bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determination of the Number and Distribution of Macrophages, Lymphocytes, and Granulocytes in the Mouse Uterus From Mating Through Implantation
Authors: De Mamata , Choudhuri Rajani , Wood Gary W 
Published: January 2018

Abstract
The concentration and distribution of F4-80 positive cells (macrophages) and common leukocyte antigen (CLA) positive (bone marrow derived) cells were assessed in mouse uterus between days 1 and 8 of pregnancy. High numbers of polymorphonuclear leukocytes and lymphocytes were present on days 1 and 2, but not thereafter. Granulocytes were found both in the endometrium and within the luminal epithelium. The percentage of total cells contributed by macrophages was high on days 1 and 2. That percentage decreased significantly on day 3, then increased again on day 5 and remained high through day 8. Macrophages always were found in myometrial stroma. Macrophages were found throughout the endometrium on days 2 through 8. High numbers of macrophages were observed near epithelia, particularly on days 1,2,4, and 5. Few F4-80+ or CLA+ cells were observed within the developing primary and secondary decidua. The results demonstrate that an inflammation-like cellular response occurs in the uterus following mating and that macrophages are a major cellular component of the uterus during early pregnancy.
Role of 5-Lipoxygenase Products of Arachidonic Acid in Cell-to-Cell Interaction Between Macrophages and Natural Killer Cells in Rat Spleen
Authors: Chang Ke-Jian , Saito Hiroyuki , Tatsuno Ichiro , Tamura Yasushi , Yoshida Sho 
Published: January 2018

Abstract
In the present study we performed experiments to reveal the role off 5-lipoxygenase products of arachidonic acid in cell-to-cell interaction between rat peritoneal macrophages and spleen natural killer (NK) cells. Peritoneal macrophages were found to significantly enhance NK cell activity. It was found that the enhancing activity of macrophages was significantly inhibited by the ingestion of highly purified eicosapentaenoic acid-ethyl ester (EPA-E). But direct cytotoxic action of macrophage on target cells (YAC-1) was unchanged by the ingestion of EPA-E. In addition, the depressed enhancing activity of EPA-enriched macrophages (EPA macrophages) was partially, but significantly, restored by the addition of either 10-10 M leukotriene B4 (LTB4) or 10-12 M 5-hydroperoxyeicosatetraenoic acid (5-HPETE). The partial restoring effect of 10-10 M LTB4 was further significantly enhanced by the addition of 5-HPETE. In contrast 5-hydroxyeicosatetraenoic acid (5-HETE) had no modulatory effect on the depressed activity of EPA macrophages. LTB4,5-HPETE, and 5-HETE had no direct effect on NK cell activity itself. Significantly less amounts of LTB4 and 5-HETE were produced in EPA macrophages as compared with that in control macrophages. The present study indicates that macrophage modulatory action on NK cells can be partly mediated by LTB4 and 5-HPETE, which are produced in macrophages.
Intracellular Survival of Virulent Bordetella pertussis in Human Polymorphonuclear Leukocytes
Authors: Steed Lisa L , Setareh Morey , Friedman Richard L 
Published: January 2018

Abstract
Little is known regarding the interaction of Bordetella pertussis with polymorphonuclear leukocytes (PMNL) or the role PMNL play as an initial line of defense against B. pertussis infection. An in vitro system was developed to establish conditions for the study of phagocytosis and killing of virulent B. pertussis by human PMNL. Phagocytosis of B. pertussis strains BP504, BP165, and BP338 occurred by opsonization with anti-B. pertussis antibody, while autologous normal human sera did not induce significant phagocytosis. In PMNL bacterial killing assays virulent B. pertussis strains survived PMNL bactericidal activities while Escherichia coli controls were readily killed. Electron microscopy studies using acid phosphatase as a lysosomal marker strongly suggested that B. pertussis inhibits phagosome-lysosome fusion in PMNL. These results indicate that virulent B. pertussis strains are capable of surviving intracellularly within PMNL and that such survival may be due to inhibition of phagosome-lysosome fusion.
Activation of Human Neutrophils by Phorbol Ester Decreases the Cytoplasm Compactness and the Lactoferrin Content of the Granulocytes
Authors: Esaguy Nair , águas Artur P , Vilanova Manuel , Silva Manuel T 
Published: January 2018

