bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mitogenic signal transduction in T lymphocytes in microgravity
Authors: Cogoli Augusto , Bechler Birgitt , Cogoli-Greuter Marianne , Criswell Sue B , Joller Helen , Joller Peter , Hunzinger Elisabeth , Muller Otfried 
Published: January 2018

Abstract
The activation by concanavalin A Con A of human peripheral blood lymphocytes (PBLs) in the presence of monocytes as accessory cells was investigated in cultures exposed to microgravity conditions in Spacelab. Activation of T cells was measured as incorporation of [3H] thymidine into DNA, secretion of interleukin-2 (IL-2), and interferon-7, and expression of IL-2 receptors. Whereas, as discovered in earlier experiments, the activation of resuspended T cells is strongly inhibited, activation of cells attached to microcarrier beads is more than doubled in microgravity. The results suggest that the depression of the activation in resuspended cells may be attributed to a malfunction of monocytes acting as accessory cells. In fact, although the ultrastructure of resuspended monocytes is not altered in microgravity, the secretion of IL-1 is strongly inhibited. Our data suggest that (1) IL-2 is produced independently of IL-1, (2) IL-1 production is triggered only when monocytes (and lymphocytes?) adhere to microcarriers, (3) the expression of IL-2 receptors depends on IL-1, and (4) provided sufficient IL-1 is available, activation is enhanced in microgravity. Finally, cultures of resuspended PBLs and monocytes in microgravity constitute a complete and natural system in which monocytes are not operational. This may be useful for studies of the role of accessory cells and cell-cell interactions in T lymphocyte activation. J. Leukoc. Biol. 53: 569–575; 1993.
Granulocyte activation induced by intense interval running
Authors: Gray AB , Telford RD , Collins M , Baker MS , Weidemann MJ 
Published: January 2018

Abstract
Activation of granulocytes has been associated with normal immune function, inflammation, and exercise-induced muscle damage. The effect of intense interval running on granulocyte activation was examined by use of flow cytometry, monoclonal antibodies, and spectrophotometric techniques. Eight trained males [maximal oxygen uptake Vo2max, mean (SD) = 64.4 (3.6) ml/kg/min; age 30.1 (4.8) years] undertook an intense interval exercise (treadmill running) protocol to exhaustion. Subjects completed an average of 16.5 one- minute runs. Granulocyte expression of CR3 (GDI lb), receptor for complement component C3bi (6 and 24 h post-test), and FcγRIII (GD16) (24 h post-test) and the plasma concentration of elastase-inhibitor complex (1 h post-test) increased significantly (all P &lt; .05). Subjects (8 of 8) exhibited a post-test decrease at either 1 or 6 h (P &lt; .01) and a 24-h post-test significant increase (7 of 8; P &lt; .05) in granulocyte 90° light scattering (LS). Plasma lactoferrin (Lf) concentration, although increased by 17% at 6 h post-test, was not significantly different from resting values at any sampling point. Changes in plasma Lf and median channel 90° LS were significantly correlated (r = - .43, P = .04), raising the possibility of monitoring exercise-induced granulocyte activation (degranulation) by flow cytometry. Intense interval exercise appears to induce granulocyte activation, as manifested by release of granule proteins and changes in 90° LS and expression of both Fc and complement receptors. J. Leukoc. Biol. 53: 591–597; 1993.
Characterization of a 64-kd protein phosphorylated during chemotactic activation with IL-8 and fMLP of human polymorphonuclear leukocytes. II. Purification and amino acid analysis of phosphorylated 64-kd protein
Authors: Shibata Michio , Yamakawa Yoshio , Ohoka Tadakazu , Mizuno Satoshi , Suzuki Kazuo 
Published: January 2018

Abstract
Lung giant cell carcinoma-derived chemotactic protein (LUCT)/IL-8 and fMet-Leu-Phe stimulate phosphorylation of a 64-kd protein (p64) in 32P-labeled human polymorphonuclear leukocytes (PMNs). The p64 was purified from cytosol of human PMNs (1.8 × 109 cells) by DEAE-Sepharose CL6B column chromatography, hydroxyapatite HPLC, and reverse-phase HPLC. By hydroxyapatite HPLC, p64s were separated and produced two peaks containing both nonphosphorylated and phosphorylated p64. Amino acid composition of each p64 was determined. Each p64 was directly subjected to amino acid sequencing, but the amino acid residue in the amino-terminal of the proteins could not be detected. From the results of amino acid composition and other characters of p64, it is suggested that p64 is identical to I-plastin, which is a leukocyte-specific protein.
Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells
Authors: Park Eunkyue , Quinn Michael R , Wright Charles E , Schuller-Levis Georgia 
Published: January 2018

