bluuebunny/crossref_metadata_2025_split huggingface dataset:
Splenic macrophage activation and functions in amyloid enhancing factor-induced secondary amyloidosis Study of phagocytosis, killing, respiratory burst, and MHC class II surface expression
Authors: Reid Caroline , Hébert Lise , Pozzulo Gina , Gervais Francine 
Published: January 2018

Abstract
Secondary amyloidosis is a systemic disease characterized by the extracellular tissue deposition of insoluble fibrillar amyloid A protein. Aberrant metabolism of serum amyloid A protein by reticuloendothelial cells is thought to result in the accumulation of fibrils within the tissue. Treatment of mice with amyloid-enhancing factor (AEF) in conjunction with an inflammatory stimulus (i.e., AgNOs) induced amyloid deposition within 48-72 h. The activation state of a macrophage largely defines its enzymatic capabilities. In the studies reported here, we examined the effect of AEF on spleen macrophage activation using both functional and phenotypic assays. We found that while AEF in the presence or absence of AgNOs has no apparent effect on the ability of spleen and liver macrophages to phagocytose or kill Listeria monocytogenes, it appears to block enhanced respiratory burst function (as measured by O2− production) observed with AgNOs alone. AEF therefore seems capable of inhibiting certain macrophage activation-associated functions while not affecting others. Our activation phenotype studies, using surface Ia expression, reveal that AEF blocks the increase in number of splenic macrophages expressing Ia seen with AgNO3 alone. Treatment with interferon-7 was found to restore decreased Ia expression in animals given AEF + AgNO3 but did not prevent amyloid A fibril deposition. J. Leukoc. Biol. 53: 651–657; 1993.
Comparison of cytosolic calcium shifts, superoxide generation, and lactoferrin secretion in the neutrophils of atopies and nonatopics
Authors: Zweiman Burton , von Allmen Carolyn , Moskovitz Anne , Atkins Paul , Taylor Megan , Korchak Helen 
Published: January 2018

Abstract
We previously found that platelet-activating factor (PAF) stimulated greater lactoferrin secretion by neutrophils of atopies than nonatopics. To help understand underlying mechanisms, we compared agonist- stimulated lactoferrin secretion with another response, superoxide generation, to determine whether there is a global alteration in the reactivity of atopic neutrophils to these stimuli. We also determined Ca2+ mobilization in such neutrophils because such mobilization is a signaling pathway for both superoxide generation and granule content exocytosis. Although PAF again stimulated greater lactoferrin secretion in atopic than in nonatopic neutrophils, the peak superoxide secretion and cytosolic Ca2+ mobilization were not significantly different in atopies and nonatopics. Leukotriene B4-induced superoxide secretion and cytosolic Ca2+ shifts were also similar in atopies and nonatopics. These findings suggest that (1) the enhanced PAF-induced lactoferrin secretion in atopic neutrophils is not a reflection of greater PAF binding or broad-based cell hyperreactivity and (2) a selective signaling pathway in atopic neutrophils may be responsible for the enhanced lactoferrin secretion. These findings may be relevant to in vivo events because we have found increased PAF and lactoferrin release in skin chambers overlying immunoglobulin E-mediated human skin reactions. J. Leukoc. Biol. 53: 727–731; 1993.
Monocyte 1α-hydroxylase regulation: induction by inflammatory cytokines and suppression by dexamethasone and uremia toxin
Authors: Gyetko Margaret R , Hsu Chen Hsaing , Wilkinson Camille C , Patel Sanjeev , Young Eric 
Published: January 2018

Abstract
Abstract: Alveolar macrophages acquire lα-hydroxylase activity in inflammation, and thereby metabolize 25 hydroxyvitamin D3 (25 D3) to the active metabolite, la,25-dihydroxyvitamin D3 (1,25 D3, calcitriol). Cal- citriol is a potent differentiation agent that modulates mononuclear phagocyte activation and effector functions. The mediators that induce macrophage lα-hydroxylase activity are not well delineated. Furthermore, it is unclear whether calcitriol is a product only of terminally differentiated macrophages or whether less mature mononuclear phagocytes can produce it as well. The ability of newly recruited monocytes to produce calcitriol as an autocrine differentiation agent is particularly important in inflammation, as it may substantially expand the functional repertoire of these cells. To assess the effects of cytokines on lα-hydroxylase activity, blood monocytes were cultured in the presence and absence of human recombinant tumor necrosis factor a (TNF-α), interferon-7 (IFN-γ), and interleukins 1 and 2 and then incubated with 25 D3 substrate. The conditioned media were assayed for calcitriol by high-performance liquid chromatography and competitive receptor binding assay. No detectable calcitriol was produced by unstimulated monocytes. However, all the cytokines markedly increased monocyte calcitriol production (range 133-151 pg/mg protein; in all cases P &lt; .001). We then determined whether calcitriol production was suppressed by preincubation with either dexamethasone or the putative uremia toxin guanidinosuccinic acid (GSA). Dexamethasone pretreatment significantly inhibited subsequent cytokine-induced calcitriol production by monocytes, as did GSA (average 69 and 63% of control, respectively).
In vivo distribution and characterization of two novel mononuclear phagocyte differentiation antigens in mice
Authors: Jutila Mark A , Berg Ellen L , Kroese Franz G M , Rott Lusijah , Perry Virginia , Butcher Eugene C 
Published: January 2018

