-term marrow cultures (LTMG) using marrow from murine immunodeficient mice (MAIDS). Normal C57BL6 mice were infected with LP-BM5 (MuLV) immunodeficiency virus (10μg total protein) intraperitoneally. Five weeks after viral infection, mice were sacrificed and marrow was harvested from normal non-virus-infected and virus-infected animals. LTMC were established in the presence or absence of dose escalation of AZT, that is, 10−6, 5 × 10−7, and 10−7 M in vitro. Compared with controls prepared from normal bone marrow, LTMC using MAIDS-infected marrow failed to establish and subsequently release supernatant-derived mononuclear cells. The addition of AZT was ineffective in either establishing LTMC or consistently producing mononuclear cells. Measurements of erythroid (BFU-E), myeloid (CFU-GM), and megakaryocyte (CFU-Meg) precursors were all depressed and none were observed after 5 weeks of culture. Treatment with AZT failed to reverse this depression of stem cell progenitors. Microscopic examination of cultures at 10 weeks demonstrated a failure of MAIDS-LTMC to establish an adequate stromal layer compared to LTMC prepared form non-virus-infected controls. This data indicate that LP-BM5 MuLV infection alters the establishment of a normal functioning hematopoietic microenvironment or stroma. Acknowledging that important differences between MAIDS and human AIDS exist, the implications of these findings concerning the establishment of the immunodeficiency disease state in human immunodeficiency virus infection is discussed. J. Leukoc. Biol. 53: 658–665; 1993.
Enhancement in vitro of the low interferon-γ production of leukocytes from human newborn infants
Authors: McKenzie Steven E , Kline Jane , Douglas Steven D , Polin Richard A 
Published: January 2018

Abstract
Interferon-γ (IFN-γ), a lymphokine produced by lymphocytes with the help of monocytes, is essential for host resistance to intracellular pathogens. Leukocytes from normal term newborn infants cannot produce IFN-γ in vitro in response to stimulation by antigen or mitogens in vitro or in vivo. We investigated the production of IFN-γ in vitro using endotoxin from Salmonella typhimurium as a stimulus. In contrast to those from adults, mononuclear cells derived from the cord blood of newborn infants did not produce IFN-γ in response to this endotoxin. We investigated the contribution of the functional immaturity of cord blood monocytes to this relative inability to produce IFN-γ. Aging of the monocytes for 2 weeks in vitro or treatment of freshly isolated cord blood monocytes with conditioned medium (from cultures of mononuclear cells from healthy adults) greatly enhanced IFN-γ production stimulated by endotoxin. Furthermore, recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony- stimulating factor (M-CSF), or IFN-γ was able to substitute in part for the conditioned medium from adult cells. Thus correction of the functional immaturity of monocytes derived from newborn infants can result in enhanced production of IFN-γ in vitro. J. Leukoc. Biol. 53: 691–696; 1993.
Uniform detection of HIV-1 in alveolar macrophages of pediatric but not adult AIDS patients
Authors: Pearce Tillman E , Nowakowski Maja , Eden Edward , Huang Zheng-Bo , Steiner Phillip , Shahabuddin Muhammad , Potash Mary Jane , Volsky David J 
Published: January 2018

Abstract
Manifestations of pulmonary disease in pediatric AIDS patients differ from those in adults. To evaluate whether differences in the frequency of alveolar macrophage (AM) infection with human immunodeficiency virus type 1 (HIV-1) could account for these clinical distinctions, we undertook a comparative analysis of HIV-1 DNA in AMs from pediatric and adult AIDS patients by enzymatic amplification. A higher frequency of viral DNA detection in pediatric cases (100%) compared with adults (67%) was observed. The sensitivity of detection was 1 viral DNA copy per 4000 AMs; matched peripheral blood mononuclear cells from six of seven pediatric and eight of nine adult patients tested HIV-1 DNA positive. Adult but not pediatric patients exhibited a marked alveolar lymphocytosis, 32% mean lymphocyte count compared with 7.0%, respectively. These results suggest that the burden of HIV-1 in the lungs of pediatric AIDS patients is greater than that in adults. J. Leukoc. Biol. 53: 722–726; 1993.
Characterization of a 64-kd protein phosphorylated during chemotactic activation with IL-8 and fMLP of human polymorphonuclear leukocytes. I. Phosphorylation of a 64-kd protein and other proteins
Authors: Shibata Michio , Ohoka Tadakazu , Mizuno Satoshi , Suzuki Kazuo 
Published: January 2018

