bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of Stimulant-Induced Activation of Phagocytic Cells With Tetrandrine
Authors: Castranova Vincent , Kang Ji-Hee , Moore Mark D , Pailes William H , Frazer David G , Schwegler-Berry Diane 
Published: January 2018

Abstract
Tetrandrine is an alkaloid obtained from the root of a medicinal herb which is employed in China as a treatment for silicosis. One proposed mechanism for the development of silica-induced fibrosis is lung damage resulting from particle-induced inflammation and secretion of reactive compounds from alveolar phagocytes. Therefore, the objective of the present study was to determine if tetrandrine exhibited the ability to inhibit respiratory burst activity of pulmonary phagocytes. The data indicate that although tetrandrine is not cytotoxic to phagocytic cells, it is a potent inhibitor in vitro of zymosan-stimulated oxygen consumption, superoxide anion release, and hydrogen peroxide secretion by alveolar macrophages. Tetrandrine is also effective in vivo in preventing activation of alveolar macrophages after inhalation or intratracheal instillation of silica. Tetrandrine also inhibits stimulant-induced chemiluminescence by polymorphonuclear leukocytes. Since tetrandrine does not alter stimulant-induced depolarization of phagocytic cells, its inhibitory action is not via interference with receptor-ligand binding but rather must occur elsewhere in the stimulus-secretion coupling scheme.
Kinetics of the Biosynthesis of Complement Subcomponent C1q by Murine Macrophages: LPS, Immune Complexes, and Zymosan Alone and in Combination With Interferon-γ
Authors: Zhou Anqiang , Herriott Mary J , Leu Richard W 
Published: January 2018

Abstract
We investigated the effects of bacterial lipopolysaccharide (LPS), immune complexes (IC), and C3b opsonized zymosan (AZ) alone and in combination with lnterferon-γ (IFN-γ) priming on macrophage synthesis and secretion of C1q. Our results indicated that LPS, IC, and AZ alone stimulated C1q mRNA and secretion in the absence of IFN-γ. The increase in mRNA accumulation was detectable after 3 h, peaked at 6h and was maintained at constitutive levels for 24 h. There was a corresponding early burst of increased secretion of functional C1q after 3 to 6 h which declined rapidly after 9 to 24 h culture of LPS-stimulated macrophages. Priming of macrophages with IFN-γ and simultaneous triggering with LPS, IC, or AZ produced additive rather than synergistic increases in C1q mRNA accumulation. These same agents inhibited constitutive secretion of C1q in the absence of IFN-γ priming as determined by autoradiographic analysis of metabolically radiolabeled secretory C1q. Triggering of IFN-γ primed macrophages with LPS, IC, or AZ also markedly suppressed the increased rate of C1q secretion induced by IFN-γ in a dose-related fashion. A corresponding dose-dependent increased accumulation of endogenous C1q in cell lysates was detected by Western blot analysis of macrophages which had been stimulated by LPS, IC, or AZ alone or in combination with IFN-γ. Our findings indicate that LPS as well as FcR and C3bR triggering agents stimulate early and sustained C1q synthesis accompanied by an early and short-lived burst of C1q secretion which rapidly diminished and results in an increased intracellular accumulation of C1q due to ongoing synthesis. IFN-γ appeared to further amplify the same kinetics of increased C1q mRNA accumulation and decreased extracellular accumulation mediated by LPS, IC, and ZM. Our results suggest that LPS, IC, and AZ alone or in combination with IFN-γ stimulate early C1q production to modulate macrophage effector functions followed by an inhibition of C1q secretion when the activation process has been culminated.
Protein kinase C isoforms in human neutrophil cytoplasts
Authors: Smallwood Joan I , Malawista Stephen E 
Published: January 2018