Abstract
Flow cytometry, immunohistology, and SDS- PAGE Western blot analysis were used to characterize two novel anti-mouse mononuclear phagocyte differentiation antigens defined by monoclonal antibodies. One antibody, Monts-4, recognized an 80-100 kd cell-surface protein expressed on resident macrophages in the peritoneum and stained macrophages in the splenic white pulp and marginal zone, liver, lymph node paracortical regions, Peyers patches, and cortex of the thymus. Monts-4 did not stain blood monocytes or monocyte-derived inflammatory macrophages in the peritoneal cavity. Macrophages that were Monts-4 positive became Monts-4 negative within 24-72 h after culturing in vitro. Monoclonal antibody SK39 recognized a 180 kd cell-surface molecule expressed on inflamed peritoneal monocytes/macro- phages and stained macrophages in the splenic red pulp, cortex of the thymus, subcapsule and medullary regions of lymph nodes, and in sites of acute and chronic inflammation. No differences were seen in the expression of these antigens in the immunodeficient SCID versus normal BALB/c mouse. A comparison of the distribution and molecular weights of the Monts-4 and SK39 antigens with other described mononuclear phagocyte-specific antigens, including F4/80 and those defined by the Ml/70, ERTR9, MOMA1, MOMA2, and SER4 monoclonal antibodies, shows these to be novel mononuclear phagocyte-specific differentiation antigens.
Differential surface expression of cell adhesion molecules during granulocyte maturation
Authors: Lund-Johansen Fridtjof , Terstappen Leon W Μ M 
Published: January 2018

Abstract
Individual steps of granulocyte maturation, such as lineage commitment, proliferation, maturation, and migration from the marrow to the peripheral blood, may be influenced by distinct interactions with the bone marrow stroma. To identify candidates of membrane components involved in maturational stage-specific interactions, we studied changes in the expression of cell adhesion molecules along the granulocyte maturational pathway. Three-color flow cytometric measurements were used to measure levels of cell adhesion molecules along this pathway. The α chains of VLA-4 (CD49d) and VLA-5, the inte- grin 01 chain (CD29), and CD31 (PECAM-1) were expressed in high density on all early myeloid cells but down-modulated during postproliferative maturation. CD44 and L-selectin were expressed on CD34+ myeloid progenitor cells and mature granulocytes but down- modulated during the intermediate stages of maturation. The granulocyte receptor for endothelial selectins, sLex, was specifically expressed by myeloid progenitor cells. sLex was down-modulated during the intermediate stages of granulocyte maturation but up-regulated again during terminal maturation. In contrast, CD67, a putative granulocyte adhesion molecule, was negative on progenitors, transiently up-regulated during the intermediate stages of maturation, and almost absent from the surface of mature granulocytes. These results show that each stage of granulocyte maturation is associated with the expression of a unique combination of cell adhesion molecules. L-selectin, CD44, and 01 integrins were regulated as previously described for immature lymphopoietic cells and may therefore play general roles in the compartmen- talization and development of leukocytes. In contrast, sLex and CD67 were specifically expressed by myeloid cells and could be specifically important for compartmen- talization of distinct phases of granulocyte maturation.
Hepatic removal of 125I-DLT gelatin after burn injury: a model of soluble collagenous debris that interacts with plasma fibronectin
Authors: Blumenstock Frank A , La Celle Peter , Herrmannsdoerfer Axel , Giunta Corinne , Minnear Fred L , Cho Eshin , Saba Thomas M 
Published: January 2018