Abstract
Interleukin-8 (IL-8) such as LUCT (lung giant cell carcinoma-derived chemotactic protein), NAP (neutrophil activating protein) and MDNCF (monocyte- derived neutrophil chemotactic factor), and formylmethionyl- leucyl-phenylalanine (fMLP) are well-known chemoattractants for human polymorphonuclear leukocytes (PMNs) and are able to stimulate phosphorylation of 64-kd protein (p64) in these leukocytes. To elucidate the molecular mechanism of PMN activation with chemoattractants, we investigated the phosphorylation process of p64 in an intact cell. 32P-Labeled PMNs were stimulated with LUCT/IL-8, fMLP, leukotriene B4, or C5a, and phosphorylated proteins were analyzed by two-dimensional electrophoresis and autoradiography. A marked phosphorylation of p64 was observed after stimulation. A new spot of phosphorylated p64 (pp64) could be detected on the gel stained with Coomassie Brilliant Blue, indicating that the isoelectric point (pI) of p64 shifted from 5.3 to a more acidic pI by the phosphorylation forming pp64. The spot of pp64 was shown to be dephosphorylated to p64 by treatment with calf intestine alkaline phosphatase. Other proteins having molecular masses 82, 66, 58, 55 and 50 kd were also phosphorylated. The fMLP- stimulated phosphorylation was time-dependent and saturated within 5 min. Maximum stimulation was achieved with 10 nM fMLP. Phosphoamino acid analysis revealed phosphorylation of serine residues in pp64. Staurosporine (100 nM) and W-7 (100 μΜ) significantly inhibited the phosphorylation of p64, but H-7 slightly inhibited it. H-8 and herbimycin A did not effect phosphorylation. Phorbol myristate acetate was found to stimulate significantly. Protein kinase C did not stimulate the phosphorylation. These data suggest that protein kinase C and calmodulin-like protein are indirectly involved in the phosphorylation of p64 during chemoattractant-activation of PMN.
Retinoic acid inhibits interleukin-1-induced cytokine synthesis in human monocytes
Authors: Gross Volker , Villiger Peter M , Zhang Baoping , Lotz Martin 
Published: January 2018

Abstract
Retinoids are pluripotent morphogens whose effects on gene expression are mediated through specific intracellular receptors. They have certain anti-inflammatory effects in vivo, the basis of which is not clearly understood. To characterize mechanisms involved with potential anti-inflammatory actions of retinoids, we studied the effects of retinoic acid (RA) on cytokine production in human peripheral blood monocytes. RA differentially modulated the expression of interleukin-1β (IL-10), IL-6, and IL-8 mRNAs depending on the inducing stimulus. While phorbol myristate acetate-induced IL-lβ and IL-8 mRNA expression was increased by RA (IL-6 could not be induced by this pathway in monocytes), IL-lβ-induced expression of IL-1β and IL-8 was markedly reduced and IL-6 gene expression was almost completely suppressed. Lipopolysaccharide (LPS)-induced cytokine synthesis was only slightly reduced and this required a longer preincubation (&gt; 72 h) of monocytes with RA. IL-l-induced de novo synthesis of IL-6 protein and secretion of biologically active IL-6 were also inhibited by RA. The inhibition pattern of RA was different from that of dexamethasone, which inhibited both IL-1 and LPS effects. In summary, our data show that RA regulates monocyte cytokine expression selectively in response to the particular stimuli. Inhibition of IL-lβ-induced cytokine expression provides a mechanism that can explain some of the anti-inflammatory effects of RA.
Immune changes in test animals during spaceflight
Authors: Lesnyak A T , Sonnenfeld G , Rykova M P , Meshkov D O , Mastro A , Konstantinova I 
Published: January 2018

Abstract
Over the past two decades, it has become apparent that changes in immune parameters occur in cosmonauts and astronauts after spaceflight. Therefore, interest has been generated in the use of animal surrogates to better understand the nature and extent of these changes, the mechanism of these changes, and to allow the possible development of countermeasures. Among the changes noted in animals after spaceflight are alterations in lymphocytic blastogenesis, cytokine function, natural killer cell activity, and colony-stimulating factors. The nature and significance of spaceflight-induced changes in immune responses will be the focus of this review.
Autocrine amplification of PAF-acether formation in immunologically activated murine macrophages
Authors: Ninio Ewa , Maiza Hassina , Bidault Jocelyne 
Published: January 2018