Abstract
Taurine is present in high concentrations in most mammalian tissues, including those that prodigiously produce oxidants. Taurine protects against bronchiolar damage induced by NO2, ozone, bleomycin, and amio- darone. Taurine is chlorinated to form taurine chloramine (Tau-Cl) by the halide-dependent myeloperoxidase system and, under physiological conditions, reduces HOC1 toxicity. Although NO and its metabolites, ΝO2− and NOs−, are thought to be major mediators of tissue damage resulting from oxidant exposure, cytokines, including tumor necrosis factor (TNF), are also involved. We examined the effects of Tau-Cl on NO production and TNF release by using RAW 264.7 cells activated with recombinant interferon-γ (rIFN-γ; 50 U/ml) and lipopoly- saccharide (LPS; 10 μg/ml). NO was measured spec- trophotometrically as ΝO2− after reaction with Griess reagent and TNF was measured by FLISA. Tau-Cl (0.5 mM) inhibits NO and TNF released into the medium by 47% and 43%, respectively. Tau-Cl is actively transported into RAW 264.7 cells by an uptake system that is energy, temperature, and Na+ dependent. Competition experiments demonstrate that the uptake system for Tau- Cl is distinct from that for taurine. In addition, the NO synthase activity of cytosolic preparations from activated RAW 264.7 cells is irreversibly inhibited by pretreatment with Tau-Cl. We demonstrate that Tau-Cl inhibits production of NO and TNF by activated macrophages and suggest a mechanism through which taurine supplementation may protect against oxidant-induced tissue damage.
Inhibition of apoptosis and prolongation of neutrophil functional longevity by inflammatory mediators
Authors: Lee Alison , Whyte Moira K B , Haslett Christopher 
Published: January 2018

Abstract
Neutrophil apoptosis leads to macrophage ingestion of intact senescent neutrophils. This may represent a neutrophil removal mechanism that is important both in the control of inflammatory tissue injury and for the normal resolution processes of inflammation. Because apoptosis is likely to be a key control process in cell and tissue homeostasis, a number of inflammatory mediators were tested for their ability to modulate the rate of apoptosis in populations of neutrophils aging in culture. Endotoxic lipopolysaccharide, human recombinant complement factor 5a, and human recombinant granulocyte- macrophage colony-stimulating factor all markedly inhibited the rate of neutrophil apoptosis in a concentration-dependent fashion, without inducing necrosis (as assessed by trypan blue exclusion). This inhibitory effect on the rate of neutrophil apoptosis was shown by morphological criteria and confirmed by gel electrophoresis of extracted DNA. Inhibition of apoptosis of aging neutrophil populations was associated with prolongation of the functional life span of the population as assessed by the ability of neutrophils to spread on glass surfaces, to polarize in response to deliberate stimulation with N-formyl-Met-Leu-Phe (fMLP), and to release the granule enzyme marker myeloperoxidase on fMLP stimulation. These observations show that inflammatory mediators prolong the functional life span of neutrophils through modulation of apoptosis. Further elucidation of these mechanisms will lead to a better understanding of the processes controlling neutrophil residence and function in inflamed tissues and may provide further insights into the molecular mechanisms of apoptosis, which is of widespread importance in tissue biology.
The in vivo effects of rhIL-lα therapy on human monocyte activity
Authors: Lee Anna M , Vadhan-Raj Saroj , Hamilton Raymond F , Scheule Ronald K , Holian Andrij 
Published: January 2018