Abstract
The decline of plasma fibronectin after surgery, trauma, and burn, as well as during severe sepsis after injury, appears to limit hepatic Kupffer cell phagocytic activity. Intravenous infusion of gelatin-coated particles to simulate blood-borne particulate collagenous tissue debris in the circulation after injury also depletes plasma fibronectin. We used soluble gelatin conjugated with 1251-labeled dilactitol tyramine (DLT-gelatin) as a model of soluble collagenous tissue debris. We studied its blood clearance as well as organ localization in normal and postburn rats. Fibronectin-deficient plasma harvested early after burn exhibited limited ability to support in vitro phagocytic uptake of the gelatinized microparticles by Kupffer cells in liver tissue from normal rats. However, Kupffer cells in liver tissue from normal and postburn rats phagocytized the test particles at a normal rate when incubated in normal plasma. The DLT-gelatin ligand bound to fibronectin in a dose- dependent manner as verified by its capture with anti- fibronectin coated plastic wells when coincubated with purified fibronectin. By gel filtration chromatography, the binding of fibronectin with the DLT-gelatin ligand was readily detected, resulting in the formation of a high- molecular-weight complex. In normal animals the plasma clearance and liver localization of 125I-DLT-gelatin was competitively inhibited by infusion of excess nonradioactive gelatin. The blood clearance and liver localization of the soluble gelatin ligand were also impaired after burn injury during periods of fibronectin deficiency similarly to the pattern observed with gelatin-coated microparticles. By autoradiography, the cellular site for the uptake of the 1251-DLT-gelatin was primarily but not exclusively hepatic Kupffer cells; 125I-DLT-asialofetuin and 125I- DLT-ovalbumin were removed by hepatocytes and sinusoidal endothelial cells, respectively. Thus, gelatin conjugated with 125I-DLT can be used to simulate blood- borne soluble collagenous tissue debris after burn. It rapidly binds to plasma fibronectin before its hepatic Kupffer cell removal, and its blood clearance is markedly delayed after burn injury during periods of plasma fibronectin deficiency.
Lipopolysaccharide-induced suppression of erythrocyte binding and phagocytosis via FCγRI, FCγRII, FCγRIII, and CR3 receptors in murine macrophages
Authors: Sundaram Ramani , O’Connor Maeve , Cicero Mary , Ghaffar Abdul , Gangemi J David , Mayer Eugene R 
Published: January 2018

Abstract
Abstract: In this study we have investigated the ability of lipopolysaccharide (LPS) to suppress binding and phagocytosis of erythrocytes via various receptors on mouse macrophages. Thioglycollate-elicited peritoneal macrophages were treated in vitro with LPS and the ability to bind and phagocytose radiolabeled sheep red blood cells was determined. We show that LPS can directly suppress phagocytosis of immunoglobulin G-opsonized and nonopsonized sheep red blood cells (SRBCs) by inflammatory macrophages. Suppression was dose dependent and was observed after 4 h of exposure. This effect lasted for at least 24 h following the removal of LPS. LPS suppressed the binding, rate, and absolute level of phagocytosis via Fc receptors. Phagocytosis via all Fc receptors (FcγRI, FcγRII, and FcγRIII) was suppressed by LPS. Furthermore, suppression was not limited to Fc receptor-mediated phagocytosis because binding and uptake of C3bi-opsonized SRBCs to CR3 receptors was also decreased following LPS treatment. LPS did not exert its effects via the production of interleukin-1 (IL-1), IL-6, tumor necrosis factor a, or interferon a/β, because antibodies to these cytokines did not abrogate the effect. The ability of LPS to suppress binding and phagocytosis of microorganisms may contribute to the toxic effects of LPS during gram-negative sepsis by preventing or delaying elimination of bacteria by host macrophages.
Selective inactivation of lymphocytes after psoralen/ultraviolet light (PUVA) treatment without affecting systemic immune responses
Authors: Laskin Jeffrey D , Mermelstein Fred H , Heindel Ned D , Ron Yacov 
Published: January 2018

