bluuebunny/crossref_metadata_2025_split huggingface dataset:
Silica induces apoptosis in macrophages and the release of interleukin-1 α and interleukin-1β
Authors: Sarih M’hammed , Souvannavong Vongthip , Brown Spencer C , Adam Arlette 
Published: January 2018

Abstract
Resident adherent peritoneal cells selectively released high amounts of interleukin-1 (IL-1) activity when treated with silica. The use of anti-IL-1 antisera showed that both IL-Ια and IL-1β were present in supernatants of silica-treated macrophages. In contrast, intracellular IL-1 activity was totally neutralized by anti- IL-Ια antibodies and was easily converted into the mature IL-Ια form by autolysis in cytoplasmic extracts. Anion exchange chromatography clearly separated the two IL-1 species present in supernatants of silica- stimulated macrophages. Natural IL-1β was further characterized by chromatofocalization; it had an apparent isoelectric point, pI, in the range 8.3-8.6. In agreement with previous findings showing that IL-1/3 was released only by apoptotic cells, we have found that silica-treated macrophages underwent apoptosis. This was demonstrated by the characteristic laddering electrophoretic pattern of DNA extracted from silica-treated cells and by the morphology of macrophage nuclei stained with the DNA-specific dye DAPI. In addition, quantification of apoptotic cells was performed by a flow cytometric analysis based on the reduction of cellular DNA content exhibited by apoptotic cells. Treatment of macrophages with silica, therefore, results in an active process that promotes the processing and liberation of IL-1β.
Interplay between superantigens and the immune system
Authors: Irwin Michael J , Gascoigne Nicholas R J 
Published: January 2018

Abstract
Superantigens interact with the immune system by binding to major histocompatibility complex (MHG) class II proteins and activating T cells through the variable region of the T cell receptor β-chain. Through this means they can cause massive proliferation and then death of a large proportion of T cells. Superantigens are produced by bacteria, mycoplasmas, retroviruses, and probably by other organisms. In some cases, the superantigen is crucial to the organism’s life cycle. Mouse mammary tumor virus disseminates by activating T cells which stimulate the proliferation of B cells harboring the virus. In other cases, the superantigen may be responsible for the pathogenesis of the infection, such as in the case of Toxic Shock Syndrome. In this article, we review information on the diseases in which superantigens are involved, and the mechanisms by which the superantigens interact with T cell receptor and class II molecules.
A carboxyl-terminal tail peptide of neutrophil chemotactic receptor disrupts its physical complex with G protein
Authors: Bommakanti Rajani K , Klotz Karl-Norbert , Dratz Edward A , Jesaitis Algirdas J 
Published: January 2018

Abstract
The binding of G protein to the N-formyl peptide receptor of human neutrophils was investigated with site-specific synthetic peptides. Peptide CT336/332 (322RALTEDSTQTSDTAT336) from the carboxyl-terminal tail region of the receptor competed with the receptor for binding to bovine Gi protein. The peptide competition was assayed by dissociation of a GTP-sensitive, rapidly sedimenting (7S) form of receptor-G protein complex as analyzed by velocity sedimentation on linear sucrose density gradients. An IC50 of 590 μΜ was determined for CT336/332 peptide. A control peptide, with the reverse sequence, rCT 336/332(336 TATDSTQTSDETLAR322)did not perturb the sedimentation of the reconstituted receptor-G protein complex up to the highest tested concentration, 3 mM. Other peptides tested, corresponding to central portions of the predicted intracellular loop regions CII140/127 (127VLHPVWT QNHRTVS140) and CIII239/227 (227KIHKQGLIKSSRP239) of the receptor, failed to dissociate the reconstituted receptor-G protein complex. Control peptides from the extracellular region EII184/170 (170KTGTVACTFNFSPWT184) and an unrelated sequence matching a portion of neutrophil cytochrome b, CYT306/296 (296KWITKWTHPFKTIE306), were also ineffective. Our results suggest that the cytoplasmic tail of the formyl chemotactic peptide receptor is involved in its coupling to the signal-transducing G protein.
Influence of suspension on the expression of protective immunological memory to murine Listeria monocytogenes infection
Authors: Miller Edwin S , Sonnenfeld Gerald 
Published: January 2018