Abstract
Pleiotropic cytokines such as interleukin-lα (IL-lα) have multiple effects on peripheral blood monocytes (PBMs). This study examined the ability of in vivo recombinant human IL-lα (rhIL-lα) therapy to enhance clinically important monocyte functions in ovarian cancer patients prior to chemotherapy. After 4 days of continuous infusion, in vivo rhIL-lα therapy amplified both the number and activity of PBMs. Therapy with rhIL-lα increased the number of PBMs sixfold. These monocytes had a significantly increased ability to produce superoxide anion in response to phorbol 12,13- dibutyrate stimulation. Their ability to secrete spontaneously the immunomodulatory cytokines IL-lα and IL-1β was significantly increased, but their ability to secrete tumor necrosis factor a (TNF-α) was not significantly elevated. These effects of rhIL-lα infusion on cytokine secretion by PBMs appear to be related to rhlL-lα-in- duced increases in the mRNA levels for these cytokines. In contrast, rhIL-lα therapy did not significantly alter PBM response to lipopolysaccharide (10 μg/ml). In summary, infused rhIL-lα, in addition to its use as a myelo- protective agent, has enhancing effects on the number and activity of PBMs. The effects of rhIL-lα infusion on PBM function demonstrated here should at least transiently increase the ability of monocytes to combat infection and enhance host immune response.
Monocyte adherence to human vascular endothelium
Authors: Beekhuizen Henry , van Furth Ralph 
Published: January 2018

Abstract
An acute inflammatory response requires that circulating monocytes bind to and migrate across the endothelium of the vessel wall to gain access to inflamed sites. Various mediators of inflammation - cytokines and chemoattractants - have been shown to initiate and regulate the margination and extravasation of monocytes. This review summarizes evidence that the mechanism underlying the initial adhesion of monocytes to normal and cytokine-stimulated endothelial cells and their subsequent transendothelial migration are successive events in monocyte-endothelial cell interaction. Special emphasis is given to the current knowledge of the contribution of adhesion molecules belonging to the family of 13i- and 132-integrins, the immunoglobulin supergene family, and the selectins to such cellular interaction. The sequence of events that allow monocytes to attach to, migrate over and finally pass the endothelium is discussed in detail.
NADPH-oxidase activity: the probable source of reactive oxygen intermediate generation in hemocytes of the gastropod Lymnaea stagnalis
Authors: Adema C M , van Deutekom-Mulder E C , van der Knaap W P W , Sminia T 
Published: January 2018

Abstract
Macrophage-like defense cells (hemocytes) of the pond snail Lymnaea stagnalis generate reactive oxygen intermediates (ROIs) upon contact with non-self, following kinetics similar to those of ROI production by mammalian leukocytes during respiratory burst. In this study, several inhibitors of NADPH-oxidase, the key enzyme of the respiratory burst in mammalian phagocytes, were tested for their effect on oxidative activities [as demonstrated by nitroblue tetrazolium (NBT) reduction and luminol-dependent chemiluminescence (LDCL)] of phagocytosing snail hemocytes. In the presence of di- phenylenc iodonium, zymosan-stimulated hemocytes of L. stagnalis failed to reduce NBT and showed a markedly reduced LDCL response. Also, compounds that prevent assembly of functional NADPH-oxidase complexes in activated mammalian cells were effective; preincubation of hemocytes with 1,4-naphthoquinone inhibited the LDCL response and NBT reduction upon phagocytic stimulation. Furthermore, coincubation but not preincubation with five different catechol-like phenols inhibited oxidative activities of zymosan-stimulated hemocytes. These results imply similarities in composition and regulation of the ROI-generating mechanisms of both mammalian and snail defense cells. It is postulated that in L. stagnalishemocytes, (1) NADPH-oxidase activity is responsible for ROI production, (2) an active NADPH-oxidase enzyme complex has to be assembled from putative cytosolic and membrane-associated components, and (3) continuous replacement of active NADPH-oxidase enzyme complexes is necessary to sustain respiratory burst-like oxidative activities during interactions with non-self.
Restoration of postburn impaired lymphocyte responsiveness by nonsteroidal anti-inflammatory drugs is independent of prostaglandin E2 inhibition
Authors: Mathieu Jacques , Masson Isabelle , Chancerelle Yves , Chanaud Brigitte , Strazlko Suzanne , De Sousa Martine , Kergonou Jean-François , Giroud Jean-Paul , Florentin Irene 
Published: January 2018