Abstract
Psoralens, together with ultraviolet light A (PUVA), are used for the treatment of several proliferative diseases. It has been suggested that the effectiveness of this treatment is due to induction of a specific immune response by PUVA-treated lymphocytes that down- regulates untreated cells of the same specificity. The present studies show that the clinically used psoralen analogue 8-methoxypsoralen (8-MOP), as well as 4,8-dimethyl- 5′-(pyridiniummethyl)psoralen bromide (4NQ), a derivative that does not cross the cell membrane, when activated by UVA light, render lymphocytes unresponsive to mitogenic, antigenic, or phorbol myristate acetate + ionomy- cin-induced stimulation. This state of unresponsiveness was not reversed by exogenous recombinant interleukin-2. Treatment of lymphocytes with 4NQ and UVA light had no effect on the viability or the homing pattern of the cells to spleen or liver, whereas 8-MOP induced toxicity in about 50% of cells after 3 days in culture. Using an adoptive transfer mouse model, we found that antigen- specific lymphocytes treated with PUVA (8-MOP or 4NQ) had no effect on the ability of these mice to respond to a subsequent challenge with the same or an irrelevant antigen. This was tested by measuring the T cell proliferative responses of lymph node cells from mice primed with keyhole limpet hemocyanin (KLH) or fowl gamma globulin (FGG) before or after adoptive transfer of large numbers of KLH- or FGG-specific PUVA-treated lymph node cells. No effects of antigen-primed PUVA-treated cells on antigen-primed untreated cells were observed in vitro in mixed lymphocyte cultures responding to the relevant antigen. These results suggest that, in our model system, PUVA induces cell inactivation but does not affect systemic T cell responses.
Response of blood leukocytes to thrombin receptor peptides
Authors: Hoffman Maureane , Church Frank C 
Published: January 2018

Abstract
Thrombin has receptor mediated effects on a variety of cell types. A recently cloned platelet thrombin receptor exerts its effects by a tethered-ligand mechanism. A similar receptor was shown in at least two nonplatelet cell types, fibroblasts and endothelial cells. Thrombin has biologically important effects on leukocytes, but the type of receptor mediating the effects is not known. Therefore, we examined the responses of monocytes, neutrophils, and lymphocytes to thrombin and to an agonist specific for the platelet-type thrombin receptor. We compared the effects of a peptide (SFLLRNPNDKYEPF) corresponding to residues 42-55 of the cloned platelet thrombin receptor on calcium flux in platelets and leukocytes. The thrombin receptor peptide induced increases in intracellular calcium in platelets and monocytes that reached a maximum at 5 μΜ peptide. The maximal increase was similar in magnitude to the response to thrombin. Lymphocytes showed a small and variable increase in intracellular calcium in response to thrombin or the thrombin receptor agonist. The thrombin receptor peptide had no effect on neutrophil calcium concentrations. When the amino acid corresponding to Arg 46 was replaced with Ala in the synthetic peptide, the ability to increase intracellular calcium was abolished for both platelets and monocytes. The peptide instead had thrombin antagonist activity. Thus, monocytes respond to thrombin receptor peptides similarly to platelets. We conclude that human monocytes possess a thrombin receptor similar to that present on platelets. Furthermore, the residue corresponding to Arg 46 of the thrombin receptor is critical for receptor agonist activity.
Activated neutrophils and neutrophil activators in human milk: increased expression of CD11b and decreased expression of L-selectin
Authors: Keeney Susan E , Schmalstieg Frank C , Palkowetz Kimberly H , Rudloff H Elizabeth , Le Binh-Minh , Goldman Armond S 
Published: January 2018

Abstract
Human milk neutrophils and macrophages were examined by flow cytometry to determine whether they displayed phenotypic markers of activation. The markers were CDllb and L-selectin, which are increased or shed, respectively, from the surface of activated neutrophils. Phenotypic features of milk neutrophils and macrophages were similar to blood neutrophils stimulated with fMLP: plasma membrane expression of CDllb was increased and L-selectin was decreased. After blood neutrophils were incubated in acellular milk, their expression of CDllb increased and L-selectin decreased. The activation was not affected by trypsin but was significantly decreased by treating acellular milk with chloroform or ether. Sedimentation studies suggested that particulate fractions of milk were active. Further, the activation was partly blocked by treating target blood neutrophils with cytochalasin B. Thus, human milk neutrophils are activated, and the activation may be due partly to phagocytosis of membranous structures in milk.
Inhibition of human mononuclear cell proliferation, interleukin synthesis, mRNA for IL-2, IL-6, and leukotriene B4 synthesis by a lipoxygenase inhibitor
Authors: Atluru Durgaprasadarao , Gudapaty Seshagirirao , O’Donnell Michael P , Woloschak Gayle E 
Published: January 2018