Abstract
Human neutrophils isolated from the blood were incubated in vitro for 30 min with 25 ng/ml of phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, to study its effect on the fine structure of granulocytes and on the subcellular distribution of lactoferrin (Lf). Flow cytometry analysis of the human neutrophils showed that PMA induced a decrease in size and granularity of the cells. By electron microscopy, the PMA-treated cells showed numerous empty vesicles, smoothing of the cell surface, and a marked decrease in the compactness of the cytoplasmic ground substance. High-resolution immunogold ultracytochemistry showed that neutrophils lost most of their content in Lf after the PMA incubation. In thin sections, the cytoplasmic compartment of PMA-treated neutrophils contained an average of 1.03 ± 0.3 Lf-positive vesicles per μm2, whereas control granulocytes showed an average of 5.72 ± 1.49 Lf vesicles per μm2 of cytoplasm. Most of PMA-treated neutrophils kept some Lf-positive vesicles; a significant minority (10–15%) of the granulocytes showed cytological features of cell death. We conclude that the PMA-induced neutrophil activation is associated with microanatomical changes that include i) exocytosis of most, but not all, of the Lf-bearing vesicles; ii) rounding up of the cell outline; and iii) decrease in the compactness of the cytoplasmic ground substance.
Murine Eosinophil Granulocytes Bind the Murine Macrophage-Monocyte Specific Monoclonal Antibody F4/80
Authors: McGarry M P , Stewart C C 
Published: January 2018

Abstract
Studies designed to identify a panel of monoclonal antibodies useful for the separation of murine eosinophil myeloid progenitors revealed that F4/80, an antigen heretofore thought to be expressed only by murine monocyte/macrophage lineage cells, was expressed by eosinophil granulocytes. Eosinophils from several strains of mice stained positively with specific antibody for the epitope. A novel pathway for myeloid differentiation is proposed in which neutrophil progenitors exit a common lineage prior to a common progenitor of monocytes and eosinophils. Moreover, the results demonstrate that binding of anti-F4/80 can no longer be viewed as exclusive for mononuclear phagocytes.
Critically III Anergic Patients Demonstrate Polymorphonuclear Neutrophil Activation in the Intravascular Compartment With Decreased Cell Delivery to Inflammatory Focci
Authors: Tellado Jose M , Christou Nicolas V 
Published: January 2018

Abstract
Skin test anergy, the failure to produce a delayed type hypersensitivity (DTH) response, is associated with an increase in infection-related complications and death usually due to multiple organ failure (MOF). Refractory intravascular activation of polymorphonuclear neutrophils (PMNs) has been implicated in the development of MOF. We studied 20 critically ill surgical patients with life threatening infections to determine if PMN intravascular activation was present and how this affected essential PMN functions such as exudation. The 11 anergic patients had a more intense inflammatory response to their infection. Plasma lactoferrin was 6.1 ± 0.3 μg/ml in anergic patients compared to 3.9 ± 1.5 in reactives P &lt; 0.05, accompanied by reduced total primary (3.3 ± 1.9 vs 4.7 ± 2.1 μg/106 PMN P &lt; 0.01) and secondary (2.8 ± 0.4 vs 5.0 ± 0.9 μg/106 PMN P &lt; 0.01) granule content, respectively. In vitro superoxide production following 100 ng/ml PMA stimulation was 0.44 ± 0.1 in anergics vs 0.36 ± 0.1 nmol/μg PMN protein in reactivities, P &lt; 0.05. PMN chemotaxis was 8.2 ± 0.6 PMNs/HPF in anergics compared to 10.2 ± 1.6 PMNs/HPF in reactives P &lt; 0.05, accompanied by decreased PMN delivery to skin blister windows (3.2 ± 1.4 vs 4.5 ± 1.9 × 107 PMN/ml, respectively, P &lt; 0.05). We conclude that critically ill anergic surgical patients have increased intravascular PMN activation, which may contribute to oxygen-derived tissue damage in the vascular space, as well as a deficient delivery of effector cells in areas of bacterial invasion. This may lead to inability to clear the inflammatory signals which set up the vicious circle of MOF leading to death.
Effect of Interleukin-1, GM-CSF, Erythropoietin, and Lithium on the Toxicity Associated With 3′-Azido-3′-Deoxythymidine (AZT) In Vitro on Hematopoietic Progenitors (CFU-GM, CFU-MEG, and BFU-E) Using Murine Retrovirus-Infected Hematopoietic Cells
Authors: Gallicchio Vincent S , Hughes Nedda K , Hulette Ben C , Noblitt Lynette 
Published: January 2018

