bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellular pH Changes During Neutrophil Activation: Na+ /H+ Antiport
Authors: Weisman Steven J , Punzo Amalia , Ford Charles , Sha'afi Ramadan I 
Published: January 2018

Abstract
Activation of the Na+ /H+ antiport mechanism was studied in human neutrophils by monitoring intracellular pH with a carboxyfluorescein derivative. N-formyl-methionylleucyl-phenylalanine (FMLP) and phospholipase C (PLC) induced biphasic pH changes. Amiloride, which inhibits the antiport, completely blocked alkalinization but enhanced acidification. Polymyxin B, which inhibits protein kinase C, only blocked alkalinization. Activation with phorbol 12-myristate 13-acetate (PMA) led to alkalinization only; this was inhibited by amiloride or polymyxin B. Thus, during polymorphonuclear leukocyte (PMN) activation, Intracellular alkalinization appears to be mediated by an amiloride-sensitive Na+ /H+ antiport. Antiport activity can also be blocked indirectly by inhibition of protein kinase C activity. Early intracellular acidification does not appear to require kinase activity but is observed when phospholipids are remodeled with PLC. The antiport was also activatable by hypertonic buffered media. This response did not appear to be mediated by protein kinase C because it was unaffected by polymyxin B. Finally, superoxide generation was investigated. It is affected by, but not soley controlled by, either antiport or protein kinase C activity.
Respiratory Burst of Normal Human Eosinophils
Authors: Petreccia David C , Nauseef William M , Clark Robert A 
Published: January 2018

Abstract
Oxidative metabolism of eosinophils has generally been studied in cells from patients with eosinophilia. We isolated eosinophils with purity of &gt;95% from normal donors. Oxygen metabolism of eosinophils and neutrophils was compared using O2 production as a measure of the stimulus-induced respiratory burst. During 10 min of stimulation, using phorbol myristate acetate (PMA) or opsonized zymosan (OPZ), eosinophils produced two to three times as much O2 as did neutrophils. Continuous kinetic analysis was used to measure the latency period and maximal rate of O2 production. Eosinophils had a shorter latency period and greater rate of O2 production than did neutrophils at all concentrations of PMA. With OPZ stimulation, O2 production rates by both cells were similar. The latency periods were similar with high concentrations of OPZ but at limiting amounts of OPZ eosinophils had a longer latency period than did neutrophils. In addition, the kinetic assay demonstrated that the respiratory burst in eosinophils was more sustained than in neutrophils.
These results indicate substantial differences in the oxidative burst of eosinophils and neutrophils with respect to activation, capacity, and regulation. These distinctive features of O2 production by eosinophils may be important in host defense against metazoan parasites or in tissue injury during inflammation.
In Vitro Tumoricidal Activity of Resting and Glucan-Activated Kupffer Cells
Authors: Sherwood Edward R , Williams David L , McNamee Rose B , Jones Ernest L , Browder I William , Di Luzio Nicholas R 
Published: January 2018

Abstract
Kupffer cells compose 80-90% of fixed tissue macrophages and have been suggested to play an important role in hepatic antitumor resistance. In the present study, the ability of resting and activated Kupffer cells to lyse syngeneic mammary adenocarcinoma BW10232 cells was evaluated. Activated Kupffer cells were isolated from C57BI/6J mice following single of multiple intravenous (IV) injections of glucan (0.45 mg/mouse), a potent macrophage-activating agent. Mice receiving 5% (w/v) dextrose served as control. Resting Kupffer cells induced significant (P &lt; .05) 4% and 12% specific lysis of adenocarcinoma cells at target:effector ratios of 1:10 and 1:50, respectively. Kupffer-cell-mediated tumoricidal activity was depressed on day 1 following a single IV injection of glucan. By day 3 postglucan, the antitumor activity of Kupffer cells returned to control levels and was enhanced on days 5 and 10. Following multiple IV injections of glucan on days -5, -3, and -1, Kupffer-cell-mediated cytotoxicity was elevated on days 1 and 4. These observations demonstrate that 1) resting Kupffer cells are significantly cytotoxic to adenocarcinoma cells at T:E ratios of 1:10 and 1:50 and 2) following a transient inhibition of Kupffer-cell-mediated tumoricidal activity, glucan was effective in significantly enhancing the antitumor activity of Kupffer cells.
Differential Prostaglandin Production by Unfractionated and Density-Fractionated Human Monocytes and Alveolar Macrophages
Authors: Elias Jack A , Ferro Thomas J , Rossman Milton D , Greenberg Jo Ann , Daniele Ronald P , Schreiber Alan D , Freundlich Bruce 
Published: January 2018

