bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of transforming growth factor-beta and prostaglandin E2 production by ethanol in human monocytes
Authors: Szabo Gyongyi , Verma Bikash K , Fogarasi Miklos , Catalano Donna E 
Published: January 2018

Abstract
To test our hypothesis that monocytes (MØ) and their mediators are major contributors to ethanol- related immunodepression, the modulating capacity of acute ethanol treatment was assessed on the production of transforming growth factor-beta (TGFβ) and prostaglandin E2 (PGE2) by human peripheral blood MØ. We demonstrate that acute in vitro treatment of adherent MO with either 50 or 150 mM ethanol induced a significant increase in the production of TGFβ (P &lt; 0.045 and β &lt; 0.001, respectively). Furthermore, MØ pretreatment with both 50 and 150 mM ethanol augmented TGFjS production in response to subsequent stimulation with the synthetic bacterial analog, muramyl dipeptide (MDP) (P &lt; 0.05 and β &lt; 0.001, respectively). Ethanol also increased TGFØ production in interferon β (IFNβ)- activated MØ in response to MDP stimulus (P &lt; 0.05). MØ TGFβ levels, however, were always lower in IFNβ- activated than in non-IFNβ-activated MØ after the same stimulation with ethanol plus MDP, suggesting that MØ preactivation by IFN7 can partially counteract the TGFβ inducing potential of ethanol. Similar to its TGFβ - inducing potential, ethanol (150 mM) had the capacity to induce PGE2 production in adherent human MØ (P &lt; 0.045). However, ethanol failed to augment MØ PGE2 production induced by the PGE2 secretagogue, MDP. TGFjS induction by ethanol was unaffected by the presence of cyclooxygenase inhibitor, suggesting that ethanol-induced MØ TGFß production does not require MØ PG£2 production. These results indicate that ethanol is a potent inducer for inhibitory MØ mediators, TGFjS and PGE2, and also has the capacity to augment MØ TGFß production in response to subsequent stimulation. Thus, ethanol-induced elevation of MØ TGFß and PGE2 production might contribute to decreased β cell proliferation and abnormal MØ functions after alcohol exposure, resulting in a depressed immune response.
Fibronectin cell-binding domain triggered transmembrane signal transduction in human monocytes
Authors: Chang Zong-Liang , Beezhold Donald H , Personius Christine D , Shen Zong-Lu 
Published: January 2018

Abstract
Fibronectin (Fn) fragments have recently been shown to stimulate tumor necrosis factor (TNF) secretion by human monocytes. In this study, we investigated the signal transduction mechanisms involved in Fn-induced TNF secretion. Treatment of human monocytes with Fnl20, a chymotryptic cell-binding fragment of plasma Fn, failed to cause a detectable rise in Ca2+ mobilization. Fnl20-induced TNF secretion could be inhibited with Ca2+ channel blockers. The protein kinase C (PKC) inhibitors H-7 and sphingosine inhibited the TNF-inducing activity of Fnl20. HA1004 was used as a control for the isoquinoline sulfonamide derivatives and did not change Fnl20-induced TNF secretion by monocytes. H-8 inhibited TNF secretion at higher concentrations. A calmodulin-dependent kinase inhibitor, W-7, was found to be effective, with 50% inhibition of Fnl20-induced TNF secretion at 5 μM. The activation and translocation of PKC were measured directly. In unstimulated monocytes, approximately 70% of PKC activity was found in the cytosol and 30% in the membrane. Following the stimulation of monocytes with phorbol myristate acetate (100 nM), rapid and sustained translocation of PKC from the cytosol to the membrane was observed. The stimulation of monocytes with Fnl20 triggered a rapid translocation of PKC within 2 to 5 min, followed by a return to normal levels within 8 min. These findings support the conclusion that Fnl20-induced TNF secretion requires the activation of PKC. J. Leukoc. Biol. 53: 79–85; 1993.
MRP-8 and MRP-14, two abundant Ca2+-binding proteins of neutrophils and monocytes
Authors: Hessian Paul A , Edgeworth Jonathan , Hogg Nancy 
Published: January 2018