Abstract
The drug 3′-azido-3′-deoxythymidine (AZT), a synthetic thymidine analogue, has been used clinically in the management of acquired immune deficiency syndrome (AIDS). The drug is an effective antiviral agent due to its ability to block reverse transcriptase activity. This action of AZT was demonstrated in the Rauscher leukemia virus (RLV)-induced murine erythroleukemia model system. Unfortunately, associated with AZT has been the development of hematopoietic toxicity manifested by anemia, neutropenia, and overall bone marrow suppression. Hematopoietic growth factors (GM-CSF, erythropoietin), cytokines (interleukin-1), and agents known to potentiate hematopoiesis (lithium) have been demonstrated to modulate drug and/or radiation-induced hematopoietic toxicity. We report the results of further studies designed to investigate the ability of GM-CSF, erythropoietin, interleukin-1, and lithium to modulate AZT toxicity on murine hematopoietic granulocyte-macrophage (CFU-GM), megakaryocytic (CFU-Meg), and erythroid (BFU-E) progenitors cultured from bone marrow and spleen cells from mice infected with RLV. Hematopoietic progenitors from either normal or RLV-infected animals when exposed to AZT demonstrated concentration-dependent toxicity and differed for each progenitor with BFU-E being the most sensitive (ID50 concentration, 5 × 10-9 M) and CFU-GM the least sensitive (ID50 concentration, 5 × 10-5 M). As has been previously demonstrated using normal murine hematopoietic progenitors, when cultured with RLV-infected marrow or spleen cells, addition of GM-CSF, Meg-CSF or erythropoietin failed to inhibit AZT toxicity in vitro on CFU-GM, CFU-Meg, and BFU-E, respectively. However, in the presence of interleukin-1 (recombinant human IL-1α, 30 ngm) or lithium chloride (ultra-pure, 1.0 mM), AZT toxicity CFU-GM, CFU-Meg, and BFU-E cultured from RLV-infected marrow or spleen cells was reduced. These results further demonstrate interleukin-1 and lithium are effective in modulating the toxic action of ACT on hematopoietic progenitors and that RLV-infected animals serve as a useful viral model system to study the effect of agents capable of modulating hematopoiesis in the presence of the anti-viral drug AZT.
Role of Antibody-Dependent Cellular Cytotoxicity and Lymphokine-Activated Killer Cells in AIDS and Related Diseases
Authors: Brenner Bluma G , Gryllis Chryssa , Wainberg Mark A 
Published: January 2018