Abstract
Granule-poor human neutrophil cytoplasts, prepared without heat or cytochalasin B treatment so as to preserve both motile function and activatable respiratory burst oxidase, were investigated for their content of several isoforms of protein kinase C (PKC). Immunoblotting with isoform-specific rabbit antibodies (Abs) to PKC revealed that both the α-specific and the β(I and II)-specific Abs recognized a protein band of 78 kd comigrating with PKC from rat brain cytosol. The γ-specific antiserum did not detect any protein of this molecular mass. The cytoplast β-PKC band was more readily detected than the cytoplast α-PKC band. Antibodies to βI- or β-II-specific PKC sequences showed the βII subtype to be the predominant form of β-PKC, although some βI was also found. The identity of the 78-kd cytoplast bands as PKC was established by the fact that phorbol ester treatment of intact cytoplasts induced translocation of the bands from cytosol to membrane fractions. However, whereas PKC specific activity was similar in cytoplast lysates and brain cytosol, immunoreactivity of cytoplast α- and β-PKC bands was considerably less than that of rat brain. Hydroxylapatite chromatography of partially purified cytoplast PKC revealed two major peaks of PKC activity precisely coeluting with brain a- and β-PKC and displaying comparable enzymatic activities despite the relatively weak immunoreactivity of cytoplast α- and β-PKC. To our knowledge, this is the first demonstration that human neutrophil–derived cytoplasts contain α, βI, and βII forms of PKC and that each isoform translocates from cytosol to membrane upon exposure to phorbol ester at concentrations that induce superoxide production. In addition, our evidence raises the possibility that cytoplasts may also possess other isoforms of PKC that we are unable to detect with our α, β, and γ antibodies. Finally, the granule-poor cytoplasts seem a particularly useful preparation in which to examine the role of individual PKC isoforms in neutrophil activation.
Chronic granulomatous disease with partial deficiency of cytochrome b558 and incomplete respiratory burst: variants of the X-linked, cytochrome b558-negative form of the disease
Authors: Roos Dirk , de Boer Martin , Borregard Niels , Bjerrum Ole W , Valerius Niels H , Soger Reinhard A , Mühlebach Tony , Belohradsky Bernd H , Weening Ron S 
Published: January 2018

Abstract
Five male patients from four different families presented with a clinical record of chronic granulomatous disease (CGD): recurrent infections of the skin and/or respiratory tract with catalase-positive microorganisms, sometimes in combination with granulomata and/or abscesses in various organs. These patients differed from “classical” forms of the disease in that their neutrophils, although deficient in killing in vitro of Staphylococcus aureus, contained a decreased but measurable amount of cytochrome b558 (10–60% of normal on a heme basis), causing weak staining in the nitroblue tetrazolium dye test and a depressed respiratory burst after contact of the cells with fluid or particulate activators of the NADPH:O2 oxidoreductase. In the cell-free activation system, the defect in the patients' cells was localized in the membrane fraction. In each of the four families, the cellular abnormalities showed an X-linked inheritance. Fusion experiments performed with the monocytes from these patients and those from patients with classical X-linked, cytochrome b558–negative (Xb0) or autosomal, cytochrome b558–positive (Ab+) CGD showed complementation of NADPH:O2 oxidoreductase activity in the latter but not in the former combination. Thus, the unusual CGD patients represent variant forms of Xb0 CGD, with mutations in the gene coding for the beta subunit of cytochrome b558 that do not cause complete loss of this protein.
Expression and distribution of CD11a/CD18 and CD54 during human T cell–B cell interactions
Authors: Tohma Shigeto , Ramberg Jane E , Lipsky Peter E 
Published: January 2018

Abstract
Interactions between intercellular adhesion molecule 1 (ICAM-1, CD54) and leukocyte function–associated antigen 1 (LFA-1, CD11a/CD18) play a critical role in T cell–B cell collaboration. The current experiments were carried out to determine the expression and distribution of these adhesion molecules on human peripheral T cells and B cells during T cell–B cell collaboration. Resting CD4+ T cells were largely ICAM-1 negative, whereas immobilized anti-CD3 monoclonal antibody (mAb) rapidly induced ICAM-1 expression. By contrast, most B cells expressed ICAM-1 before activation, and further increases in density were noted with stimulation. Both B cells and CD4+ T cells expressed LFA-1 before activation, although the density on CD4+ T cells was considerably greater. A double staining method for electron microscopic analysis was developed that permitted analysis of the expression and distribution of ICAM-1 to be assessed during T cell–B cell collaboration. Under the experimental conditions examined, B cells showed a uniform distribution of ICAM-1. In contrast, ICAM-1 was highly mobile on the surface of CD4+ T cells. If the T cells were not fixed, staining, even at 4°C, caused rapid redistribution of ICAM-1 into aggregates. However, by fixing cells before the staining procedures, the distribution of ICAM-1 on CD4+ T cells could be accurately assessed. Most (85%) of the fixed activated CD4+ T cells showed a uniform distribution of ICAM-1. However, when activated CD4+ T cells were cocultured with B cells, redistribution of ICAM-1 on CD4+ T cells but not B cells occurred, such that the majority (85%) was found at or immediately adjacent to the point of attachment to the B cells. No redistribution of LFA-1 on either T cells or B cells was found. These findings suggest that rapid changes in density of ICAM-1 expression and the mobility of ICAM-1 on activated T cells may play a role in providing activation signals to B cells during T cell–B cell collaboration.
Effects of glucocorticoids on the TPA-induced monocytic differentiation
Authors: Hoff Torsten , Spencker Torsten , Emmendoerffer Andreas , Goppelt-Struebe Margarete 
Published: January 2018