Abstract
Mononuclear phagocyte elaboration of E series prostaglandins (PGE) may be important in the regulation of inflammatory and fibrotic reactions. Mononuclear phagocytes are morphologically and functionally heterogeneous cells. To further understand the processes controlling inflammation and fibrosis, in particular that in the human lung, we characterized the ability of unfractionated and density-fractionated human alveolar macrophages and blood monocytes to elaborate PGE. Alveolar macrophages and blood monocytes constitutively elaborated small amounts of PGE, and their elaboration of PGE was increased with lipopolysaccharide (LPS) stimulation. Monocytes elaborated more PGE than autologous alveolar macrophages. In addition, denser monocytes (specific gravity &gt; 1.055) and denser alveolar macrophages (specific gravity &gt; 1.044) elaborated more PGE than less dense monocytes and alveolar macrophages, respectively. When monocytes were incubated in vitro, their constitutive PGE elaboration decreased with time. However, in vitro incubation did not cause monocytes to lose their capacity to elaborate PGE in response to LPS. Thus, mononuclear phagocyte populations differ in their ability to elaborate PGE. These differences can be only partially attributed to differences in cell maturation.
Shift in Subfractions of Rat Alveolar Macrophages In Vivo During Endotoxin-Induced Alveolitis
Authors: Rinaldo Jean E , Moore Susan A , Lee Robert E , Dauber James H 
Published: January 2018

Abstract
To elucidate changes in alveolar macrophages that accompany sepsis-induced lung injury, this study analyzed the subfractions of alveolar macrophages (AM) recovered by lung lavage during the onset of endotoxin-induced acute neutrophilic alveolar inflammation in the rat model. Centrifugation on continuous self-generated density gradients of Percoll was used to fractionate AM into subpopulations between density limits 1.012 and 1.130. Two-thirds of AM recovered from pathogen-free control rats (group C) were in a fraction with a density range of 1.058-1.078 [“normal” density fraction, (ND)]. Only 6% were located in a very low density (VLD) fraction 1.037-1.048. Neutrophils accounted for less than 1% of recovered cells and usually were found in the fraction with density range of 1.079-1.130. By contrast, if rats underwent lung lavage 15 hours after the administration of endotoxin (group E), only 38% of macrophages were recovered in the “normal” density fraction, whereas 26% of the AM recovered were in the VLD fraction. This shift in the relative sizes of the density based subpopulations coincided with the onset of acute bronchoalveolar inflammation as indicated by the recovery of neutrophils by bronchoalveolar lavage (PMN = 7 × 104 in C, vs. 9.4 × 105 in E, p &lt; .001). The macrophages on the low density subfractions showed functional impairment: they were less viable in culture and migrated poorly in response to endotoxin-activated serum compared to macrophages in the “normal” density fraction from the endotoxin-treated animals. The rapid emergence of the low density population after endotoxin could represent an influx of new cells, but more likely indicates that injury to or previous activation of resident macrophages has caused their density to decrease. We speculate that the emergence of a population of AM in airspaces with low density and impaired function could weaken pulmonary host defense following endotoxemia.
Chemotactic Factor Binding and Functional Capacity: A Comparison Between Human Granulocytes and Differentiated HL-60 Cells
Authors: Dahlgren Claes , Andersson Tommy , Stendahl Olle 
Published: January 2018

Abstract
In the presence of dimethyl sulfoxide (DMSO), the leukemic promyelocytic cell line HL-60 will differentiate into mature polymorphonuclear granulocytes. In the present report, we compare chemotactic factor binding and function in HL-60 cells with that of normal human granulocytes using the chemotactic peptide N-formylmethionyl-leucyl-phenylal-anine (FMLP) as ligand. The cellular response measured as CL was changed as a result of storage or conditioning of normal peripheral blood cells. With these cells, a conditioning procedure at room temperature resulted in a pronounced increase in the CL response. The increase of the CL response was probably a result of increased expression of cryptic receptors, since the changes of the oxidative response to FMLP was accompanied by increased binding of the peptide to the cell surface. Scatchard analysis revealed that the increased binding was due to an increased number of receptors. In differentiated HL-60 cells, conditioning neither led to increased production of oxidative metabolites, nor to any increased binding of the peptide. The data thus indicate that many FMLP receptors could reside in a cryptic site that is not accessible to extracellular ligands, and that conditioning results in an increased exposure of these receptors, followed by an increased oxidative response to the ligand in normal cells but not in mature HL-60 cells.
Murine Glia Cells in Culture Can be Stimulated to Generate Reactive Oxygen
Authors: Sonderer Bruno , Wild Peter , Wyler Robert , Fontana Adriano , Peterhans Ernst , Schwyzer Martin 
Published: January 2018

