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Deep vein puncture under ultrasonographic guidance-an alternative approach for vascular access of apheresis therapies.
Hanafusa N, Torato T, Katagiri D, Usui T, Matsumoto A, Noiri E, Nangauku M
(2015) J Clin Apher 30: 380-1
MeSH Terms: Adult, Blood Component Removal, Colitis, Ulcerative, Granulocytes, Humans, Middle Aged, Monocytes, Punctures, Retrospective Studies, Ultrasonography, Interventional, Veins
Added February 11, 2016
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11 MeSH Terms
Cysteinyl leukotriene overproduction in aspirin-exacerbated respiratory disease is driven by platelet-adherent leukocytes.
Laidlaw TM, Kidder MS, Bhattacharyya N, Xing W, Shen S, Milne GL, Castells MC, Chhay H, Boyce JA
(2012) Blood 119: 3790-8
MeSH Terms: Adult, Aged, Arachidonate 5-Lipoxygenase, Aspirin, Asthma, Aspirin-Induced, Blood Platelets, Bronchoconstriction, Cysteine, Female, Granulocytes, Humans, Integrins, Leukocytes, Leukotriene E4, Leukotrienes, Male, Middle Aged, Nasal Polyps, Platelet Aggregation Inhibitors, Young Adult
Show Abstract · Added March 26, 2014
Cysteinyl leukotriene (cysLT) overproduction is a hallmark of aspirin-exacerbated respiratory disease (AERD), but its mechanism is poorly understood. Because adherent platelets can convert the leukocyte-derived precursor leukotriene (LT)A(4) to LTC(4), the parent cysLT, through the terminal enzyme LTC(4) synthase, we investigated the contribution of platelet-dependent transcellular cysLT production in AERD. Nasal polyps from subjects with AERD contained many extravascular platelets that colocalized with leukocytes, and the percentages of circulating neutrophils, eosinophils, and monocytes with adherent platelets were markedly higher in the blood of subjects with AERD than in aspirin-tolerant controls. Platelet-adherent subsets of leukocytes had higher expression of several adhesion markers than did platelet nonadherent subsets. Adherent platelets contributed more than half of the total LTC(4) synthase activity of peripheral blood granulocytes, and they accounted for the higher level of LTC(4) generation by activated granulocytes from subjects with AERD compared with aspirin-tolerant controls. Urinary LTE(4) levels, a measure of systemic cysLT production, correlated strongly with percentages of circulating platelet-adherent granulocytes. Because platelet adherence to leukocytes allows for both firm adhesion to endothelial cells and augmented transcellular conversion of leukotrienes, a disturbance in platelet-leukocyte interactions may be partly responsible for the respiratory tissue inflammation and the overproduction of cysLTs that characterize AERD.
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20 MeSH Terms
Adenosinergic regulation of the expansion and immunosuppressive activity of CD11b+Gr1+ cells.
Ryzhov S, Novitskiy SV, Goldstein AE, Biktasova A, Blackburn MR, Biaggioni I, Dikov MM, Feoktistov I
(2011) J Immunol 187: 6120-9
MeSH Terms: 5'-Nucleotidase, Adenosine, Animals, CD11b Antigen, Carcinoma, Lewis Lung, Cell Differentiation, Cell Proliferation, Cell Separation, Female, Flow Cytometry, Granulocytes, Male, Mice, Mice, Inbred C57BL, Myeloid Cells, Real-Time Polymerase Chain Reaction, Receptors, Purinergic P1
Show Abstract · Added May 29, 2014
Extracellular adenosine and purine nucleotides are elevated in many pathological situations associated with the expansion of CD11b(+)Gr1(+) myeloid-derived suppressor cells (MDSCs). Therefore, we tested whether adenosinergic pathways play a role in MDSC expansion and functions. We found that A(2B) adenosine receptors on hematopoietic cells play an important role in accumulation of intratumoral CD11b(+)Gr1(high) cells in a mouse Lewis lung carcinoma model in vivo and demonstrated that these receptors promote preferential expansion of the granulocytic CD11b(+)Gr1(high) subset of MDSCs in vitro. Flow cytometry analysis of MDSCs generated from mouse hematopoietic progenitor cells revealed that the CD11b(+)Gr-1(high) subset had the highest levels of CD73 (ecto-5'-nucleotidase) expression (Δmean fluorescence intensity [MFI] of 118.5 ± 16.8), followed by CD11b(+)Gr-1(int) (ΔMFI of 57.9 ± 6.8) and CD11b(+)Gr-1(-/low) (ΔMFI of 12.4 ± 1.0) subsets. Even lower levels of CD73 expression were found on Lewis lung carcinoma tumor cells (ΔMFI of 3.2 ± 0.2). The high levels of CD73 expression in granulocytic CD11b(+)Gr-1(high) cells correlated with high levels of ecto-5'-nucleotidase enzymatic activity. We further demonstrated that the ability of granulocytic MDSCs to suppress CD3/CD28-induced T cell proliferation was significantly facilitated in the presence of the ecto-5'-nucleotidase substrate 5'-AMP. We propose that generation of adenosine by CD73 expressed at high levels on granulocytic MDSCs may promote their expansion and facilitate their immunosuppressive activity.