Abstract
The human monocytic cell line U937 was used as a model system to investigate the effects of glucocorticoids on monocytic differentiation. Upon incubation with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (5 × 10-9 M) for 48 to 72 h, the immature U937 cells ceased to proliferate and became morphologically and functionally macrophage-like. Preincubation of the cells with glucocorticoids (dexamethasone and prednisolone, 10-7 and 10-6 M) but not progesterone (10-6 M) had marked effects: The cells remained in suspension and developed very little cell-cell interaction. This correlated with decreased expression of the surface molecules ICAM-1 and CD18 as determined by fluorescence-activated cell sorter analysis. The TPA-induced ability of the cells to release lysozyme or to generate reactive oxygen radicals (determined as reduction of nitroblue tetrazolium) was markedly reduced. The induction of cyclooxygenase activity and thus the ability to release prostanoids was almost completely abolished. Inhibition of prostanoid synthesis was also observed when the glucocorticoids were administered 24 or 48 h after TPA. The primary step of TPA induction, the activation and translocation of protein kinase C, however, was not affected by glucocorticoids as determined by activity measurements and Western blot analysis. There was no change in the subsequent TPA-induced induction of c-fos. The down-regulation of the differentiation-related oncogenes c-myc and c-myb was the same in cells treated with TPA in the presence or absence of glucocorticoids. Furthermore, no significant effect of glucocorticoids on the TPA-induced growth arrest was observed. Glucocorticoids thus interfere with TPA-induced functions, which are typical for activated macrophages; however, they do not impair the differentiation process and concomitant growth inhibition.
Effects of antiorthostatic suspension and corticosterone on macrophage and spleen cell function
Authors: Kopydlowski Karen M , McVey D Scott , Woods Keith M , Landolo John J , Chapes Stephen K 
Published: January 2018

Abstract
The purpose of this study was to determine whether antiorthostatic suspension of C3HeB/FeJ mice for a period of 11 days affected macrophage and spleen cell function. We found that antiorthostatic suspension did not alter macrophage secretion of prostaglandin E2, tumor necrosis factor α, and interleukin-1. Antiorthostatic suspension also did not affect macrophage-mediated contact-dependent cytotoxicity, TNF-mediated cytotoxicity, expression of class II histocompatibility molecules, or concanavalin A and Bandeiraea simplicifolia lectin binding sites. The proliferative response of splenic T cells in response to mitogens and staphylococcal exotoxins was significantly enhanced in antiorthostatically suspended mice. We detected significantly higher concentrations of corticosterone in the plasma of antiorthostatically suspended mice. Therefore, there did not appear to be any direct immunosuppressive effects of corticosterone on the parameters tested.
Lectinophagocytosis of type 1 fimbriated (mannose-specific) Escherichia coli in the mouse peritoneum
Authors: Bernhard Wolfgang , Gbarah Awni , Sharon Nathan 
Published: January 2018

Abstract
Bacteria can bind specifically to phagocytic cells via lectin-carbohydrate interactions and such binding is often followed by activation and degranulation of the phagocytes, as well as uptake and killing of the bacteria, a phenomenon designated lectinophagocytosis. Although extensively studied in vitro, no direct evidence for the occurrence of lectinophagocytosis in vivo has been available. To obtain such evidence, we injected type 1 fimbriated (mannose-specific) or nonfimbriated Escherichia coli into the peritoneal cavity of mice (107–1010 bacteria/animal) in the absence or presence of sugars and quantified the phagocytic activity by assaying the release of lysosomal N-acetyl-β-d-glucosaminidase into the peritoneal fluid, up to 45 min after injection. Following injection of the type 1 fimbriated bacteria, significant release of the enzyme was observed which was time dependent and increased with the number of bacteria injected, whereas the nonfimbriated bacteria caused only little release. Methyl α-d-mannoside (50 mM), but not methyl α-d-galactoside or sucrose, inhibited the release by 60 to 100%. No release of N-acetyl-β-d-glucosaminidase was induced by bacteria injected into a peritoneal cavity from which the macrophages had been removed. Our findings show that lectinophagocytosis can occur in vivo and may contribute to the host's defence against type 1 fimbriated bacteria.
Quartz selectively down-regulates CR1 on activated human granulocytes
Authors: Lundahl J , Dahlgren C , Eklund A , Hed J , Hernbrand R , Tornling G 
Published: January 2018