Abstract
When murine macrophages activated in vivo with bacille Calmette-Guérin were triggered with either acetyl-CoA or propionyl-CoA to form PAF-acether (PAF), similar amounts of platelet-aggregating product were recovered. Liquid chromatographic purification and reversed-phase analysis showed that the composition of PAF molecular species formed in the presence of acetyl- CoA was an equimolar mixture of PAF bearing Cl 6:0 alkyl chain (57% ± 7, mean ± SD, n = 3) and PAF Cl8:1. The PAF-like material obtained from the propionyl-CoA- supplemented macrophages was a mixture of the propi- onyl analogue of PAF (66% ± 11, n = 3) and native PAF. The rate of lyso-PAF:acetyl-CoA acetyltransferase (EC 2.3.1.67) reaction in a macrophage lysate was similar for either substrate in the presence of an equimolar mixture of propionyl-CoA and acetyl-CoA. We conclude that the exogenously added propionyl-CoA is transferred to lyso- PAF acceptor to form propionyl-PAF by the PAF-forming acetyltransferase. Propionyl-PAF triggers the formation of native PAF probably from the endogenous acetyl-CoA pool. Two specific PAF antagonists, BN 52021 (60 μΜ) and WEB 2086 (3 μΜ), did not influence the rate of PAF synthesis in the presence of either acetyl-CoA or pro- pionyl-CoA and did not prevent native PAF formation when propionyl-CoA was added alone, suggesting that the classical PAF receptors are not involved. This is the first description of a possible mechanism of autocrine amplification of PAF biosynthesis in macrophages.
Modulation of the cytoskeleton and intracellular calcium in leukocytes exhibiting a cancer-associated chemotaxis defect
Authors: Janeczek A H , van Alten P J , Reyes H M , Walter R J 
Published: January 2018

Abstract
Monocyte chemotaxis is severely depressed in patients with advanced tumors, but the cellular basis for this chemotactic defect is not known. Because the ac- tomyosin cytoskeleton is thought to play a primary role in chemotaxis, we have employed flow cytometry to examine several aspects of the contractile machinery including myosin II, myosin light chain kinase (MLCK), actin, and cytoplasmic calcium in unstimulated and in formylpeptide- stimulated neutrophils and monocytes. Serum-pretreated polymorphonuclear leukocytes (PMNs) and monocytes from healthy blood donors or PMNs and monocytes isolated from tumor patients were studied. Leukocytes pretreated with serum from cancer patients exhibited decreased baseline myosin staining and a vastly different response to formylpeptide stimulation compared with leukocytes pretreated with normal human serum. In contrast, similar amounts of MLCK were observed in neutrophils and monocytes preincubated with normal or cancer serum with or without stimulation with formylpeptide. The fluorescent calcium indicator fluo-3 showed that resting and fMLP-stimulated levels of intracellular calcium were not significantly different in control and cancer serum-pretreated human leukocytes or in leukocytes isolated from tumor patients. Similarly, resting and fMLP-stimulated levels of F-actin in cancer patients’ leukocytes as assessed by NBD-phallacidin staining did not differ significantly from those of normal leukocytes. Because the actomyosin cytoskeleton is intricately involved in leukocyte chemotaxis, alterations in the cytoskeleton may dramatically affect cell motility. The cytoskeletal alterations and changes in the response of leukocytes pretreated with cancer patients’ serum to formylpeptide stimulation as described here may result in decreased chemotaxis by these cells.
Lipopolysaccharide structure-function relationship in activation versus reprogramming of mouse peritoneal macrophages
Authors: Zhang Xiaoke , Morrison David C 
Published: January 2018

Abstract
Lipopolysaccharide (LPS) is one of the most potent stimuli for macrophages. The activities of LPS have been attributed to the lipid A region of the molecule. We have previously shown that pretreatment of macrophages with very low doses of LPS can selectively “reprogram” these cells to respond differentially to subsequent activation, as assessed by tumor necrosis factor-α and nitric oxide (NO) production. Here we demonstrate that the relative capacity of various LPS preparations for induction of down-regulation of subsequent LPS-activated NO production correlates well with their relative potency for initiation of NO formation. Although LPS-dependent activation can be regulated by a pertussis toxin (PT)-sen- sitive factor, the LPS pretreatment-induced reprogramming is shown here to be refractory to regulation by PT. These results suggest that, although the structural components of LPS dictating the relative activities of the molecule for activation versus reprogramming are similar, there may exist different pathways in initiation of LPS-induced activation versus reprogramming.
Soluble FCγ receptors
Authors: Fridman Wolf H , Teillaud Jean-Luc , Bouchard Caroline , Teillaud Christophe , Astier Anne , Tartour Eric , Galon Jerome , Mathiot Claire , Sautes Catherine 
Published: January 2018

Abstract
Soluble FCγ receptors have been identified in biological fluids of mice and humans. They are produced either by alternative splicing of the exon encoding the transmembrane region of the receptor (FcγRII) or by proteolytic cleavage at the cell membrane (FCγRII and FC7RIII). They inhibit B cell proliferation and immunoglobulin production. Their concentrations in plasma seem to be modified during the development of certain diseases, as for instance in multiple myeloma, where plasma concentrations oi soluble FCγKIll are correlated with the stage of the disease.