Abstract
Female BDF1 mice were immunized with virulent Listeria monocytogenes, which resulted in the generation of a long-lived state of protective immunological memory for this facultative intracellular bacterial pathogen. The influence of antiorthostatic suspension, a ground-based model employed to simulate certain aspects of weightlessness that occur during spaceflight, on the capacity of these mice to express memory immunity was evaluated. Memory-immune mice were suspended by the tail in the orthostatic or antiorthostatic position and were reinfected with a lethal dose of virulent L. monocyto- genes. It was found that suspension did not influence the kinetics of bacterial growth in vivo when the rechallenge infection was started concurrently with the suspension. However, mice that were reinfected on day 2 or 4 of the suspension exhibited an enhanced capacity to eliminate the infection. Attenuation of this enhancing effect was observed when mice were infected on day 7 of the suspension. These results indicate that the stress of antiorthostatic suspension can influence the capacity of the murine host to express protective immunological memory to pathogenic bacteria.
Processing and intracellular transport of cathepsin G and neutrophil elastase in the leukemic myeloid cell line U-937—modulation by brefeldin A, ammonium chloride, and monensin
Authors: Lindmark Anders , Gullberg Urban , Olsson Inge 
Published: January 2018

Abstract
The effects of brefeldin A, monensin, and the weak base NH4C1 on the biosynthesis and processing of cathepsin G and neutrophil elastase of myeloid cells were investigated. Monoblast-like U-937 cells were biosynthetically labeled with [35S]methionine, followed by subcellular fractionation, immunoprecipitation, and analysis by sodium dodecyl sulfate-polyacrylamide gel electrophore-sis and fluorography. Brefeldin A inhibited proteolytic processing, intracellular transport, and secretion. The effects were reversible inasmuch as removal of brefeldin A resulted in a normal pattern of processing and transfer to high-density organelles, corresponding to lysosomes, and restitution of constitutive secretion of precursor forms. Both cathepsin G and neutrophil elastase acquired resistance to endoglycosidase-H, suggesting that conversion to complex oligosaccharide side chains also occurs in the presence of brefeldin A. Monensin and NH4Cl inhibited final proteolytic processing, indicating either that acidification is necessary for directing cathepsin G and neutrophil elastase to lysosomal-like organelles or that the protease(s) responsible for processing requires an acid pH. We conclude that pH-dependent proteolytic processing of cathepsin G and neutrophil elastase occurs in post-Golgi structures and that transfer to lysosomes or an immediately prelysosomal compartment is mandatory for complete processing. J. Leukoc. Biol. 55: 50–57; 1994.
Inhibition by all-trans-retinoic acid of tumor necrosis factor and nitric oxide production by peritoneal macrophages
Authors: Mehta Kapil , McQueen Teresa , Tucker Stanley , Pandita Raj , Aggarwal Bharat B 
Published: January 2018

Abstract
Besides their growth-inhibiting and differentiation-inducing properties, retinoids have been shown to exert immunomodulatory and anti-inflammatory functions by mechanisms that are not well understood. Tumor necrosis factor-α (TNF), a cytokine produced by mononuclear phagocytes, has been shown to be an important mediator of endotoxin-induced septic shock, cachexia, bone resorption, and inflammation. Nitric oxide may also have a role in septic shock, hypotension, and vasodilatation. In this study, we examined the effects of retinoids on the production of TNF and nitric oxide by murine peritoneal macrophages. Of the various retinoids studied, all-trans-retinoic acid (RA) was most potent; it almost completely inhibited the production of TNF by macrophages activated with endotoxin and interferon-γ. The inhibitory effect was dependent on the dose and duration of RA exposure to macrophages. RA also blocked phorbol ester-induced TNF production in a macrophage cell line (RAW 264.7). Besides TNF, the retinoid suppressed the production of nitric oxide from activated peritoneal macrophages. The importance of these results in relation to controlling various harmful effects of cytokines released by activated macrophages is discussed. J. Leukoc. Biol. 55: 336–342; 1994.
Influence of antiorthostatic suspension on resistance to murine Listeria monocytogenes infection
Authors: Miller Edwin S , Sonnenfeld Gerald 
Published: January 2018