Abstract
Two calrium-binding proteins, named migration inhibitory factor-related proteins-8 (MRP-8) and MRP-14, are primarily expressed by circulating human neutrophils and monocytes. Evidence accumulating from the investigations of several independent groups is now leading to an improved understanding of the biology of these proteins. Both MRP-8 and MRP-14 display features characteristic of members of the S100 family of calciumbinding proteins. Some of these features predict functions for MRP-8 and MRP-14 but to date an exact and well-defined function remains elusive. Here we review the available information and highlight evidence that suggests the function of MRP-8 and MRP-14 may be associated with both monocyte and neutrophil activation and the accumulation of these cells in inflammatory sites. J. Leukoc. Biol. 53: 197–204; 1993.
Inhibition of interleukin-1 release and activity by the rat seminal vesicle protein SV-IV
Authors: Vuotto Maria Luisa , Peluso Gianfranco , Mancino Domenico , Colonna Giovanni , Facchiano Antonio , Lelpo Maria Teresa , Ravagnan Giampietro , Metafora Salvatore 
Published: January 2018

Abstract
SV-IV, a 9.8-kd protein isolated from rat seminal vesicle secretion, has been shown to have strong non-species-specific immunosuppressive, anti-inflammatory, antithrombotic, and antiphospholipase A2 properties. The present investigation was undertaken to determine the mechanism of action of its immunosuppressive effects. It was found that SV-IV is a potent inhibitor of interleukin-1 (EL-1) release from lipopolysaccharide (LPS)-activated human adherent monocytes and an effective inhibitor of ILrl-induced thymocyte proliferation. The ability of SV-IV to form a noncovalent dimeric association with IL-1α but not with IL-1β, its ability to induce a marked decrease of IL-1 binding to its own receptors on the thymocyte surface, and its capacity to bind specifically to the macrophage plasma membrane might play an important role in the molecular mechanism of these inhibitory effects. J. Leukoc. Biol. 53: 214–222; 1993.
Aspergillus fumigatus antigen induced eosinophilia in mice is abrogated by anti-IL-5 antibody
Authors: Murali Pazhayannur S , Kumar Anoopa , Choi Hongyung , Bansal Naveen K , Fink Jordan N , Kurup Viswanath P 
Published: January 2018

Abstract
A murine model of allergic bronchopulmonary aspergillosis (ABPA), developed by exposure to Aspergillus fumigatus antigens, demonstrated eosinophilia of peripheral blood (PB), bone marrow (BM), and lung. The eosinophilia was abrogated by monoclonal anti-inter-leukin-5 (IL-5) antibody (TRFK-5) and not by an isotype control antibody (GL 113). Eosinophils in PB were enumerated from stained smears and their relative increase or decrease in cells from BM and lung was determined by an eosinophil peroxidase (EPO) assay (measured in optical density). Intraperitoneal injection of TRFK-5 in mice exposed to A. fumigatus antigen produced a significant reduction in eosinophils (PB 6.6 ± 1.14% vs. 3.8 ± 0.8%, P&lt; .01) and EPO production in BM (0.935 ± 0.03 vs. 0.615 ± 0.02, P &lt; .001). A similar reduction in EPO production in the lung (0.691 ± 0.12 vs. 0.495 ± 0.05, not significant) was also reflected in the histopathol-ogy for the different groups of mice. These findings confirming the role of IL-5 in eosinophilia, although not surprising, are significant in elucidating the immu-nopathogenesis of ABPA in the murine model. We conclude that in this model, eosinophilia may be due largely to the Th2 cytokine -IL-5 induced by A. fumigatus antigens. J. Leukoc. Biol. 53: 264–267; 1993.
Affinity purification and subcellular localization of kinesin in human neutrophils
Authors: Rothwell Stephen W , Deal Carolyn C , Pinto Jay , Wright Daniel G 
Published: January 2018

Abstract
Studies of granule-microtubule interactions in human neutrophils have suggested that mechanochemical ATPases such as kinesin or dynein may play a role in granule mobilization during neutrophil activation by inflammatory signals. In this study we show that proteins extracted from the surface of neutrophil granules, found previously to contain microtubule-dependent ATPase activity, caused microtubules polymerized from phospho- cellulose-purified rat brain tubulin to move across glass slides. Antibodies were generated against peptides based on two regions of the amino acid sequence of Drosophila kinesin: the ATPase active site (amino acids 86-99) in the head of the kinesin heavy chain and the tail of the heavy chain (residues 913-933). These antibodies were found to recognize kinesin in rat brain extracts as well as kinesin- like polypeptides in extracts of human neutrophils. Furthermore, when used in immunoaflmity chromatography, these antibodies permitted the isolation of a protein from neutrophil granule extracts that was recognized by Drosophila kinesin antibodies. Subcellular localization by immunofluorescence microscopy showed this protein to be associated principally with the cytoplasmic granules of neutrophils. J. Leukoc. Biol. 53: 372–380; 1993.
Functional alterations of human neutrophils by medium-chain triglyceride emulsions: evaluation of phagocytosis, bacterial killing, and oxidative activity
Authors: Bellinati-Pires R , Waitzberg DL , Salgado MM , Carneiro-Sampaio MMS 
Published: January 2018