Abstract
We have investigated the interaction between quartz and granulocytes with respect to complement receptor expression. When N-formylmethionyl-leucyl- phenylalanine (fMLP)-stimulated leukocytes were exposed to quartz at 37°C, CR1 was down-regulated but CR3 was not affected. This was a direct effect on granulocytes because it occurred in a similar fashion when mixed leukocyte suspensions and isolated granulocyte populations were used as targets for quartz. The observed down- regulation by quartz was not affected by the microfilament-disrupting agent cytochalasin B and the total detectable pool of CR1 was reduced after quartz exposure. When protease inhibitors, such as aprotinin or phenylmethanesulfonyl fluoride, were present during quartz exposure, the down-regulation of GR1 was less pronounced, but this was not the case not when protease inhibitors such as £DTA-Na2 and pepstatin were present. Exposure to quartz was not accompanied by a pronounced release of β-glucoronidase (marker for the rprimary granules) or vitamin B12 binding protein (mar- er for the secondary granules). In contrast to quartz, exposure to alumina did not affect the expression of CR1 and CR3. The spontaneous mobilization of CR1 at 37°G was reduced when quartz was present but the GR3 mobilization was unaffected. Our results indicate that quartz induces a granule protease-dependent selective shedding of CR1 but not CR3 despite a low degree of degranulation. J. Leukoc. Biol. 53: 99–103; 1993.
Differential expression of bovine MHC class II antigens identified by monoclonal antibodies
Authors: Taylor Bernadette C , Choi K Yeon , Scibienski Robert J , Moore Peter F , Stott Jeffrey L 
Published: January 2018

Abstract
Four monoclonal antibodies (mAbs), UC-A4, UC-D3, UC-H9, and IL-A21, specific for bovine major histocompatibility complex class II proteins are described. Sequential immunoprecipitation experiments using biotin-labeled peripheral blood mononuclear cells suggested, but did not conclusively establish, that each of these antibodies recognized a different epitope. The epitope identified by IL-A21 appeared to be common to all of the class II proteins precipitated by the four mAbs, and UG-D3 and UC-H9 each appeared to react with distinct epitopes on separate subsets of these class II proteins. Monoclonal antibody UC-A4 appeared to identify an epitope on a subset of the class II molecules identified by UC-H9. Differences found in the expression by lymphoid cells of class II proteins identified by the four mAbs were indicative of each mAb recognizing a different epitope. UC-H9 and IL-A21 class II proteins were detected on all surface immunoglobulin (S’lg) positive cells in peripheral blood, but UC-A4 and UC-D3 class II proteins were not. Expression of UC-A4 class II proteins, detected at low density on a strikingly reduced number of S’lg+ cells from the blood of some bovine leukosis virus-infected cattle, could be increased by culturing these B cells with lipopolysaccharide. All peripheral blood monocytes expressed UG-H9 and IL-A21 class II proteins, but only a proportion of monocytes expressed detectable UC-A4 and UG-D3 class II proteins. Almost all mitogen-stimulated BoCD4+ and BoCD8+ T cells expressed UC-H9 and IL- A21 class II proteins, whereas fewer stimulated T cells of both subsets expressed UC-A4 and UC-D3 class II proteins. All gamma/delta receptor (γ/δ R) T cells expressed UC-D3, UG-H9, and IL-A21 class II proteins, but no cells (of γ/δ R+ or CD4+/CD2+ phenotype) from γ/δ R+ T cell-enriched cultures expressed UC-A4 class II proteins. J. Leukoc. Biol. 53: 479–489; 1993.
Analysis of differential HLA-DQB expression in autologous B cell lines
Authors: Woolfrey Ann E , Andersen L Christina , Shewey Linda , Chung JoSan , Nepom Gerald T 
Published: January 2018

