bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytochalasin D inhibits lipopolysaccharide-induced tumor necrosis factor production in macrophages
Authors: Shinji Hitomi , Akagawa Kiyoko S , Yoshida Takeshi 
Published: January 2018

Abstract
We reported previously that a reorganization of microfilaments can be observed when macrophages are stimulated with lipopolysaccharide (LPS). This reorganization is not detected with current methods in macrophages of an LPS-nonresponsive C3H/HeJ mouse. These results suggest that the observed microfilament response might be involved in a macrophage-activating process induced by LPS. To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production. A concentration of CD incapable of affecting filamentous actin by itself was used in these experiments. When this concentration of CD was added after LPS stimulation, microfilament reorganization and TNF production were inhibited. The suppressive effect of CD on TNF production was confirmed by the observation that TNF-α mRNA expression was also inhibited by CD. This inhibitory effect of CD was not specific to TNF, because the production of interleukin-1 and prostaglandin E2 were also inhibited. These effects of CD were observed only when CD was added within the first 20 min after LPS stimulation. These results suggest that the CD- sensitive microfilament response is essential in the signaling pathway for the production of certain monokines in LPS-stimulated macrophages.
Ex vivo clonotype primer-directed gene amplification to identify malignant T cell repertoires
Authors: Beers Teri , Du Tian-Long , Rickert Michael , Overturf Phyllis , Choi Youngnim , Greenberg Steven J 
Published: January 2018

Abstract
A novel strategy that utilizes input genomic DNA and overcomes limitations encountered with traditional RNA reverse transcription-polymerase chain reaction (PCR) amplification methodology is described to screen for T cell receptor (TCR) repertoires. The methodology has been developed to identify individual T cell clonotypes with regard to their unique receptor beta chain variable/diversity/joining (VDJ) region gene rearrangement. The technique avoids preselection for a given antigen specificity and is therefore independent of artificial bias introduced by in vitro cell population expansion. This technique was used to detect and identify genetically of malignant clones from heterogeneous mononuclear cell populations from an array of hemato- oncological disorders, including mycosis fungoides/Sézary Syndrome, adult T cell leukemia, and large granular lym- phoproliferative disease. An initial primary PCR, directed by a TCR-Jβ generic primer and a complement of family-specific TCR-Vβ primers, defines predominant T cell receptor variable gene usage. Use of a TCR-Jβ generic primer supplants the use of a constant region primer anchor and thus eliminates the need to target mRNA. The process of variable gene screening also expedites gene sequencing. By sequencing through the VDJ juxtaposed region, i.e·, the third complementarity determinant region, clonotype-specific primers are developed and used in a secondary clonotype primer-directed PCR (CPD-PCR) to detect, with extreme sensitivity and specificity, unique T cell clonal repertoires. Analysis of the products of the CPD-PCR permits the detection of a single malignant cell among one million polyclonal cells and supercedes the constraints of prior studies that provide a limited evaluation of family variable gene repertoire usage. This strategy may be applied in the detection of minimal residual disease, in surveillance after induction of disease-free states, and in analyzing the effectiveness of purging autologous bone marrow of malignant clones
Lipopolysaccharide and a phorbol ester stimulate secretion of tumor necrosis factor-α from alveolar macrophages through action on overlapping subsets of cells
Authors: Taylor Michael J , Hehnke Karen , Clark Cheryl L 
Published: January 2018

Abstract
A cell-by-cell analysis of the secretory ability of stimulated, individual alveolar macrophages (AMs) was performed through use of a tumor necrosis factor a (TNF-α) reverse hemolytic plaque assay. Two functional end points were measured: the percentage of AMs that were TNF-α secretors and the cumulative amount of TNF-α secreted by AMs (average plaque area, μm2). Lipopolysaccharide (LPS; 100 μg/ml) increased cumulative TNF-α release at both 7 and 20 h of incubation. On the other hand, a phorbol ester (phorbol myristate acetate, PMA) stimulated TNF-α release at 20 h of incubation but not at 7 h. Under nonstimulated culture conditions, 5-10% of all AMs released detectable TNF-α. PMA (but not LPS) induced a significant increase in the fraction of AMs capable of releasing TNF-α (15.1 ± 1.1% vs. 9.0 ± 1.6%, PMA vs. control, P &lt; .05). Differences in the time course of secreted TNF-α, together with the recruiting effect of PMA, suggest that LPS and PMA target TNF-α- secretory subpopulations of AMs that differ in number and secretory characteristics.
Immunoglobulin G-mediated phagocytosis activates a calcium-independent, phosphatidylethanolamine-specific phospholipase
Authors: Lennartz Michelle R , Lefkowith James B , Bromley Frances A , Brown Eric J 
Published: January 2018