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17 MeSH Terms
Selective roles for antiapoptotic MCL-1 during granulocyte development and macrophage effector function.
Steimer DA, Boyd K, Takeuchi O, Fisher JK, Zambetti GP, Opferman JT
(2009) Blood 113: 2805-15
MeSH Terms: Animals, Apoptosis, Apoptosis Regulatory Proteins, Bcl-2-Like Protein 11, Bone Marrow Cells, Escherichia coli, Filgrastim, Gene Deletion, Granulocyte Colony-Stimulating Factor, Granulocytes, Macrophage Activation, Macrophages, Peritoneal, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Myeloid Cell Leukemia Sequence 1 Protein, Myelopoiesis, Organ Specificity, Phagocytosis, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Recombinant Proteins, Specific Pathogen-Free Organisms, Tumor Suppressor Proteins, bcl-2 Homologous Antagonist-Killer Protein, bcl-2-Associated X Protein
Show Abstract · Added March 5, 2014
During hematopoiesis, myeloid cell leukemia-1 (MCL-1) mediates the survival of bone marrow progenitors and lymphocytes. However, its requirement during myeloid cell differentiation, development, and effector function is less clear. Lineage-specific deletion of MCL-1 in myeloid precursors results in neutropenia due to death during differentiation. The loss of mature neutrophils induced by Mcl-1 deletion was not rescued by genetic deletion of proapoptotic Bim and Puma or by exogenous cytokine treatment. However, blockade of intrinsic apoptosis by lineage-specific deletion of both multidomain proapoptotics Bax and Bak was capable of rescuing the neutropenia associated with Mcl-1 deletion. In the monocytic lineage, despite efficient Mcl-1 deletion, monocytes and macrophages undergo normal development. During the phagocytosis of extracellular bacteria, macrophages concomitantly increase the expression of both MCL-1 and BIM. However, Mcl-1-deficient macrophages exhibit increased sensitivity to death during bacterial phagocytosis that can be abolished by codeletion of Bim. These data suggest that MCL-1 may be necessary to antagonize BIM during macrophage effector responses. Thus, MCL-1 plays selective roles in myeloid development, being required for neutrophil development and setting the threshold for apoptosis during a macrophage effector response.
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27 MeSH Terms
Hemocyte-mediated phagocytosis and melanization in the mosquito Armigeres subalbatus following immune challenge by bacteria.