Abstract
Induction of luminol-enhanced chemiluminescence (CL) indicative of reactive oxygen formation was studied in glia cell cultures from newborn mice. A burst of CL could be induced by phorbol myristate acetate, zymosan, and antibody-coated bovine red blood cells, whereas Sendai virus and several other agents known to induce CL in myeloid cells were ineffective. Sodium azide failed to inhibit CL, indicating a myeloperoxidase-independent mechanism of light emission. In parallel experiments we identified the cells binding antibody-coated erythrocytes as macrophages characterized by the reduction of nitroblue tetrazolium and phagocytosis of zymosan and latex particles. Brain macrophages may use reactive oxygen intermediates (ROI) as a mechanism of antimicrobial defence; and, on the other hand, ROI formed by these cells may contribute to immunopathology in the brain.
Evidence of Polymorphonuclear Neutrophils (PMN) Activation in Patients With Insulin-Dependent Diabetes Mellitus
Authors: Wierusz-Wysocka B , Wysocki H , Sieklerka H , Wykretowicz A , Szczepanik A , Klimas R 
Published: January 2018

Abstract
Polymorphonuclear neutrophils' chemotaxis, surface charge, superoxide anions generation, NBT (nitro blue tetrazolium) reduction and intracellular lysozyme, and β-glucuronidase content were estimated in patients with type I diabetes mellitus in a similar state of metabolic control. The chemotaxis of diabetic cells toward bacterial chemotactic factors was similar to controls, whereas migration toward complement-derived chemoattractants was significantly reduced. Polymorphonuclear neutrophils isolated from diabetic patients, when unstimulated, produced significantly greater amounts of superoxide anions and reduced NBT more efficiently. They also revealed reduced surface charge and lower intracellular content of lysozyme, whereas β-glucuronidase content was similar to controls. The results obtained seem to indicate that neutrophils in patients with insulin-dependent diabetes manifest signs of being in the activated state. The possible mechanisms of such stimulation are discussed.
The Activation of L3T4+ Helper T Cells Assisting the Generation of Anti-Tumor Lyt-2+ Cytotoxic T Lymphocytes: Requirement of 1a-Positive Antigen-Presenting Cells for Processing and Presentation of Tumor Antigens
Authors: Kosugi Atsushi , Yoshioka Takayuki , Suda Takashi , Sano Haruo , Takahama Yousuke , Fujiwara Hiromi , Hamaoka Toshiyuki 
Published: January 2018

Abstract
The present study investigates the mechanisms of the recognition of tumor antigens by L3T4+ helper T cells responsible for the generation of Lyt-2+ cytotoxic T lymphocytes (CTL) against a major histocompatibility complex (MHC) Class II (1a) antigen-negative syngeneic X5563 plasmacytoma. Treatment of X5563-immunized spleen cells with anti-L3T4 antibody plus complement (C) diminished the generation of Lyt-2+ anti-X5563 CTL. Since the contribution of L3T4+ cells was completely replaced by the addition of exogenous lymphokines, it was demonstrated that L3T4+ cells functioned as helper T cells assisting the generation of anti-X5563 CTL responses. Elimination of 1a-positive accessory cells (AC) from X5563-immunized spleen cells resulted in the abrogation of CTL generation, whereas the addition of exogenous lymphokines to AC-depleted X5563 immunized spleen cells restored the CTL response. The addition of anti-self la antibody to the culture also eliminated CTL responses. These observations demonstrated the requirement of 1a-positive AC for and the involvement of self la antigens in the activation of helper T cells. Moreover, use of tumor cells pretreated with paraformaldehyde to cultures of X5563-immunized spleen cells or adding back of AC pretreated with chloroquine to cultures of AC-depleted immune spleen cells failed to generate CTL responses. Finally, the addition of exogenous lymphokines to the above cultures resulted in appreciable restoration of CTL responses. Taken collectively, these results indicate that L3T4+ helper T cells are activated with tumor antigens processed and presented by 1a-positive AC.
Suppressor Alveolar Macrophages in Mice Bearing Metastatic Lewis Lung Carcinoma Tumors
Authors: Young M Rita , Endicott Roger A , Duffie G Patrick , Wepsic H Terry 
Published: January 2018