Abstract
This overview summarizes current knowledge on the overall efficacy and potential contribution of antibody-dependent cellular cytotoxicity (ADCC) and lymphokine-activated killer cell (LAK) activities in evoking non-major histocompatibility complex (non-MHC) cytolytic responses to human immunodeficiency virus-1 (HIV-1)-infected targets. High titers of ADCC antibodies to the HIV-1 virion are present in HIV-1-seropositive populations at all stages of disease. These antibodies are broadly reactive with a large number of HIV-1 strains and are predominantly directed against envelope determinants spanning both gp120 and gp41. However, the relative ability of natural killer (NK) effectors, derived from HIV-seropositive individuals, to evoke ADCC responses becomes increasingly impaired with disease progression. HIV-1-seropositive individuals also show marked decreases in both production of and responsiveness to interleukin-2 (IL-2). HIV-1-seropositive individuals generally have the ability to generate ex vivo propagated LAK cells; however, these cytolytic effectors are less effective than their counterparts derived from healthy controls. Increased understanding and control of non-MHC-restricted cytotoxic-responses to HIV, and their induction by lymphokines, may lead to improved treatment strategies for the management of AIDS and related diseases.
Neutrophil-induced immunoglobulin binding to erythrocytes involves proteolytic and oxidative injury
Authors: Weiss Douglas J , Aird Betsy , Murtaugh Michael P 
Published: January 2018

Abstract
Neutrophil-induced alterations in feline erythrocytes were studied to better understand the pathogenesis of erythrocyte destruction associated with inflammatory diseases. As in previous studies, addition of superoxide dismutase/catalase to a coculture of erythrocytes and activated neutrophils attenuated neutrophil-induced immunoglobulin G (IgG) binding. However, incubation of erythrocytes with hydrogen peroxide or neutrophil-derived anuclear cytoplasts (neutroplasts) failed to induce IgG binding. Addition of phenylmethylsulfonyl fluoride, a serine protease inhibitor, to the erythrocyte-neutrophil coculture attenuated IgG binding. These observations suggest that neutrophil-derived serine protease activity is involved in IgG binding to erythrocytes. Further, incubation of erythrocytes with serine proteases, but not metalloproteases or sulfhydryl proteases, induced immunoglobulin binding. Freeze-fracture replicas of the erythrocyte membrane failed to demonstrate clustering of band 3 protein, suggesting that spatial rearrangement of band 3 protein was not the cause of the IgG binding. Neutrophil-induced IgG binding due to the combined action of proteases and oxidants may explain the accelerated destruction of erythrocytes in inflammatory diseases.
Characterization of bilirubin transport system by human peripheral blood mononuclear cells
Authors: Haga Yoshio , Tempero Margaret A , Kay H David , Zetterman Rowen K 
Published: January 2018

Abstract
Decreased immune responses have been observed in hyperbilirubinemic patients. This study investigates bilirubin transport into human peripheral blood mononuclear cells (PBMNCs). In vitro incubation of PBMNCs at 37° with 0–12 mg/dl bilirubin in solution with a fixed bovine serum albumin (BSA) concentration (3.0 g/dl) resulted in a dose-dependent increase of intracellular bilirubin in both monocytes and lymphocytes. Bilirubin uptake in monocytes was significantly higher (up to 2.7 times) than in lymphocytes under the same culture conditions. When PBMNCs were incubated with varying concentrations of bilirubin (0–16 mg/dl) in fixed BSA (3.0 g/dl) solution or at a fixed bilirubin/albumin molar ratio (0.4), the initial velocity of uptake in both cell fractions was proportional to the free (unbound to albumin) bilirubin concentration rather than the total bilirubin concentration. Bilirubin uptake by both cell fractions was significantly inhibited by treatment with metabolic inhibitors. Bilirubin uptake by monocytes continued to increase in parallel with incubation temperature from 0° to 40°, whereas uptake by lymphocytes reached a maximal level at 20° and remained constant thereafter. These results suggest that monocytes and lymphocytes incorporate bilirubin in proportion to the free bilirubin concentration and this function may rely on different energy-dependent mechanisms.
Regulation of phospholipase A2 activation and arachidonic acid metabolism in an interleukin-3–dependent macrophage-like cell line
Authors: Shibata Yoshimi , McCaffrey Patricia G , Minowada Jun , Volkman Alvin , Oghiso Yoichi 
Published: January 2018