Abstract
The present study was designed to evaluate the influence of antiorthostatic suspension, a ground-based modeling system employed to simulate certain aspects of weightlessness that occur during space flight, on the capacity of mice to resist infection with the facultative intracellular bacterial pathogen Listeria monocytogenes. Female BDF1 mice were suspended by the tail in the orthostatic or antiorthostatic position and were infected with a sublethal dose of virulent L. monocytogenes at various times during the suspension. It was found that suspension did not influence the kinetics of bacterial growth in vivo if the infection was started concurrently with the suspension. However, mice that were antiorthostatically suspended 2, 4, or 7 days before the onset of infection exhibited an enhanced capacity to eliminate the challenge infection. Suspending mice on day 2 of the infection did not alter the kinetics of bacterial growth. Finally, the enhancement of resistance to the primary Listeria infection was accompanied by failure of the mice to generate long-term protective immunological memory to the challenge organism. Collectively, these results indicate that the stress of antiorthostatic suspension can influence the capacity of mice to resist bacterial infection. J. Leukoc. Biol. 55: 371–378; 1994.
Expression of p47-phox and p67-phox proteins in murine bone marrow–derived macrophages: Enhancement by lipopolysaccharide and tumor necrosis factor α but not colony stimulating factor 1
Authors: Green Simon P , Hamilton John A , Uhlinger David J , Phillips Wayne A 
Published: January 2018

Abstract
We have investigated the relationship between the expression of the p47-phox and p67-phox cytosolic components of the NADPH oxidase and priming of the macrophage respiratory burst. Western blot analysis revealed that murine bone marrow-derived macrophages (BMM) contain immunoreactive proteins detected by antisera raised against recombinant human p47-phox and p67-phox. Priming BMM by exposure to tumor necrosis factor or (TNF-α) or lipopolysaccharide (LPS) increased the levels of p47-phox and p67-phox. Colony-stimulating factor 1 (CSF-1), which we previously found to have a negative effect on the priming of murine macrophages, had no effect on the level of p47-phox but down-regulated that of p67-phox. Our results suggest that the regulatory effects of LPS, TNF-α, and CSF-1 on the respiratory burst of BMM may be due to modulation of the expression of the p47-phox and p67-phox cytosolic components of the NADPH oxidase. J. Leukoc. Biol. 55: 530–535; 1994.
Quantification of neutrophil migration following myocardial ischemia and reperfusion in cats and dogs
Authors: Albertine Kurt H , Weyrich Andrew S , Ma Xin-liang , Lefer David J , Becker Lewis C , Lefer Allan M 
Published: January 2018

Abstract
Endothelial cell dysfunction and cardiac myocyte injury resulting from ischemia and reperfusion have been associated with accumulation of neutrophils in the myocardium. To determine whether the accumulation is related primarily to intravascular sequestration or extra-vascular infiltration of neutrophils during the early period of reperfusion, we morphometrically quantified the tissue distribution of neutrophils in cats and dogs. At the end of the reperfusion period, the base of the heart was cross-clamped to preserve neutrophil location at the moment of death. Point-counting methods were used to determine the distribution of neutrophils inside and outside coronary arterioles and venules (≤100 μm in diameter) as well as coronary capillaries 5–10 μm in diameter in 0.5-μm-thick, plastic-embedded sections. Ischemia-reperfusion resulted in a threefold increase in neutrophil number in the lumen of arterioles and venules at 60 min of reperfusion and up to a sevenfold increase at 270 min of reperfusion (P &lt; .05) compared to time-matched control nonischemic hearts. The ratio of intravascular neutrophils in venules to arterioles was 2:1. Intracapillary neutrophils increased, but not significantly, at 60 min of reperfusion. At 270 min of reperfusion, intracapillary neutrophils increased 11-fold (P &lt; .05). The percentage of total neutrophils that accumulated outside arterioles and venules in cat hearts was 8% at 60 min of reperfusion (not significant, NS) and 28% at 270 min of reperfusion (P &lt; .05). In dog hearts, the percentages were 26% (NS) and 44% (P &lt; .05), respectively. The percentage of total neutrophils that accumulated outside capillaries was &lt;6% in both cat and dog hearts (NS). The combination of rapid intravascular sequestration, delayed extravascular infiltration, and low incidence of neutrophil–cardiac myocyte contact in situ in these two species suggests that neutrophil-mediated cardiac myocyte injury during early reperfusion may initially depend on diffusion of inflammatory mediators and subsequently require direct contact between neutrophils and cardiac myocytes. J. Leukoc. Biol. 55: 557–566; 1994.
The role of G-CSF in mature neutrophil function is not related to GM-CSF-type cell priming
Authors: Treweeke Andrew T , Aziz Khalil A , Zuzel Mirko 
Published: January 2018