Abstract
Prostaglandin E2 (PGE2) has been implicated in postburn immunosuppression, which is responsible for septic complications. In the present work, seven nonsteroidal anti-inflammatory drugs (NSAIDs), differing by their capacity to inhibit the cyclooxygenase pathway, were compared for their ability to restore T lymphocyte proliferative responses evaluated 4 days after thermal injury in rats. Salicylic acid, 5-aminosalicylic acid, and niflumic acid, given daily, fully restored spleen cell responses to concanavalin A (Con A) and phytohemagglutinin. These drugs were active only at doses that were below the anti-inflammatory doses and did not modify normal spleen cell responses. In these conditions, indomethacin slightly restored lymphocyte reactivity, whereas acetylsalicylic acid, ketoprofene, and piroxicam were ineffective. PGE2 production by Con A-stimulated spleen cells from untreated burned rats and after treatment with niflumic acid or 5-aminosalicylic acid did not correlate with the intensity of the proliferative response. Indomethacin, niflumic acid, and 5-aminosalicylic acid were added in vitro to spleen cells from normal and burned rats, at concentrations from 10-7 to 10-4 M. PGE2 production was strongly depressed by indomethacin and niflumic acid and not modified by 5-aminosalicylic acid. The proliferative response of normal spleen cells was depressed in a concentration-dependent manner by niflumic acid and slightly inhibited at the highest concentrations of indomethacin. In contrast, indomethacin concentration dependently restored the burn-impaired proliferative response, whereas niflumic acid further depressed it and 5-aminosalicylic acid had no effect. These results demonstrate that only some NSAIDs are able to restore T lymphocyte reactivity impaired after thermal injury and that this property is not related to inhibition of PGE2 production. J. Leukoc. Biol. 55: 64–72; 1994.
Functional characterization of interstitial macrophages and subpopulations of alveolar macrophages from rat lung
Authors: Prokhorova Svetlana , Lavnikova Natasha , Laskin Debra L 
Published: January 2018

Abstract
The specific function of interstitial macrophages (IM) in the lung is poorly understood because of difficulties in isolating these cells in high purity or large number. In the present studies, a pure population of en-zymatically isolated IM and lung macrophages obtained mechanically from the lung were compared functionally with alveolar macrophages recovered by lavage (AM). Macrophages isolated mechanically from the tissue and AM displayed similarly high levels of Fc-receptor mediated phagocytosis. In contrast, IM phagocytized significantly fewer opsonized sheep red blood cells per macrophage than AM. In addition, although some variations in the amounts of nitric oxide and superoxide anion produced by AM and macrophages obtained by mechanical tissue disruption were observed, these subpopulations released significantly more of these mediators than IM. These data support the concept that macrophages isolated by mechanical disruption of the tissue represent a subpopulation of AM. We also found that, in contrast to AM, IM did not respond synergistically to combinations of IFN-γ and lipopolysaccharide (LPS) or tumor necrosis factor α in terms of nitric oxide production. Furthermore, regulation of superoxide anion release in AM and IM by LPS and/or IFN-γ was distinct. Taken together, these studies demonstrate that IM are functionally different from other macrophage subpopulations which might reflect their unique location within the lung. J. Leukoc. Biol. 55: 141–146; 1994.
Effects of spaceflight on the number of rat peripheral blood leukocytes and lymphocyte subsets
Authors: Allebban Zuhair , Ichiki Albert T , Gibson Linda A , Jones Jimmy B , Congdon Charles C , Lange Robert D 
Published: January 2018

Abstract
Experiments were carried out on peripheral blood leukocytes and spleen lymphocytes from 29 male rats that were flown during the Spacelab Life Sciences 1 (SLS-1) nine-day mission on the shuttle Columbia in June 1991 and on appropriate ground controls. On the day of landing, there was a significant decrease in the total white blood cell counts (P &lt; 0.0001) of flight animals in comparison to controls. There was also a significant decrease in the absolute number of lymphocytes (P &lt; 0.0001) and monocytes (P &lt; 0.0001) in the flight animals. A slight decrease in the absolute number of eostinophils and a slight increase in the number of neutrophils were observed at landing, compared with preflight values. Immunophenotyping of the peripheral blood and spleen lymphocytes of flight and control animals indicated that, on the day of landing, there was a decrease in the absolute number of CD4 and CD8 positive cells and B lymphocytes. However, relative percentages of peripheral blood CD4 +, CD8 +, and B cells were lot found to be depressed. No differences were discerned in the percent reactivity of spleen lymphocytes of flight animals compared with controls. The observed decrease in the number of leukocytes and lymphocytes at the immediate postflight period was transient and all values returned to the control levels by nine days postflight. J. Leukoc. Biol. 55: 209–213; 1994.
Partial characterization of the proliferative activity for fetal lung epithelial cells produced by silica-exposed alveolar macrophages
Authors: Melloni Boris , Lesur Olivier , Bouhadiba Tayeb , Cantin André , Bégin Raymond 
Published: January 2018