Abstract
Inhibition of arachidonate release down- regulates immunoglobulin G-mediated phagocytosis. This arachidonate requirement is selective for IgG- opsonized targets, suggesting that arachidonate may act as a second messenger for Fcγ receptor-mediated phagocytosis. Here we report the characterization of a phospholipase, activated during phagocytosis, that releases arachidonate from phosphatidylethanolamine in the absence of intracellular calcium ([Ca]i ≤ 2 nM). In vitro, a phospholipase with these characteristics was detected in soluble and particulate fractions of human monocyte homogenates. (E)-6-(Bromomethylene)tetrahydro-3-(l- naphthalenyl)-2H-pyran-2-one, a drug that selectively inhibits Ca-independent phospholipase A2S, is shown to inhibit IgG-mediated phagocytosis and its associated arachidonate release in intact monocytes as well as the in vitro enzyme activity. These findings provide a link between the whole-cell and in vitro data and present the initial characterization of a receptor-activated, calcium- independent phospholipase from human monocytes.
Differential effects of interferon-γ and glucocorticoids on FcγR gene expression in murine macrophages
Authors: Sivo Judit , Politis Alexander D , Vogel Stefanie N 
Published: January 2018

Abstract
Interferon-γ (IFN-γ) was shown previously to increase Feγ receptor (FcyR)-mediated binding and phagocytosis of immunoglobulin G-opsonized erythrocytes in mouse peritoneal exudate macrophages. Glucocorticoids potentiated this effect. We have extended these observations to an investigation of the effects of IFN-γ and glucocorticoids on steady-state mRNA levels of the three FcyR genes expressed on murine macrophages: FcyRI, FcγRII, and FcγRIIIα. FcγRI mRNA was present at a barely detectable level in unstimulated cells but was induced 5- to 10-fold by IFN-γ. FcγRIIIα mRNA was expressed constitutively and was induced significantly but very modestly (1.5-fold) by IFN-γ. FcγRII mRNA also exhibited high constitutive expression, but it was not altered by IFN-γ treatment. Dexamethasone (DEX) significantly increased the expression of IFN-γ-induced FcγRI mRNA but had no effect on the expression of FcγRII or FcγRIIIa transcripts in untreated or IFN- γ-treated cells. The effect of DEX on FcγRI mRNA was seen after about 10 h of simultaneous treatment with IFN-γ, was dose-dependent, and was glucocorticoid specific. DEX did not modulate the rate of decay of the FcγRI mRNA, suggesting that the up-regulatory effect of DEX may occur, in part, at the level of transcription. In the same culture system, the steady-state level of IFN- γ-induced Ia mRNA was concurrently inhibited by DEX. The up-regulation of the IFN-γ-induced high-affinity FcγRI mRNA, the failure to modulate the expression of the two low-affinity FcγR mRNA species, and the down- regulation of IFN-γ-induced la mRNA by DEX in the same cell population illustrate the diverse, gene-specific influence of glucocorticoids on the expression of IFN- γ-inducible genes.
Both mannose and β-glucan receptors are involved in phagocytosis of unopsonized, heat-killed Saccharomyces cerevisiae by murine macrophages
Authors: Giaimis Jean , Lombard Wes , Fonteneau Paul , Muller Christian D , Levy Rachel , Makaya-Kumba Madeleine , Lazdins Janis , Poindron Philippe 
Published: January 2018

Abstract
We studied the involvement of lectin-like receptors in phagocytosis of unopsonized heat-killed yeast (Saccharomyces cerevisiae) by murine macrophagelike cell lines and murine peritoneal resident macrophages. For this purpose we used a technique that allowed us to discriminate ingested and adsorbed heat-killed yeast. The internalization can be partly inhibited by soluble polyosides such as laminarin (β-glucan) or a- mannan. However, when they were used together (0.4 mg/ml α-mannan and 0.4 mg/ml laminarin), almost complete inhibition of phagocytosis was obtained. These observations suggest that phagocytosis of unopsonized heat- killed yeast by murine macrophage-like cell lines as well as murine peritoneal resident macrophages is mediated by both mannose and β-glucan receptors. The respective activity of these two types of receptors is a function of in vitro cell differentiation. To achieve maximal phagocytosis of unopsonized heat-killed yeast, coexpression of both mannose and β-glucan receptors is required.
Histamine modulation of Ca2+ homeostasis in human neutrophils
Authors: Leino Lasse , Tuominen Helena B , Åkerman Karl E O 
Published: January 2018