Abstract
An interleukin 3 (IL-3)–dependent macrophage-like cell line, 11-1-B3, was newly established from CBA/J mouse bone marrow cell cultures. Assay of eicosanoids in the culture supernatants of the intact and [3H]arachidonic acid (AA)–prelabeled cells showed that, after stimulation with the Ca2+ ionophore A23187, the 11-1-B3 cells synthesized and released relatively large amounts of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) but not LTC4. In addition, 11-1-B3 cells showed Ca2+-dependent and alkaline pH–optimal phospholipase A2 (PLA2) activity that preferentially hydrolyzed cleavage of sn-2-arachidonyl- but not sn-2-oleoylphosphatidylcholine. The cellular enzyme was distributed with 90% of the activity in the cytosol and 10% in the membrane fraction. Treatment of cells with A23187 for 5–10 min resulted in five- to sevenfold increases in the membrane-associated PLA2 but activity in the cytosol was unchanged. This increase in membrane-associated enzyme activity was transient, returning to the pretreatment distribution after 30 min. In sharp contrast, phorbol myristate acetate (PMA) stimulation failed to induce either eicosanoid release or PLA2 activation, although PMA induced translocation of protein kinase C (PKC) to the membrane fraction within 10 min. The data suggest that increases in cellular Ca2+ directly activate membrane-associated PLA2 and consequently initiate AA metabolism; PKC activation by PMA requires additional steps to activate PLA2, a mechanism that is apparently deficient in the IL-3–dependent Mø-like cells.
In vivo latex phagocytosis primes the Kupffer cells and hepatic neutrophils to generate superoxide anion
Authors: Bautista Abraham P , Schuler Agnes , Spolarics Zoltan , Spitzer John J 
Published: January 2018

Abstract
Activation of liver macrophages during clearance of endotoxins, bacteria, or other particulate materials may be accompanied by the migration of polymorphonuclear neutrophils (PMNs) into the liver and priming of the hepatic phagocytes to release toxic oxygen metabolites. In the present study we investigated the effect of in vivo administration of latex particles on the hepatic sequestration of PMNs and the release of superoxide anion (O2-) by the in situ perfused rat liver and isolated hepatic phagocytes. One hour after an intravenous injection of latex beads, a significant amount of O2- (0.7 nmol/min/g) was produced by the in situ perfused liver. Administration of latex particles into the perfused liver also elicited O2- production. Hepatic phagocytes from latex-treated rats generated large amounts of O2- (2–14 nmol/60 min/106 cells) when these cells were stimulated in vitro with opsonized zymosan or phorbol myristate acetate (PMA), whereas phagocytes from saline-treated rats released less than 0.8 nmol O2-. Intravenous infusion of superoxide dismutase or ibuprofen did not prevent the immigration of PMNs to the liver. However, ibuprofen inhibited the production of O2- by the perfused liver. Also, after addition of ibuprofen in vitro to isolated cells, there was more than 50% inhibition of O2- generation by Kupffer cells and hepatic PMNs treated with either zymosan or PMA. These observations suggest that arachidonic acid metabolites play a role in O2- release under these conditions. Thus, activation of the reticuloendothelial system by latex phagocytosis induces the migration of PMNs into the liver and enhances the production of toxic oxygen-derived radicals by these cells and the resident Kupffer cells. The toxic oxygen radicals may also contribute to hepatic injury.
Differential immunocompetence of macrophages derived using macrophage or granulocyte-macrophage colony-stimulating factor
Authors: Rutherford Mark S , Schook Lawrence B 
Published: January 2018