Hillyer JF, Schmidt SL, Christensen BM
(2003) Cell Tissue Res 313: 117-27
MeSH Terms: Acid Phosphatase, Animals, Bacteria, Bacterial Capsules, Cell Adhesion, Culicidae, Escherichia coli, Glycogen, Granulocytes, Green Fluorescent Proteins, Hemocytes, Histocytochemistry, Immunity, Innate, Immunohistochemistry, Lectins, Luminescent Proteins, Mannose-Binding Lectins, Melanins, Micrococcus luteus, Microscopy, Electron, Microscopy, Fluorescence, Microscopy, Immunoelectron, Microscopy, Phase-Contrast, Microspheres, Monophenol Monooxygenase, Phagocytosis, Plant Lectins, Wheat Germ Agglutinins
Show Abstract · Added February 5, 2016
Mosquitoes are important vectors of disease. These insects respond to invading organisms with strong cellular and humoral immune responses that share many similarities with vertebrate immune systems. The strength and specificity of these responses are directly correlated to a mosquito's ability to transmit disease. In the current study, we characterized the hemocytes (blood cells) of Armigeres subalbatus by morphology (ultrastructure), lectin binding, enzyme activity, immunocytochemistry, and function. We found four hemocyte types: granulocytes, oenocytoids, adipohemocytes, and thrombocytoids. Granulocytes contained acid phosphatase activity and bound the exogenous lectins Helix pomatia agglutinin, Galanthus nivalis lectin, and wheat germ agglutinin. Following bacteria inoculation, granulocytes mounted a strong phagocytic response as early as 5 min postexposure. Bacteria also elicited a hemocyte-mediated melanization response. Phenoloxidase, the rate-limiting enzyme in the melanization pathway, was present exclusively in oenocytoids and in many of the melanotic capsules enveloping bacteria. The immune responses mounted against different bacteria were not identical; gram(-) Escherichia coli were predominantly phagocytosed and gram(+) Micrococcus luteus were melanized. These studies implicate hemocytes as the primary line of defense against bacteria.
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28 MeSH Terms
Rapid phagocytosis and melanization of bacteria and Plasmodium sporozoites by hemocytes of the mosquito Aedes aegypti.
Hillyer JF, Schmidt SL, Christensen BM
(2003) J Parasitol 89: 62-9
MeSH Terms: Aedes, Animals, Escherichia coli, Female, Granulocytes, Green Fluorescent Proteins, Hemocytes, Immunity, Cellular, Indicators and Reagents, Insect Vectors, Luminescent Proteins, Melanins, Micrococcus luteus, Microscopy, Electron, Microscopy, Fluorescence, Microscopy, Interference, Microspheres, Phagocytosis, Plasmodium gallinaceum
Show Abstract · Added February 5, 2016
Mosquitoes are vectors of many deadly and debilitating pathogens. In the current study, we used light and electron microscopies to study the immune response of Aedes aegypti hemocytes to bacterial inoculations, Plasmodium gallinaceum natural infections, and latex bead injections. After challenge, mosquitoes mounted strong phagocytic and melanization responses. Granulocytes phagocytosed bacteria singly or pooled them inside large membrane-delimited vesicles. Phagocytosis of bacteria, Plasmodium sporozoites, and latex beads was extensive; we estimated that individual granulocytes have the capacity to phagocytose hundreds of bacteria and thousands of latex particles. Oenocytoids were also seen to internalize bacteria and latex particles, although infrequently and with low capacity. Besides phagocytosis, mosquitoes cleared bacteria and sporozoites by melanization. Interestingly, the immune response toward 2 species of bacteria was different; most Escherichia coli were phagocytosed, but most Micrococcus luteus were melanized. Similar to E. coli, most Plasmodium sporozoites were phagocytosed. The immune response was rapid; phagocytosis and melanization of bacteria began as early as 5 min after inoculation. The magnitude and speed of the cellular response suggest that hemocytes, acting in concert with the humoral immune response, are the main force driving the battle against foreign invaders.
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19 MeSH Terms
Characterization of hemocytes from the yellow fever mosquito, Aedes aegypti.