Abstract
The influence of histamine on the basal intracellular free Ca2+ concentration ([Ca2+]i) and agonist- induced increases of [Ca2+], was studied in Fura-2-loaded neutrophils. Histamine was unable to change the basal [Ca2+]i at concentrations (10−6-10-4 M) that have been shown to cause a rapid increase in [Ca2+]i in a variety of cell types. Histamine, in contrast, was found to inhibit dose-dependently the rise in [Ca2+]i induced by two neutrophil receptor agonists, IV- formylmethionyl-leucyl- phenylalanine (fMLP) and serum-opsonized zymosan particles. The histamine inhibition was shown to be specific for H2 receptor activation by blocking experiments with selective H1 and H2 receptor antagonists. In the absence of extracellular Ca2+, histamine failed to inhibit the agonist-induced rise in [Ca2*]i, indicating that histamine does not affect the release of Ca2+ from internal pools. Forskolin, which mimics the biochemical effects of H2 receptor activation by directly stimulating adenylate cyclase, also decreased the Ca2+ transients induced by receptor agonists. Similarly, 3-isobutyl-l-methylxanthine (IBMX), a phosphodiesterase inhibitor, reduced the Ca2+ response of activated neutrophils. These data suggest that in human neutrophils (1) no functional H1 receptors are present or alternatively H1 receptors are not coupled to cellular Ca2+ metabolism, and (2) H2 receptors modulate the receptor-triggered Ca2+ flux via the cAMP second messenger system.
Docosahexanoic acid (22:6, n-3) but not eicosapentaenoic acid (20:5, n-3) can induce neutrophil-mediated injury of cultured endothelial cells: involvement of neutrophil elastase
Authors: Bates Edna J , Ferrante Antonio , Harvey Dianne R , Nandoskar Madhuri , Poulos Alf 
Published: January 2018

Abstract
Previously published work has indicated that polyunsaturated fatty acids (PUFA) may enhance neutrophil-mediated damage to host tissues. We have found that endothelial detachment was significantly increased by neutrophils pretreated with docosahexaenoic (22:6, n-3) and arachidonic (20:4, n-6) acids at 10-40 μΜ but not by eicosapentaenoic acid (20:5, n-3). Endothelial cell lysis as measured by 51Cr release was unaffected. The extent of detachment was dependent on both fatty acid and neutrophil pretreatment concentrations. A specific leukocyte elastase inhibitor abrogated the increased detachment but catalase had no effect. Measurement of prostaglandin I2 synthesis as an alternative nonlytic assay of endothelial function indicated that 20:4 but not 20:5 was able to stimulate neutrophil-induced endothelial PGI2 synthesis. Although all three PUFA (3-33 μΜ) were found to stimulate release from neutrophil-specific granules, only 22:6 and 20:4 could stimulate release of the azurophilic granules containing elastase to any significant extent. Saturated fatty acids (20:0 and 22:0) and the methyl ester of 22:6 did not cause either neutrophil-mediated endothelial detachment or degranulation. We conclude that neutrophils pretreated with 22:6 or 20:4 but not 20:5 can decrease endothelial integrity through detachment involving neutrophil elastase. These findings may have important implications for the dietary use of fish oils rich in n-3 fatty acids.
Function and regulation of leukocyte homing receptors
Authors: Jutila Mark A 
Published: January 2018

Abstract
In vivo studies in the mid-1960s showed that lymphocytes home to various lymphoid compartments of the body in a tissue-specific manner. A central event in this process is adhesion of the leukocyte in the blood to specialized endothelial cells within the lymphoid organs. Leukocyte binding to the vascular endothelial cells involves many diverse adhesion molecules expressed by both cell types. Those adhesion molecules which contribute to the tissue specificity of the leukocyte-endothelial cell interactions are called “homing receptors.” The study of homing receptors has progressed tremendously in recent years. The intent of this treatise is to review our current understanding of these molecules in the context of the lymphocyte and outline studies showing that these molecules have important functions for other leukocytes as well. A general overview of leukocyte-endothelial cell adhesion will not be given: the reader can easily find many excellent and up-to-date reviews of this subject in the literature. This review is an attempt to outline the major contributions to the identification and characterization of homing receptors. Apologies are extended for any oversights made. J. Leukoc. Biol. 55: 133–140; 1994.
Hyperimmune serum modulates allergic response to spores in a murine model of allergic aspergillosis
Authors: Murali Pazhayannur S , Bamrah Bindu S , Choi Hongyung , Fink Jordan N , Kurup Viswanath P 
Published: January 2018