Abstract
Macrophages derived in vitro from bone marrow progenitors (bone marrow–derived macrophages, BMDMs) using either macrophage colony-stimulating factor (CSF-1) or granulocyte-macrophage colony-stimulating factor (GM-CSF) as the myelopoietic stimulus display differential functional, morphological, and mRNA phenotypes. The data presented here demonstrate further that CSF-1– and GM-CSF–derived BMDMs differ in immunologic capacity. GM-CSF–derived BMDMs, when compared to CSF-1–derived BMDMs, showed greater cytolytic activity against tumor necrosis factor α (TNF-α)–resistant, but not TNF-α–sensitive, tumor targets. In contrast, CSF-1–derived BMDMs produced nitrite in response to lipopolysaccharide (LPS) alone, whereas GM-CSF–derived BMDMs required interferon γ plus LPS treatment. The two BMDM populations also showed differential sensitivities to LPS for secretion of TNF-α and nitrite, but the maximal inducible amounts of these factors and prostaglandin E2 were similar between the BMDM populations. Lastly, GM-CSF–derived but not CSF-1–derived BMDMs showed an L-arginine–dependent listeriacidal activity. These results show that the functional heterogeneity of CSF-1– and GM-CSF–derived macrophages is limited and appears to result largely from differences in the activational signals required by each BMDM population to elicit a given function.
Synergistic interaction of bacterial lipopolysaccharide and the monocyte-macrophage colony-stimulating factor: potential quantitative and qualitative changes in macrophage-produced cytokine bioactivity
Authors: Evans Robert , Kamdar Sonya J , Duffy Theodore M , Fuller Jane 
Published: January 2018

Abstract
In this brief definitive report, we show that over a 6-h period and under serum-free conditions, recombinant monocyte-macrophage colony-stimulating factor 1 (rCSF-1) and lipopolysaccharide (LPS) synergize and induce macrophages to express higher levels of mRNA for interleukin 1α (IL-1α), IL-1β, tumor necrosis factor α (TNF-α), and IL-6 and to release more bioactivity than macrophages treated with LPS alone. This synergy was regulated by the amount of LPS in the culture medium. Paraformaldehyde-fixed macrophages likewise showed augmentation of IL-1 activity, but whereas all of the bioactivity associated with the fixed macrophages could be neutralized by anti-IL-1α antibody only ≍ 40% of the supernate activity could be attributed to IL-1α. Preliminary data suggest that the augmenting effect induced by CSF-1 cannot be explained solely on a quantitative basis because the addition of rIL-1α to supernates of macrophages treated with LPS alone or with the combination of LPS and CSF-1 resulted in an increase in thymocyte mitogenic activity to a level that could not be explained on an additive basis. Although the supernates contained TNF and IL-6, antibody neutralization assays made it unlikely that these were directly responsible for the augmenting effect. These results suggest that CSF-1 not only enhances basic genetic responses induced by LPS alone but also may induce a mechanism that amplifies cytokine bioactivity.
Prostaglandin E2 receptor activity and susceptibility to natural killer cells
Authors: Fulton Amy M , Chong Yen C 
Published: January 2018

Abstract
We have described a high-affinity receptor for prostaglandin E2 (PGE2) present on metastatic murine mammary tumor cells. Pharmacologic antagonism of this receptor increases metastatic potential. In the present study, we have asked whether the binding activity of PGE on tumor target cells plays a role in natural killer (NK)–target cell interactions. We have used three unrelated PGE-receptor antagonists, SC19220, LEO101, and AH6809, to show inhibition of [3H]PGE2 binding to YAC-1 cells and inhibition of PGE2-mediated elevation of intracellular cyclic AMP (cAMP). Addition of any of these three receptor antagonists to standard 4-h 51Cr-release assays inhibits YAC-1 lysis by NK-enriched populations from murine spleen. This is the first report that antagonism of PGE binding affects NK activity. Our studies demonstrate that these effects are mediated through inhibition of target-effector cell conjugate formation. Studies in which effector and target cells were pretreated separately indicate that the PGE-mediated effects are expressed at the target cell level.