Abstract
Medium-chain triglyceride (MCT) and long- chain triglyceride (LCT) emulsions currently used in nutritional therapy were evaluated for their in vitro effect on neutrophil oxidative metabolism, phagocytosis, and bacterial killing activities. Neutrophils from healthy adult male volunteers were assessed after blood incubation with commercially available fat emulsions containing LCT, MCT, or a mixture of 50% MCT and 50% LCT at a final triglyceride concentration of 20 mg/ml. It was observed that MCT-containing emulsions stimulated nitroblue tetrazolium (NBT) dye reduction by neutrophils as determined by a cytochemical NBT test performed directly on whole blood. This effect was dose dependent. However, after lipid removal by cell washing, the MCT-treated neutrophils showed decreased production of hydrogen peroxide (H2O2) and NBT reduction in response to bacterial lipopolysaccharide or phorbol my- ristate acetate stimuli as well as impaired phagocytosis and killing of Staphylococcus aureus. In contrast, the LCT emulsion did not alter any of the neutrophil functions evaluated. The present data suggest that MCTs elicit the oxidative metabolism of neutrophils, probably by phagocytosis of fat particles and, depending on the lipid concentration, this effect may not be reversible, leading to impairment of the cellular response to subsequent membrane stimuli. J. Leukoc. Biol. 53: 404–410; 1993.
Polyunsaturated fatty acids increase neutrophil adherence and integrin receptor expression
Authors: Bates Edna J , Ferrante Antonio , Harvey Dianne R , Poulos Alt 
Published: January 2018

Abstract
Fish oils are abundant in polyunsaturated fatty acids of the n-3 series (in particular eicosapen- taenoic, 20:5 and docosahexaenoic acid, 22:6). Such fatty acids are generally considered to be beneficial in the prevention of cardiac disease and to have anti-inflammatory properties. Neutrophil adherence is an essential early event in an acute inflammatory response, and we have demonstrated that both 20:5 and 22:6 stimulate adherence in vitro. Arachidonic acid (20:4, n-6) was also stimulatory. Significant stimulation of adherence was seen from 5 to 80 μM (nontoxic concentrations) 22:6, 20:5, or 20:4. At the lower fatty acid concentrations tested (≤40 μM) 20:5 was less active than 22:6 or 20:4 at stimulating adherence. Above 40 μM there was no difference in the ability of the three fatty acids to stimulate adherence. At the lower fatty acid concentrations tested (≤10 μM) 22:6 was less active than 20:4, whereas above 10 μM they were equally active. Immunofluorescent flow cytometric analysis of neutrophil integrin (adherence) receptors showed that the complement G3bi receptor (GDI lb) was up-regulated by these fatty acids. There was no change in GDI la or GDllc. Saturated fatty acids of the same chain length were without effect on adherence or receptor expression. The findings suggest that these polyunsaturated fatty acids may, under certain conditions, be proinflammatory with respect to their acute effects on the interaction of neutrophils with microbes, endothelium, and other tissues. J. Leukoc. Biol. 53: 420–426; 1993.
Reconstitution of recombinant N-formyl chemotactic peptide receptor with G protein
Authors: Schreiber Ronda E , Prossnitz Eric R , Ye Richard D , Cochrane Charles G , Jesaitis Algirdas J , Bokoch Gary M 
Published: January 2018

Abstract
A recombinant human neutrophil N-formyl peptide receptor (rFPR) expressed in transfected mouse fibroblasts (TX2 cells) was analyzed for its ability to couple physically with the heterotrimeric G protein, Gi. Im- munoprecipitation of photoaffinity-labeled rFPR and endogenous neutrophil formyl peptide receptor (nFPR) with an anti-FPR peptide antibody demonstrated that the receptors were identical in both size and extent of glycosylation. Coupling of rFPR with endogenous TX2 Gi was demonstrated by coimmunoprecipitation of the two proteins with an anti-Gi antibody. Moreover, rFPR was able to form a physical complex with purified Gi in a soluble reconstitution system. We observed similar affinities of rFPR and nFPR for Gi. This report provides the first direct evidence that rFPR associates physically with Gi and provides a foundation for analysis of the G protein coupling capacity of mutant rFPRs. J. Leukoc. Biol. 53: 470–474; 1993.
Interactions of lipopolysaccharide with neutrophils in blood via CD14
Authors: Weingarten Ronald , Sklar Larry A , Mathison John C , Omidi Shadi , Ainsworth Teresa , Simon Scott , Ulevitch Richard J , Tobias Peter S 
Published: January 2018