Abstract
Allergic bronchopulmonary aspergillosis (ABPA) is a disease in atopic asthmatics characterized by eosinophilia and elevated levels of immunoglobulin E (IgE) and IgG antibodies to the ubiquitous fungus Aspergillus fumigatus (Af). The role of specific antibodies in the disease process is not clear. In this study, BALB/c mice were injected with hyperimmune serum from syngeneic mice exposed to soluble antigen of Af. These mice were then exposed to either Af spores or soluble antigen. Total IgE, Af-specific IgG1 (enzyme-linked immunosorbent assay) in serum, and eosinophils (eosinophil peroxidase assay) in lungs and bone marrow were measured. Histologic sections of lungs were examined for cellular infiltration and morphologic changes. Results indicate a suppression of increase in levels of antibodies and eosinophilia in mice receiving immune serum and exposed to spores compared with controls receiving phosphate-buffered saline treatment. Spores being the primary source of exposure to Af in ABPA, these results are significant in understanding the role of preexisting specific antibodies in patients. J. Leukoc. Biol. 55: 29–34; 1994.
Activation of NF-κB may be necessary but is not sufficient for induction of H-2 antigens by TNF in J558L murine myeloma cells
Authors: Wolchok Jedd D , Goodman Adam R , Vilçek Jan 
Published: January 2018

Abstract
We have investigated the role of the transcription factor NF-κB in the induction of H-2 antigens by tumor necrosis factor (TNF) in murine J558L myeloma cells. An earlier report suggested that J558L cells may have a defect in NF-κB activation in response to some stimuli. Treatment of J558L cells with either TNF or lipopolysaccharide (LPS) resulted in nuclear translocation of NF-κB, as demonstrated by electrophoretic mobility shift assay. Both TNF and LPS activated the same NF-κB nuclear complexes, composed of the p50 and p65 subunits. LPS mediated a stronger and more sustained activation of NF-κB than TNF. In contrast, TNF induced higher levels of H-2 antigen surface expression than did LPS, suggesting that activation of NF-κB is not sufficient for optimal enhancement of H-2 expression. An inhibitor of NF-κB activation, pyrrolidinedithiocarbamate (PDTC), dramatically reduced the induction of H-2 antigen by TNF, supporting the view that NF-κB is required for TNF-induced H-2 antigen expression. Constitutive levels of H-2 antigen expression on the cell surface and of nuclear NF-κB also decreased after PDTC treatment. However, PDTC had a smaller inhibitory effect on LPS-induced NF-κB activation and H-2 antigen expression, suggesting that TNF and LPS activate NF-κB by somewhat different pathways. J. Leukoc. Biol. 55: 7–12; 1994.
Leishmania donovani infection enhances macrophage viability in the absence of exogenous growth factor
Authors: Moore Kathryn J , Turco Salvatore J , Matlashewski Greg 
Published: January 2018

Abstract
Bone marrow-derived macrophages rapidly die in the absence of macrophage growth factor (M-CSF). However, as demonstrated here, bone marrow-derived macrophages infected with Leishmania donovani exhibit increased viability in the absence of exogenous growth factor. Forty-eight hours after inoculation with promastigotes or amastigotes, infected cell cultures contained 180 and 95% more cells, respectively, than control cultures. This effect was specific to Leishmania infection, as uptake of latex beads or avirulent promastigotes by macrophages did not enhance cell viability. L. donovani-infected macrophages also displayed increased phagocytic capacity, as compared with control macrophages and macrophages grown continuously in M-CSF-containing medium. Supernatants collected from infected cells elaborated a factor(s) that enhanced macrophage viability but did not stimulate macrophage DNA synthesis. This activity of L. donovani-infected cell-conditioned medium could be abrogated by preincubation of macrophages with cycloheximide before inoculation with the parasite, implying that macrophage protein synthesis is required for the elaboration of this factor(s). J. Leukoc. Biol. 55: 91–98; 1994.
Secretion of TNF-α by alveolar macrophages in response to Candida albicans mannan
Authors: Garner Ronald E , Rubanowice Katherine , Sawyer Richard T , Hudson John A 
Published: January 2018