Hillyer JF, Christensen BM
(2002) Histochem Cell Biol 117: 431-40
MeSH Terms: Acid Phosphatase, Aedes, Animals, Esterases, Granulocytes, Hemocytes, Immunohistochemistry, Lectins, Microscopy, Electron, Monophenol Monooxygenase, Peroxidases, Protein Binding
Show Abstract · Added February 5, 2016
Mosquitoes are the most important arthropod disease vectors, transmitting a broad range of pathogens that cause diseases such as malaria, lymphatic filariasis, and yellow fever. Mosquitoes and other insects are able to mount powerful cellular and humoral immune responses against invading pathogens. To date, most studies have concentrated on the humoral response. In the current study we describe the hemocytes (blood cells) of the yellow fever mosquito, Aedes aegypti, by means of morphology, lectin binding, and enzyme activity and immunocytochemistry. Our light and electron microscopic studies suggest the presence of four distinct hemocyte types: granulocytes, oenocytoids, adipohemocytes, and thrombocytoids. We believe granulocytes and oenocytoids are true circulating hemocytes, but adipohemocytes and thrombocytoids are likely adhered to fixed tissues. Granulocytes, the most abundant cell type, have acid phosphatase and alpha-naphthyl acetate esterase activity, and bind the exogenous lectins WGA, HPA, and GNL. Phenoloxidase, an essential enzyme in the melanotic encapsulation immune response, was detected inside oenocytoids. This is, to our knowledge, the first report that has detected phenoloxidase inside mosquito hemocytes at the ultrastructural level. These results have begun to form a knowledge base for our ongoing studies on the function of Ae. aegypti hemocytes, and their involvement in controlling infections.
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12 MeSH Terms
The relative quiescence of hematopoietic stem cells in nonhuman primates.
Mahmud N, Devine SM, Weller KP, Parmar S, Sturgeon C, Nelson MC, Hewett T, Hoffman R
(2001) Blood 97: 3061-8
MeSH Terms: Animals, Antigens, CD34, Bone Marrow Cells, Bromodeoxyuridine, Cell Cycle, Cell Differentiation, Cell Division, Cell Separation, Clone Cells, Colony-Forming Units Assay, Female, Flow Cytometry, Fluorescent Dyes, Granulocyte Colony-Stimulating Factor, Granulocytes, Hematopoiesis, Hematopoietic Stem Cells, Leukapheresis, Mice, Papio, Rhodamine 123, Species Specificity
Show Abstract · Added November 14, 2013
Quiescence has been thought to be required for the retention of the full biological potential of pluripotent hematopoietic stem cells (PHSCs). This hypothesis has been challenged recently by the observation that all murine PHSCs cycle continuously and constantly contribute to steady-state blood cell production. It was asked whether these observations could be extrapolated to describe hematopoiesis in higher mammals. In this series of experiments, the replicative history of PHSCs was examined in baboons by continuously administering bromodeoxyuridine (BrdU) for more than 85 weeks. The results indicate that under steady-state conditions, PHSCs remain largely quiescent but do cycle, albeit at a far lower rate than previously reported for rodent PHSCs. BrdU-labeled cycling PHSCs and progenitor cells were shown to have an extensive proliferative capacity and to contribute to blood cell production for prolonged periods of time. The proportion of PHSCs entering cell cycle could, however, be rapidly increased by the in vivo administration of granulocyte-colony stimulating factor. These data indicate that during steady-state hematopoiesis, baboon PHSCs require prolonged periods of time to cycle and that the proportion of PHSCs in cycle is not fixed but can be altered by external stimuli. The relative quiescence of PHSCs observed in this nonhuman primate model, in contrast to murine PHSCs, might explain the current barriers to genetic modification and ex vivo expansion of human PHSCs.
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22 MeSH Terms
E2F-1 and E2F-3 are functionally distinct in their ability to promote myeloid cell cycle progression and block granulocyte differentiation.