Abstract
The proliferation of lung epithelial cells is a prominent feature of lung tissue response following silica-induced lung injury and alveolar macrophages are recognized as a major contributing cell to the lung inflammatory processes. In previous studies, a growth-promoting activity for fetal rat lung epithelial cells was observed in silicotic alveolar fluids and in supernatants from in vitro and in vivo silica-exposed alveolar macrophages. In the present work, the biological and physicochemical properties of the macrophage-derived growth-promoting activity for fetal lung epithelial cells were explored. Four peaks of growth-promoting activity for lung epithelial cells ranging from 32 to 7 kDa were found in both in vitro and in vivo silica-exposed macrophage supernatants. The investigations were coupled with biochemical treatments of the mitogenic peaks and blocking antibodies or antisera were used to specify further the nature of the proliferative activities. Among the established growth factors, alveolar macrophage–derived growth fractions had characteristics consistent with platelet-derived growth factor–, insulin-like growth factor 1–, and fibroblast growth factor–like molecules. The cytokine production following in vitro exposure, which reflects very early events in the pathogenesis of silicosis, was more strongly related to the high-molecular-weight PDGF-like molecules, whereas the cytokine production following in vivo exposure, which reflects later events in the pathogenesis of silicosis, was more influenced by intermediate-molecular-weight FGF- and IGF-like molecules. J. Leukoc. Biol. 55: 574–580; 1994.
Endotoxin and GM-CSF-mediated down-regulation of macrophage apo E secretion is inhibited by a TNF-specific monoclonal antibody
Authors: Zuckerman Steven H , O’Neal Laura 
Published: January 2018

Abstract
Macrophage activation is associated with increased secretion of monokines, proteases, arachidonic acid metabolites, reactive oxygen, and nitrogen intermediates and yet decreased secretion of apolipoprotein E (apo E). Although the kinetics of apo E down-regulation have been investigated, the mechanism(s) involved remains unknown. In the present study, the question of whether macrophage-activating factors such as lipopolysaccharide (LPS) and granulocyte-macrophage colony-stimulating factor (GM-CSF) directly result in apo E down-regulation or indirectly by inducing the secretion of other inflammatory mediators has been investigated. LPS-stimulated macrophages demonstrated a dose-dependent reduction in apo E secretion with a 70% decrease occurring following a 48-h incubation with 20 ng/ml LPS. Coculture of these cells with a neutralizing concentration of a hamster monoclonal antibody against murine tumor necrosis factor (TNF) inhibited the LPS-mediated reduction in apo E secretion. This inhibitory effect resulting from TNF neutralization was not observed using pooled hamster immunoglobulin G, or hamster monodonals against murine interleukin-lα (IL-lα), IL-1β, or interferon-7. Similar results were observed when GM-CSF was used to induce apo E down-regulation. The inhibitory effects of TNF neutralization on endotoxin-induced apo E down-regulation were dependent on LPS concentration and were no longer apparent at concentrations greater than 200 ng/ml. These results suggest that an autocrine, TNF-dependent mechanism may play a role in the down-regulation of apo E secretion during macrophage activation. J. Leukoc. Biol. 55: 743–748; 1994.
Surface proteins involved in T cell costimulation
Authors: Mondino Anna , Jenkins Marc K 
Published: January 2018

Abstract
The activation and eventual clonal expansion of individual antigen-specific CD4+ T cell clones are dependent on the production of autocrine growth factors such as interleukin-2 (IL-2). The specificity of CD4+ T cell activation is imparted by T cell antigen receptor (TCR) recognition of peptide antigens bound to class II major histocompatibility complex (MHC)-encoded molecules on the surface of antigen-presenting cells (APCs), for example B cells, macrophages, and dendritic cells. To induce maximal IL-2 production by T cells, however, APCs must also provide non-antigen-specific costimulatory signals. Recent work indicates that APC-derived costimulatory signals play a critical role in determining whether lymphokine production, apoptotic cell death, or functional anergy is induced by TCR engagement. This information has allowed immunologists to manipulate costimulatory molecules to prevent allograft rejection and enhance tumor immunity. Here we review current information on the biologic effects of, and signal transduction pathways engaged by, several known receptor-ligand pairs that transduce costimulatory signals in T cells. Special emphasis will be placed on the interaction of CD28 on the T cell with its ligands, B7-1, B7-2, and B7-3 on the APC. J. Leukoc. Biol. 55: 805–815; 1994.