Abstract
The capacity of alveolar macrophages from mice injected with a metastatic Lewis lung carcinoma variant, LLC-C3, to regulate T-cell Con A blastogenesis and NK cytotoxicity was studied. During the first 5 days after subcutaneous tumor injection, alveolar macrophages were stimulatory to Con A blastogenesis of normal spleen cells. After 5 days, the alveolar macrophages shifted to become suppressive. The suppressive activity was extensive by day 11, when the primary and metastatic tumor foci were first detectable. The tumor-bearer alveolar macrophages also suppressed NK cytotoxicity. Alveolar macrophage suppressive activity was sensitive to indomethacin, suggesting a prostaglandin-dependent suppressor mechanism. Suppression was not mediated by the production of hydrogen peroxide or superoxide, as it was insensitive to catalase or superoxide dismutase. When normal alveolar macrophages were cultured with LLC-C3 supernatants for over 12 hours, suppressive activity was induced. The results of these studies show that alveolar macrophages of tumor bearers become suppressive with progressive tumor growth and might, thus, facilitate the development of pulmonary metastases.
Modulation of Human Monocyte Leukotactic Responsiveness by Thromboxane A2 and 12-Hydroxyheptadecatrienoic Acid (12-HHT)
Authors: Campbell Peter B , Tolson Timothy A 
Published: January 2018

Abstract
The leukotactic responsiveness of human peripheral blood monocytes is regulated by the cell-directed inhibitor of monocyte leukotaxis, CDI-MLx. The actions of CDI-MLx on normal monocytes in vitro were abrogated by co-incubation with inhibitors of cyclooxygenase and thromboxane synthetase with indomethacin and dazmegrel (UK-38,465) being most active. The actions of CDI-MLx were mimicked by the thromboxane A2 analogue, U-46619, and by 12-HHT with half-maximal inhibition observed at 10−10M; PGE2 was 1000-fold less active. SQ 29,548, a thromboxane A2 receptor antagonist, blocked the effects of CDI-MLx, U-46619, and 12-HHT. Production of PQE2 and thromboxane B2 by purified monocytes was stimulated by CDI-MLx and this effect was also blocked by indomethacin, dazmegrel, and dazoxiben. These data suggest a major regulatory role for thromboxane synthetase products in human monocyte leukotaxis.
The Role of the Na+/H+ Antiporter in Human Neutrophil NADPH-Oxidase Activation
Authors: Wright Jonathan , Maridonneau-Parini Isabelle , Cragoe Edward J , Schwartz John H , Tauber Alfred I 
Published: January 2018

Abstract
The Na+/H+ antiporter has been shown to regulate activation of the human neutrophil. To delineate the role of the antiporter in the stimulation cascade, superoxide ((O2−) generation was observed in PMA-stimulated neutrophils in which intracellular pH (pHI) was artificially manipulated by the use of nigericin, a K+/H+ ionophore, with and without use of the Na+/H+ antiporter inhibitor, dimethyiamiloride (DA). Decreased O2− generation was observed in a Na+-free, 140 mM K+ buffer, but addition of nigericin restored this parameter of neutrophil activation to levels found in physiologic Na+ media. Further, the inhibitory effects of DA on O2− generation by cells incubated in a 10 mM Na+, 130 mM K+ buffer were totally reversed by a similar concentration of nigericin. O2− generated by a membrane preparation of the NADPH-oxidase, made from cells incubated under the same experimental conditions, paralleled whole cell studies, but the activity of the oxidase did not vary when suspended in the various reaction mixtures. These experiments support the role of the Na+/H+ antiporter in neutrophil activation as a metabolic regulator of pHi that Influences receptor-coupled reactions proximal to expression of the NADPH-oxidase itself.
Accelerated Recovery of Hematopoiesis Following Sub-Lethal Whole Body Irradiation With Recombinant Murine Interleukin-1 (IL-1)
Authors: Gallicchio Vincent S 
Published: January 2018

Abstract
This communication reports the results of studies designed to investigate the ability of recombinant murine interleukin-1 (rIL-1) to enhance the recovery of hematopoiesis following administration of sub-lethal whole body irradiation (2 Gy). Mice were administered rIL-1 (100 and 500 units) i.p. Twenty-four hours later these mice were administered 2 Gy radiation. Irradiated control mice were given only phosphate buffered saline (PBS). Animals were then serially sacrificed (on days 1, 2, 4, 7, 9, and 12 following irradiation) and their peripheral blood was analyzed for indices (packed red cell volume, WBC, platelets, and differential). Femoral bone marrow was harvested and assayed for their stem cell content—erythroid (CFU-E, BFU-E), granulocyte-macrophage (CFU-GM), and megakaryocyte (CFU-MEG). Irradiated mice pretreated with rIL-1 demonstrated accelerated hematopoietic recovery as measured by higher WBC, platelets and femoral stem cell content than PBS-treated irradiated controls. These results indicate IL-1 may be an effective radioprotective agent against the hematotoxicity induced by ionizing radiation.
Alteration of Rat Kupffer Cell Function Following Mitomycin-C Administration
Authors: Bodenheimer Henry , Charland Colette , Leith John 
Published: January 2018