Abstract
The functional characteristics of neutrophils are exceedingly sensitive to physiological conditions as well as the details of isolation. Exposure to lipopolysaccharide (LPS) or even contamination of the isolating media with traces of LPS is known to play an important role in regulating cell function and expression of receptors. Because of the suspected role of GD14 as a receptor for LPS, we used anti-CD14 monoclonal antibodies both to identify CD14 in the cell surface of polymorphonuclear leukocytes and to inhibit functional changes elicited by LPS. Cytometric techniques were used to investigate the regulation of CD14 and CR3 on the neutrophil cell surface in whole blood to minimize any effects of isolation. In whole blood neutrophils express low levels of formyl peptide receptor, CD14, and CR3, which increase substantially in response to formyl peptide and LPS. The increases in CR3 and CD14 occurred in parallel and were independent of protein synthesis and tumor necrosis factor (TNF) production. The increase in CR3 was inhibited by antibodies MY4, 3C10, and 28C5 against CD14. These findings are consistent with the notion that in blood the observed receptor up-regulation is in direct response to the action of LPS on neutrophils through CD14 and does not require products from macrophages such as TNF or the production of C5a from the plasma. J. Leukoc. Biol. 53: 518–524; 1993.
An immunohistologic study of granulomatous inflammation in SIV-infected rhesus monkeys
Authors: Horvath Christopher J , Hunt Ronald D , Simon Meredith A , Sehgal Prabhat K , Ringler Douglas J 
Published: January 2018

Abstract
We studied granulomatous inflammation in simian AIDS using histologic, immunohistologic, and in situ hybridization techniques. Complete Freund’s adjuvant was used to induce granulomas in two control animals and two macaques infected with simian immunodeficiency virus (SIV) and having low peripheral CD4+ T cell counts. Control animals developed large (&gt;2 cm diameter) epithelioid granulomas containing CD68+ macrophages (mφs), epithelioid mφs and multinucleated giant cells (MNGCs), CD4+ and CD8+ T cells, and small perivascular collections of CD20+ B cells. Lymphocytes rarely expressed proliferating cell nuclear antigen (Ki-67), and only rare endothelial cells expressed vascular cell adhesion molecule 1 (VCAM-1). In contrast, SIV+ animals had smaller (&lt;0.5 cm diameter) epithelioid granulomas characterized by numerous large, dense CD8+, CD20+ lymphocyte aggregates with prominent local division (Ki-67+). Despite low blood CD4+ T cell numbers, there was a substantial CD4+ T cell infiltrate, accompanied by enhanced endothelial VCAM-1 expression. These granulomas contained no detectable SIV antigen or RNA. Thus, in simian AIDS, experimentally induced granulomatous responses are grossly attenuated, yet associated with increased local endothelial-leukocyte signaling and lymphocyte division. J. Leukoc. Biol. 53: 532–540; 1993.
Effects of macrophage-colony stimulating factor on human monocytes: Induction of expression of urokinase-type plasminogen activator, but not of secreted prostaglandin E2, interleukin-6, interleukin-1, or tumor necrosis factor-α
Authors: Hamilton John A , Whitty Genevieve A , Stanton Heather , Meager Anthony 
Published: January 2018

Abstract
It is often assumed that macrophage-colony stimulating factor (M-CSF) or CSF-1, as well as granulocyte macrophage-CSF (GM-CSF), can induce inflammatory mediator production by monocytes/macrophages. We demonstrate with elutriation-purified human monocytes that, in contrast to lipopolysaccharide, recombinant human CSF-1 does not induce secretion of prostaglandin E2, interleukin-6 (IL-6), IL-lβ, or tumor necrosis factor a, as measured by immunoassay; however, increased urokinase-type plasminogen activator (u-PA) activity in cell lysates and mRNA was observed. Similar results were obtained when the monocytes were treated with recombinant human GM-CSF. Such increased u-PA expression may contribute to the function of CSF-1 at sites of inflammation. J. Leukoc. Biol. 53: 707–714; 1993.
Coexpression of IL-2 receptor p55 and p75 by circulating blood lymphocytes
Authors: Sheldon A , Flego L , Zola H 
Published: January 2018