Strom DK, Cleveland JL, Chellappan S, Nip J, Hiebert SW
(1998) Cell Growth Differ 9: 59-69
MeSH Terms: Apoptosis, Carrier Proteins, Cell Cycle, Cell Cycle Proteins, Cell Differentiation, Cell Line, DNA-Binding Proteins, E2F Transcription Factors, E2F1 Transcription Factor, E2F2 Transcription Factor, E2F3 Transcription Factor, E2F4 Transcription Factor, E2F5 Transcription Factor, Gene Expression Regulation, Granulocyte Colony-Stimulating Factor, Granulocytes, Humans, Interleukin-3, Retinoblastoma-Binding Protein 1, Transcription Factor DP1, Transcription Factors, Tumor Cells, Cultured
Show Abstract · Added June 10, 2010
Interleukin 3 (IL-3)-dependent 32D.3 myeloid cells are an attractive model system for the analysis of hematopoietic cell growth, differentiation, and apoptosis. In these cells, E2F-3, E2F-4, and DP-1 are regulated by both IL-3 and granulocyte colony-stimulating factor (G-CSF), whereas E2F-1 was expressed at low levels and was not regulated by either cytokine. E2F-2 and E2F-5 were not detectable. To examine phenotypes associated with the loss of normal cell cycle regulation by pRb, we established E2F-1- and E2F-3-overexpressing cell lines. In contrast to E2F-1, E2F-3 overexpression did not accelerate apoptosis or promote S-phase entry in the absence of IL-3, demonstrating that they are not functionally redundant. In addition, when cells were cultured in G-CSF to stimulate granulocytic differentiation, E2F-1 overexpression overrode survival functions provided by G-CSF and serum and induced apoptosis. In contrast, cells overexpressing E2F-3 exhibited normal granulocytic differentiation. Bcl-2 coexpression blocked E2F-1-induced apoptosis in the presence of G-CSF. However, these cells were blocked in the granulocytic differentiation program at the metamyelocyte stage and remained dependent on G-CSF for continuous culture. Cells overexpressing both E2F-1 and Bcl-2 exhibited slowed but continuous cell cycling in the absence of IL-3 until they eventually succumbed to apoptosis. Therefore, E2F-1, but not E2F-3, can temporally replace the requirement for growth factors to promote cell cycle progression, and in terminally differentiating cells, this leads to a block in differentiation and induction of apoptosis.
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22 MeSH Terms
The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation.
Westendorf JJ, Yamamoto CM, Lenny N, Downing JR, Selsted ME, Hiebert SW
(1998) Mol Cell Biol 18: 322-33
MeSH Terms: Animals, CCAAT-Enhancer-Binding Proteins, COS Cells, Cell Differentiation, Chromosomes, Human, Pair 21, Chromosomes, Human, Pair 8, Core Binding Factor Alpha 2 Subunit, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, Granulocytes, Hematopoiesis, Humans, Leukemia, Nuclear Proteins, Oncogene Proteins, Fusion, Promoter Regions, Genetic, RUNX1 Translocation Partner 1 Protein, Rats, Recombinant Fusion Proteins, Transcription Factors, Transcription, Genetic, Translocation, Genetic
Show Abstract · Added June 10, 2010
AML-1B is a hematopoietic transcription factor that is functionally inactivated by multiple chromosomal translocations in human acute myeloblastic and B-cell lymphocytic leukemias. The t(8;21)(q22;q22) translocation replaces the C terminus, including the transactivation domain of AML-1B, with ETO, a nuclear protein of unknown function. We previously showed that AML-1-ETO is a dominant inhibitor of AML-1B-dependent transcriptional activation. Here we demonstrate that AML-1-ETO also inhibits C/EBP-alpha-dependent activation of the myeloid cell-specific, rat defensin NP-3 promoter. AML-1B bound the core enhancer motifs present in the NP-3 promoter and activated transcription approximately sixfold. Similarly, C/EBP-alpha bound NP-3 promoter sequences and activated transcription approximately sixfold. Coexpression of C/EBP-alpha with AML-1B or its family members, AML-2 and murine AML-3, synergistically activated the NP-3 promoter up to 60-fold. The t(8;21) product, AML-1-ETO, repressed AML-1B-dependent activation of NP-3 and completely inhibited C/EBP-alpha-dependent activity as well as the synergistic activation. In contrast, the inv(16) product, which indirectly targets AML family members by fusing their heterodimeric DNA binding partner, CBF-beta, to the myosin heavy chain, inhibited AML-1B but not C/EBP-alpha activation or the synergistic activation. AML-1-ETO and C/EBP-alpha were coimmunoprecipitated and thus physically interact in vivo. Deletion mutants demonstrated that the C terminus of ETO was required for AML-1-ETO-mediated repression of the synergistic activation but not for association with C/EBP-alpha. Finally, overexpression of AML-1-ETO in myeloid progenitor cells prevented granulocyte colony-stimulating factor-induced differentiation. Thus, AML-1-ETO may contribute to leukemogenesis by specifically inhibiting C/EBP-alpha- and AML-1B-dependent activation of myeloid promoters and blocking differentiation.
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22 MeSH Terms