Abstract
Resident alveolar macrophages (AMø) were tested for their ability to respond to Candida albicans mannan. AMø were found to produce tumor necrosis factor alpha (TNF-α) in vitro in response to mannan stimulation. TNF-α secretion was measured using ELISA and L929B cellular cytotoxicity assays. Cytotoxicity was neutralized in parallel L929B cell cultures by the addition of rabbit anti-TNF-α antibody. Mannan preparations were found to be free of contaminating LPS by Limulus assay. When AMø were cultivated for 18 h at 37°, 67 μg of mannan stimulated the secretion of approximately 207 U/ml of TNF-α. By comparison, AMø treated with 6.7 μg of LPS secreted approximately 257 U/ml of TNF-α. Optimal TNF-α production occurred between 9 and 18 h after mannan stimulation. Disparate mechanisms for stimulation of TNF-α secretion were suggested by differential sugar blockade of LPS- and mannan-induced TNF-α secretion. The addition of 2% D-mannose or 2% alpha-methyl-D-mannoside to AMø cultures blocked mannan-but not LPS-stimulated TNF-α secretion. Furthermore, the addition of rabbit anti-mannan antibody to mannan-coated plastic culture dishes prevented TNF-α secretion by the mannan-sensitive RAW 264.7 cell line. Moreover, the data suggest that C. albicans mannan stimulated AMø to secrete TNF-α by an LPS-independent receptor mechanism which may also function as a mannose receptor. J. Leukoc. Biol. 55: 161–168; 1994.
Inhibition of human interferon-gamma expression by antisense oligodeoxynucleotides
Authors: Boeve Christine M A , De Ley Marc 
Published: January 2018

Abstract
We investigated 12 antisense oligodeoxynucleotides, complementary to different regions of the human interferon-γ (HuIFN-γ) gene, for their ability to inhibit HuIFN-γ production in cultures of single donor total leukocytes or lymphocytes (95% purity). Out of seven oligomers, specific for a sequence including the translation initiation codon, 15 to 21 nucleotides long, the one resulting in the greatest inhibition was the 16-mer. An inhibitory effect of 90% could be achieved when the oligomer was added to cultures of lymphocytes in separate doses. Three other 16-mers, complementary to a sequence in the 5′ noncoding region, in the coding region, or at the donor splice junction of the third intron respectively, were inhibitory to a lesser extent. Two 16-mers, one complementary to a sequence at the donor splice junction of the second intron and one specific for a sequence in the 3′ untranslated region, showed no effect. J. Leukoc. Biol. 55: 169–174; 1994.
Inhibition of activation-induced death in T cell hybridomas by thiol antioxidants: oxidative stress as a mediator of apoptosis
Authors: Sandstrom Paul A , Mannie Mark D , Buttke Thomas M 
Published: January 2018

Abstract
N-Acetylcysteine (NAC) is a well established thiol antioxidant which, after uptake, deacylation and conversion to glutathione functions as both a redox buffer and a reactive oxygen intermediate scavenger. We report here that NAC completely blocks activation induced death and associated DNA fragmentation of myelin basic protein (MBP) specific T cell hybridomas. Conversely, NAC had very little effect on the antigen driven proliferation of a MBP specific T cell line similar to that from which the hybridomas were derived. NAC displayed an analogous absolute inhibition of mitogen mediated activation induced death, even if added up to 3 h post activation. Although glutathione was as efficient as NAC at blocking activation induced death, dithiothreitol displayed minimal inhibition while L-cysteine had no effect at all. The observation that certain thiol antioxidants such as NAC and glutathione can completely block the activation induced death of T cell hybridomas implicates redox regulation in this process. J. Leukoc. Biol. 55: 221–226; 1994.
Activation of macrophages for cytolysis of virally infected cells by monoclonal antibody to the 73-kDa lipopolysaccharide receptor
Authors: LeBlanc Paul A 
Published: January 2018

Abstract
The abilities of lipopolysaccharide (LPS) and mAb5D3 (a monoclonal antibody specific for the 73 kDa LPS receptor) to activate bone marrow culture derived macrophages (BMCM) for cytolysis of vesicular stomatitis virus infected BALB/c3T3 (VSV-3T3) and the tumor target, P815, were compared. Activation for cytolysis of VSV-3T3 cells occurred at a lower level of either LPS or mAb5D3 than activation for cytolysis of P815. With both targets and under several stimulation conditions there was a constant differential between the two activating stimuli. These data indicate that stimulation of the 73 kDa LPS receptor at low levels of either mAb5D3 or LPS can activate BMCM for cytolysis of VSV-3T3 but not P815. Further, the constant relative efficiency of mAb5D3 to LPS in both target systems suggests that there is a common receptor for both LPS mediated effects. J. Leukoc. Biol. 55: 262–264; 1994.