Abstract
Because of uncertainties regarding the comparability of granulocyte-macrophage and granulocyte colony-stimulating factors with regard to their effects on mature neutrophils (PMNs), we compared the actions of the two cytokines on reactive oxidant production and granular secretion by these cells. We found that chemiluminescence (CL) stimulated by formylmethionyl-leucylphenylalanine (fMLP) was not influenced by G-CSF (0.1–100 ng/ml), whereas GM-CSF priming (10 ng/ml) caused a nearly twofold increase in this PMN response. Moreover, the reactivity of PMNs treated with GM-CSF and G-CSF in combination was not different from that of PMNs treated with GM-CSF alone. GM-CSF (10 ng/ml) increased the rate of O2- production by 79%, caused a fivefold increase in fMLF-induced myeloperoxidase (MPO) secretion, and strongly enhanced CD11b expression. In contrast, G-CSF (50 ng/ml) only slightly increased O2- production (by 15%), and MPO secretion and CD11b expression remained unchanged. Both cytokines together gave results similar to those obtained with GM-CSF alone. In the presence of platelets (which by themselves enhanced PMN reactivity), the differences in the effects of the two cytokines persisted. We conclude that the priming effect of G-CSF on mature PMNs is negligible compared with that of GM-CSF. Our results are in conflict with previous reports of much more pronounced G-CSF effects but in accord with recent work showing the failure of this cytokine to induce a range of effects produced by GM-CSF. We therefore suggest that the primary role of G-CSF in mature PMN function is still unclear but may be related to the control of PMN distribution in view of the mobilizing and marginating effects of the cytokine in viva J. Leukoc. Biol. 55: 612–616; 1994.
Rat CINC/gro: a novel mediator for locomotive and secretagogue activation of neutrophils in vivo
Authors: Suzuki Hidekazu , Suematsu Makoto , Miura Soichiro , Liu Yu Ying , Watanabe Kazuyoshi , Miyasaka Masayuki , Tsurufuji Susumu , Tsuchiya Masaharu 
Published: January 2018

Abstract
The effects of rat CINC/gro, a member of the interleukin-8 family, on the endothelium-neutrophil interaction and transendothelial macromolecular leakage were studied in rat mesenteric microcirculation. Thirty minutes after superfusion with 10 nM CINC/gro, the number of neutrophils adherent to the venular endothelium and those migrated across the venules were significantly increased with a concomitant elevation of luminol-dependent chemiluminescence at the site of adhesion. Transendothelial macromolecular leakage as assessed by the relative length of venular wall stained with monastral blue B was also increased at 30 min after the start of CINC/gro superfusion. Pretreatments with a CD18-directed monoclonal antibody, WT-3 (1 mg/kg), significantly attenuated the increase in number of adherent and migrated neutrophils, the increase in luminol-dependent chemiluminescence, and the venular macromolecular leakage after the application of CINC/gro. These data suggest that CINC/gro is a novel stimulator that evokes not only locomotive but also secretagogue activation of neutrophils via a CD18-dependent mechanism in viva J. Leukoc. Biol. 55: 652–657; 1994.
Nitric oxide (NO)–induced mitochondrial injury among chicken NO-generating and target leukocytes
Authors: Sung Yen-Jen , Dietert Rodney R 
Published: January 2018

Abstract
In an analysis of nitric oxide (NO) production and toxicity, chicken macrophage–generated NO inhibited mitochondrial activity in both NO-producing macrophages themselves and lymphoid tumor targets. However, differences in targeting of mitochondrial toxicity were observed among these cells. Two chicken macrophage cell lines, HD11 and MQ-NCSU, produced NO (measured as nitrite) dependent upon concentrations of l-arginine and bacterial endotoxin (lipopolysaccharide). Mitochondrial activity was negatively correlated with the amount of NO produced. Using a modified MTT assay, NO induced suppression in two mitochondrial complexes. Mitochondrial activity was significantly suppressed among HD11 cells receiving LPS alone (complex I, 63.0 ± 5.5% suppression; complex II, 27.9 ± 5.2%). In contrast, mitochondrial activities in samples receiving LPS plus inhibitor, NG-nitro-l-arginine methyl ester (NAME; 5 mM) or 2,4-diamino-6-hydroxypyrimidine (DAHP; 5 mM), were not significantly different from control values. When HD11 macrophages were cocultured with lymphoblastoid tumor targets, RECC-CU60 (T cell) or LSCC-RP9 (B cell), adding LPS (1 μg/ml), tumor cell mitochondrial activity was significantly suppressed. In the generator macrophages, complex I was more suppressed than complex II, whereas in lymphoid targets no such difference was observed. These results indicate that NO inhibits complex I and II mitochondrial activity but that differential targeting can occur among chicken leukocyte populations J. Leukoc. Biol. 56: 52–58; 1994.
Influence of interleukin-1 on neutrophil function and resistance to Streptococcus suis in neonatal pigs
Authors: Shi J , Goodband R D , Chengappa M M , Nelssen J L , Tokach M D , McVey D S , Blecha F 
Published: January 2018