Abstract
Glass II major histocompatibility complex genes are differentially expressed during cellular activation and differentiation, often in a locus-specific manner. We investigated the differential expression of the HLA- DQB gene, using B cell lines LAZ221 and LAZ388: LAZ221, derived from an early B cell leukemia, expresses HLA-DR but not HLA-DQ LAZ388, the autologous Epstein-Barr virus-transformed B cell line, expresses both DR and DQ Transfection experiments demonstrate differential function of class II gene upstream regulatory regions in the two lines, which correlates with differential class II gene expression. Using gel retardation and DNase I footprint assays, we demonstrate that absence of DQB gene expression is associated with characteristic nuclear protein-binding interactions in the proximal DQB gene upstream regulatory region. These interactions are visualized as DNA-protein complexes that are seen with nuclear proteins from the DQ-negative cell line, LAZ221, and involve consensus promoter Y box and W box elements, as well as novel upstream sites. Transcriptional regulatory proteins that differ in these autologous B cell lines may be stage-specific factors involved in the developmental regulation of HLA genes. J. Leukoc. Biol. 53: 697–706; 1993.
Effects of in vitro exposure to arachidonic acid on TNF-α production by murine peritoneal macrophages
Authors: Hubbard Neil E , Lim Debora , Somers Scott D , Erickson Kent L 
Published: January 2018

Abstract
Modifying the fatty acid composition of macrophages through diet can significantly alter some of their functions, such as tumoricidal capacity and tumor necrosis factor a (TNF-α) production. The mechanism of that modification, however, is unknown. In this report, we provide evidence that fatty acids added to macrophages in culture can significantly alter macrophage TNF-α production. For example when inflammatory macrophages were incubated with various doses of arachidonic acid [20:4(n-6)] during activation with lipopolysaccharide (LPS), we observed a dose-dependent decrease in the level of bioactive TNF-α with complete inhibition at 2-5 μΜ. This inhibition was specific for 20:4(n-6) because in vitro treatment with other fatty acids, such as eicosapentaenoic [20:5(n-3)] or docosahexaenoic [22:6(n-3)] acids, had differential effects. The inhibitory action of 20:4(n-6) did not involve toxicity because cell viability was not affected and in vitro interferon-γ and lipopolysaccharide (LPS) activation of macrophages for killing of P815 tumor targets was not altered. Inhibition by 20:4(n-6) occurred posttranscriptionally, and could be reversed when macrophages were treated with indomethacin during activation. Arachidonic acid treatment also significantly increased the production of immunoreactive prostaglandin E2 (PGE2) by LPS-treated and untreated macrophages. These results suggest that in vitro treatment of macrophages with 20:4(n-6) may inhibit TNF-α production through an alteration in the levels of PGE2 at a posttranscriptional level. These results provide evidence that some dietary fats may affect macrophage activity through modification of eicosanoid synthesis.
Calcium-binding myeloid protein (P8,14) is phosphorylated in fMet-Leu-Phe-stimulated neutrophils
Authors: Bengis-Garber Carmela , Gruener Nachman 
Published: January 2018

Abstract
In this report, we show that the pl4 subunit of calcium-binding myeloid protein complex (p8,14) is phosphorylated in human neutrophils stimulated with either fMet-Leu-Phe, phorbol myristate acetate, or a calcium ionophore. Trifluoperazine, a calmodulin antagonist, caused hyperphosphorylation of pi 4 in intact resting neutrophils. Freincubation of resting cells with 10-20 nM calyculin A, a potent protein phosphatase inhibitor, also caused enhanced labeling of pi 4, which was further progressively increased on stimulation with fMLP. Thus, the phosphorylation level of pi 4 in resting as well as in stimulated neutrophils appears to be controlled by an active protein phosphatase. The phosphorylation of pi 4 by a chemoattractant and by a phorbol ester is a novel finding supporting the current belief that p8,14 myeloid protein may play an important role in the metabolism of myeloid cells.
Immune changes during short-duration missions
Authors: Taylor Gerald R 
Published: January 2018

Abstract
Spaceflight materially influences the immune mechanism of humans and animals. Effects resulting from missions of less than 1 month are examined. Effects from longer missions are discussed in the companion paper by Konstantinova et al. Most immunology studies have involved analyses of subjects and samples from subjects obtained after flight, with the data being compared with similar data obtained before flight. These studies have demonstrated that short-duration missions can result in a postflight depression in blast cell transformation, major changes in cytokine function, and alterations in the relative numbers of immune cell populations. In addition to these post- vs. preflight studies, some data have been produced in flight. However, these in vitro analyses have been less than satisfactory because of differences between in-flight and ground-control conditions. Recently, both the U.S. and Russian space programs have started collecting in-flight, in vivo, cell-mediated immunity data. These studies have confirmed that the human cell- mediated immune system is blunted during spaceflight.