Abstract
Human peripheral blood mononuclear cells (PBMCs) were cultured in vitro with various stimuli and in the presence or absence of a 5-lipoxygenase (5-LO) inhibitor, A-63162, to measure its effects on PBMC proliferation, interleukin-2 receptor (IL-2R) expression, interleukin-2 (IL-2) synthesis, interleukin-6 (IL-6) synthesis, and accumulation of messenger RNA for IL-2 or IL-6. A-63162 inhibited PBMC proliferation stimulated by phytohemagglutinin (PHA) and phorbol myristate acetate (PMA) plus A23187, IL-2 receptor expression stimulated by PHA, and IL-2 or IL-6 synthesis induced by PHA plus PMA or PMA plus A23187. At the same concentration, A-63162 inhibited accumulation of mRNA for IL-2 or IL-6 and also inhibited leukotriene B4 (LTB.,) synthesis. Our data indicate that the 5-LO inhibitor A-63162 has immunosuppressive activity that may be due to inhibition of LTB4 production or to direct inhibitory actions of A-63162 on IL-2 and IL-6 synthesis.
Luminol-enhanced chemiluminescence induced in peripheral blood-derived human phagocytes: obligatory requirement of myeloperoxidase exocytosis by monocytes
Authors: Albrecht D , Jungi T W 
Published: January 2018

Abstract
Luminol-enhanced chemiluminescence (LCL) of phagocytes is often used to monitor for the generation of reactive oxygen mediators. A strong LCL reaction, as observed in triggered peripheral blood monocytes and neutrophils, depends on both the activation of an NAD(P)H-dependent oxidase and a functional myeloperoxidase (MPO). The aim of this work was to compare the LCL response induced by soluble and particulate stimuli in monocytes with that of polymoiphonuclear leukocytes (PMNs). In agreement with earlier results, neutrophils showed a first peak of LCL activity within 1 min and a second peak around 3 min when stimulated with soluble stimuli. The first peak is sensitive to oxygen scavengers and requires the presence of extracellular luminol, whereas the second peak is much less sensitive to oxygen scavengers and does not require the presence of extracellular luminol. The first peak of LCL is therefore thought to represent extracellular and the second peak intracellular LCL. Monocytes, in contrast, showed only the first peak of LCL activity. This peak was sensitive to oxygen scavengers, required the extracellular presence of luminol, and could be suppressed by a rapid pH shift to a pH not allowing LCL (L·, to pH 5). These results suggest that the stimulus-dependent extracellular release of oxygen metabolites and of MPO is an obligatory requirement for LCL induced in monocytes. An exclusively extracellular LCL was noted upon stimulation with aggregated immunoglobulin G, f-Met-Leu-Phe, phorbol myristate acetate, A23187, anti-CD36 antibodies, opsonized zymosan, and opsonized E. coli.. With the addition of H2O2 in excess (1 μΜ), the LCL response of monocytes therefore reflected the stimulus-dependent degranulation of MPO, and LCL-based determination of MPO release closely correlated with enzymatic MPO determination. The question of why LCL induced in monocytes, but not in PMNs, is restricted to the extracellular compartment was addressed. Although flow cytometric experiments were consistent with the hypothesis that extracellular H2O2 entered the cytoplasm of monocytes less efficiently than that of PMNs, other more important factors are assumed to contribute. Collectively, these results point to previously unrecognized differences in monocyte and PMN LCL which may reflect cellular differences of potential pathophysiological significance.
Analysis of interleukin-2-activated killer cells of rhesus monkeys: striking resemblance to the human system
Authors: Savary Cherylyn A , Lotzová Eva , Jackson Helen J , Jardine John H , Ang K Kian 
Published: January 2018

Abstract
We have found numerous and exquisite homologies between the interleukin-2 (IL-2)-activated killing systems of rhesus monkeys and humans. Lymphocytes with high oncolytic and proliferative activity were generated from peripheral blood, spleen, and bone marrow of monkeys sifter culture with IL-2. The distribution of lymphocyte subsets in IL-2 cultures closely paralleled that seen in humans, including a decrease in GD4+ and increase in CD8+, CD38+, and CD25+ lymphocytes and an increase in density of GD2 molecules. We also describe three distinct subsets of monkey lymphocytes, GD16+,56−, CD16+ 56+dim”, and CD16-,56bright, and show that the CD56+bright” subset is substantially increased (to as high as 79%) after IL-2 activation. Furthermore, as in humans, the cells with oncolytic activity were characterized as CD56+ CD16+-, and CD8+. This strong homology with humans indicates that the rhesus monkey may be a valuable preclinical model for evaluation of therapeutically relevant biological response modifiers.