Abstract
Nonspecific immunity is usually lower in neonates than adults. Consequently, enhancing the neonate’s nonspecific immune capability may be beneficial for the health and growth performance of young animals. We conducted two experiments in which neonatal pigs were injected with recombinant bovine interleukin-1β (rBoIL-1β) at 9 to 11 days of age. Three consecutive daily injections of rBoIL-1β increased neutrophil and monocyte numbers, which remained elevated until the animals were challenged with Streptococcus suis at 19 days of age. Neutrophil bactericidal activity was greater in interleukin-1-treated pigs than in saline-injected controls. At lower ratios of effector to target cells, neutrophil-mediated, antibody-dependent cellular cytotoxicity was increased in neonates treated with IL-1. However, natural killer cell activity and neutrophil production of superoxide anion were not affected by treatment with IL-1. Expression of CD18 was increased transiently on neutrophils from IL-1-treated pigs at 15 days of age. Severity of the streptococcal infection was less in pigs that were treated with IL-1 at 9 to 11 days of age. These data suggest that IL-1 treatment in neonates may augment nonspecific immune function and disease resistance. J. Leukoc. Biol. 56: 88–94; 1994.
Role of endotoxin in mononuclear phagocyte-mediated inflammatory responses
Authors: Watson R W G , Redmond H R , Bouchier-Hayes D 
Published: January 2018

Abstract
Lipopolysaccharide (LPS), which is derived from the cell wall of gram-negative and some gram-positive bacteria, plays a major role is the pathogenesis of septic shock. Initiation of these responses depends on LPS interaction with a number of immune cells, not least the mononuclear phagocyte (MP). Mononuclear phagocytes bind the LPS/lipopolysaccharide-binding protein complex through the CD14 receptor and thus mediate the release of a wide range of inflammatory mediators. Release of these mediators is teleologically beneficial but under certain circumstances may be detrimental, resulting in the systemic inflammatory response syndrome. The development of this syndrome is not clearly understood but appears, in part, to be dependent on the ability of the host to respond to these mediators. This review evaluates the mechanisms of LPS-MP interaction and the therapeutic strategies aimed at inhibiting this interaction. J. Leukoc. Biol. 56: 95–103; 1994.
Requirement for lymphocytes and resident macrophages in LPS-induced pleural eosinophil accumulation
Authors: Bozza Patricia T , Castro-Faria-Neto Hugo C , Penido Carmen , Larangeira Andréa P , Graças Maria das , Henriques M O , Silva Patricia M R , Martins Marco A , dos Santos Ricardo Ribeiro , Cordeiro Renato S B 
Published: January 2018

Abstract
In this study we investigated the involvement of inflammatory cells in the pleural accumulation of eosinophils induced by lipopolysaccharide (LPS). Intrathoracic (i.t.) injection of LPS (250 ng/cavity) into rats induced a significant eosinophil accumulation that developed within 24 h, was maximal at 48 h, and returned to control values within 120 h. This eosinophil influx was preceded by a huge neutrophil influx within 4 h and accompanied by a mononuclear cell accumulation between 24 and 48 h. Pretreatment with an antineutrophil monoclonal antibody (RP-3, 2 ml per animal) selectively reduced the number of circulating neutrophils within 8 h but failed to alter the LPS-induced eosinophilia. Similarly, platelet depletion with an anti-rat platelet antiserum did not alter the LPS-induced eosinophil accumulation. Cyclosporine (50 mg/kg, 12 and 2 h before) partially inhibited (51%) the LPS-induced pleural eosinophilia, whereas the eosinophilia was not changed by prior degranulation of pleural mast cells with polymyxin B (10 μg/cavity, 24 h before). Moreover, selective depletion of T lymphocytes using an anti-Thy 1.0 monoclonal antibody significantly inhibited the eosinophilia triggered by LPS. The i.t. injection of liposomes containing dichloromethylene diphosphonate significantly reduced (65%) the number of resident macrophages after 5 days. Under this condition, the eosinophil infiltration induced by LPS was completely inhibited. Accordingly, the i.t. injection of supernatant from macrophage monolayers, obtained from the pleural cavities of LPS-injected rats, into naive recipient animals led to a twofold increase in the number of pleural eosinophils. In conclusion, our data suggest an important role for resident macrophages and T lymphocytes in the eosinophil accumulation induced by LPS. J. Leukoc. Biol. 56: 151–158; 1994.