Abstract
By using high-sensitivity fluorescence and flow cytometry, it is possible to show that 30-40% of lymphocytes from PBL express the p55 chain of the IL-2 receptor, whereas the p75 chain is expressed at low concentrations on most lymphocytes without in vitro activation. The availability of a second fluorochrome capable of high sensitivity allows simultaneous analysis of p55 and p75, albeit with some sacrifice in sensitivity. Two-color analysis shows that a small proportion of cells (1-6%) coexpress measurable concentrations of both chains of the IL-2 receptor, and three-color studies show that these cells are predominantly CD4-positive T cells and express the CD45R0 isoform of the leucocyte-common antigen, i.e., have the phenotype of activated helper T cells. These cells may be a useful indicator of immune activation.
Isolation and confinement as a model for spaceflight Immune changes
Authors: Schmitt Didier A , Schaffar Laurence 
Published: January 2018

Abstract
The immune system of astronauts is disturbed during and after spaceflight. This situation may result from stressors encountered during the flight (microgravity, radiation, psychological stress, or confinement) or from physiological changes (demineralization or fluid shift). Therefore, ground-based investigations should be designed to determine the effects of these factors on the immune system. Very little is known about the influence of confinement or isolation on immune reactions. However, interesting data exist from experiments with animals and humans under different conditions (submarines, antarctic expeditions, single-person cave isolation, and underwater diving). The question remains as to whether these results can be extrapolated to spaceflight. Therefore, investigations of humans under isolation conditions analogous to space missions have been performed by Russian and, more recently, European investigators. Such investigations are important for understanding the physiological and psychological disturbances that occur during long periods of confinement, especially when future lunar and martian missions are considered.
Antiorthostatic suspension as a model for the effects of spaceflight on the immune system
Authors: Chapes Stephen K , Mastro Andrea M , Sonnenfeld Gerald , Berry Wallace D 
Published: January 2018

Abstract
We describe the use and appropriateness of antiorthostatic suspension in immunological investigations. This manuscript describes the model and discusses how well data obtained by using the model correlate with spaceflight data. This review concludes with some suggestions for future experiments using antiorthostatic suspension.
The effect of hypogravity and hypergravity on cells of the immune system
Authors: Cogoli Augusto 
Published: January 2018

Abstract
This article reviews the gravity effects discovered in T lymphocytes and other cells of the immune system. The strong depression of mitogenic activation first observed in an experiment conducted in Spacelab 1 in 1983 triggered several other investigations in space and on the ground in the clinostat and in the centrifuge in the past 10 years. During this period, great progress was made in our knowledge of the complex mechanism of T cell activation as well as the technology to analyze the lymphokines produced during stimulation. Nevertheless, several aspects of the steps leading to activation are not yet clear. Studies in hypogravity and hypergravity may contribute to answering some of the questions. A recent investigation in the U.S. Spacelab SLS-1, based on a new technology in which leukocytes are attached to microcarrier beads, showed that the strong inhibition of activation in microgravity is due to a malfunction of monocytes acting as accessory cells. In fact, interleukin-1 production is nearly nil in resuspended monocytes, whereas T cell activation is doubled in attached cells. In hypergravity, but not at lg, concanavalin A bound to erythrocytes activates B lymphocytes in addition to T cells. The activation of Jurkat cells is also severely impaired in space. These recent results have raised new questions that have to be answered in experiments to be conducted in space and on Earth in this decade. The experimental system, based on the mitogenic activation of T lymphocytes and accessory cells attached to microcarriers, offers an optimum model for studying basic biological mechanisms of the cell to assess the immunological fitness of humans in space and to test the feasibility of bioprocesses in space as well as on Earth.
Hapten-immune pulmonary interstitial fibrosis (HIPIF) in mice requires both CD4+ and CD8+ T lymphocytes
Authors: Hu Hui , Stein-Streilein Joan 
Published: January 2018

Abstract
We present a description and analysis of a mouse model for pulmonary interstitial fibrosis that is induced by a specific immune response to a small reactive chemical group called trinitrophenyl. We describe the model, and then we examine the cellular mechanism for the induction of the fibrosis. The specific increase in hydroxyproline reached a peak by day 7 and persisted through day 28 in all animals that were sensitized to and challenged with the hapten. Distinct patterns of fibrosis that were seen histologically correlated with antigenic pretreatment and were dependent on T lymphocytes. We also report that the inflammatory and fibrotic responses could be adoptively transferred with immune lymphocytes but not with immune serum. In vivo administration of anti-CD4 and anti-CD8 monoclonal antibodies to sensitized mice prevented the development of immune- mediated lung inflammation and was effective in reducing hydroxyproline deposition. We conclude that (activated) T lymphocytes contribute to the pathogenesis of pulmonary fibrotic diseases. The possibility arises that haptens in the environment may promote sensitization of individuals via their skin or lungs and cell-mediated immune responses to haptenated antigens within the lung may promote pulmonary fibrosis.