Abstract
Cancer chemotherapeutic agents modify the human immune system in diverse ways including both immunosuppression and immunostimulation. We evaluated the effects of mitomycin-C on rat Kupffer cell phagocytosis, C3b receptor binding, and lysosomal enzyme activity. Kupffer cell cultures were greater than 95% pure. Phagocytosis of IgG-coated sheep red blood cells was demonstrated by 84% of control cells but by only 25% of cells isolated two weeks following mitomycin-C administration (p &lt; 0.0005). This depression in phagocytic ability had returned to control levels by four weeks post-treatment. Similarly, C3b receptor binding of IgM and complement coated sheep red blood cells was observed in 88% of control Kupffer cells, but declined to 47% at two weeks after drug administration (p &lt; 0.005) and returned to normal after four weeks. Lysosomal enzyme activity was not impaired by mitomycin-C. Histologically severe ulceratlon of the colon of treated animals was seen one and two weeks after drug administration, but healed by four weeks post-mitomycin-C treatment. Depression of macrophage function as a consequence of cancer chemotherapy may have important clinical consequences in host defense against bacteria and tumor metastases.
Lung Exposure to Mineral Dusts Enhances the Capacity of Lung Inflammatory Cells to Release Superoxide
Authors: Cantin André , Dubois Frédéric , Bégin Raymond 
Published: January 2018

Abstract
In vitro exposure of macrophages and neutrophils to inorganic dusts can enhance their oxidative metabolism, however the effects of inorganic dust inhalation on lung-inflammatory cell-oxidative metabolism remain unknown. To address this issue, we studied the superoxide anion release from lung inflammatory cells obtained by bronchoalveolar lavage from 19 sheep exposed repeatedly to UICC chrysotile B asbestos (100 mg) over an 18 month period and 10 sheep exposed to a single exposure of quartz (100 mg) over a 6 month period. Exposure to asbestos and quartz did not induce an increase in the spontaneous release of superoxide from inflammatory cells. However lung-inflammatory cells from sheep exposed to asbestos released much higher levels of superoxide in the presence of phorbol myristate acetate (PMA) than did cells of unexposed sheep. In quartz exposed animals, superoxide release with PMA stimulation remained significantly increased up to 2 months after a single quartz infusion. These results suggest that inorganic dust inhalation primes lung inflammatory cells in vivo and markedly enhances their capacity to release toxic oxygen radicals.
In Vivo Labeling of Resident Peritoneal Macrophages
Authors: Melnicoff Meryle J , Morahan Page S , Jensen Bruce D , Breslin Elizabeth W , Horan Paul K 
Published: January 2018

Abstract
A novel method for labeling resident peritoneal macrophages (MO) by injection of a dye into the peritoneal cavity is described. The dye, which fluoresces green, is selectively taken up by the resident Mø. Dye labeled cells can be further characterized by labeling of cell surface antigens with monoclonal antibodies (Mabs) and phycoerythrin conjugated second antibody. After such labeling with the Mabs F4/80 or Mac 1 the resident Mø were labeled by both the green dye and the red Mab markers, while recruited Mø or neutrophils were labeled with just the red Mab; the two populations of cells were readily distinguished by two-color flow cytometry. This technique enabled identification of resident and recruited Mø in each animal without the use of radioisotopes, irradiation, or bone marrow ablation. Sufficient numbers of cells can be analyzed from each animal so that Individual animals could be evaluated.
We found no adverse effects of this labeling technique on expression of cell surface antigens or Mø mediated cytotoxicity. We did find evidence that the i.p. injection induced a mild inflammation in the peritoneal cavities of animals injected with either the dye or the balanced salt solution vehicle. Examination of the intracellular staining pattern indicated that the label rapidly sequestered in the cytoplasm of the Mø, possibly in the lysosomes. Dye solubility studies showed that the dye was partially soluble at the concentration used for in vivo labeling. We hypothesize that the Mø labeling occurred by a combination of phagocytosis of dye aggregates and endocytosis of labeled plasma membrane.