bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surface Phenotype Analysis of Human Monocyte to Macrophage Maturation
Authors: Andreesen Reinhard , Brugger Wolfram , Scheibenbogen Carmen , Kreutz Marina , Leser Hans-Georg , Rehm Annegret , Löhr Georg W 
Published: January 2018

Abstract
Cells of the mononuclear phagocyte system arise from circulating blood monocytes. Upon emigration from the vasculature, monocytes differentiate into macrophages, a process that monocytes similarly undergo in vitro. We have established primary cultures from elutriated or adherence-purified blood monocytes and analyzed the antigenic modulation during monocyte to macrophage transformation, which could be followed by the expression of specific antigens and which required as yet unknown inducer signals present in the serum. It is shown that in the absence of serum monocytes only survive in vitro when cultured adherent to plastic but rapidly die in suspension culture. Starting at 0.5%, serum induced maturation dose-dependently, with the optimal concentration being 2 to 5%. Of those antigens not present on monocyte, the low-affinity Fc receptor (CD16), the α-chain of the vitronectin receptor (CD51), gp65-MAX.1, and gp68-MAX.3 were expressed only upon serum-induced macrophage differentiation, whereas the transferrin receptor (CD71), MAX.26, and to some degree also gp65-MAX.11 appeared to be independent of maturation and were also found on primary cultures of adherent monocytes under serum-free conditions. In addition, the rapid induction of HLA class II antigens (within 24 hr) was similar with and without serum, as was the continued high-density expression in long-term culture. The monocyte-specific CD14 antigen was down-regulated in the absence of serum but kept its level of expression on differentiated macrophages. In comparison, alveolar and peritoneal macrophages, respectively, differed in their antigenic phenotype: Alveolar macrophages expressed high HLA class II antigens but low CD14, whereas for peritoneal macrophages the opposite was found. Both interferon-γ and -α suppressed macrophage maturation in vitro but had contrary effects on HLA class II and CD16 expression: Interferon-γ up-regulated the two types of antigens, which, in contrast, were down-regulated by interferon-α.
Relationship of Chemotactic Receptors for Formyl Peptide and C5a to CR1, CR3, and Fc Receptors on Human Neutrophils
Authors: Van Epps D E , Bender J G , Simpson S J , Chenoweth D E 
Published: January 2018

Abstract
The co-expression of C5a and formyl-methionine-leucine-phenylalanine-lysine (FMLPL) receptors with CR1, CR3, and Fc receptors on human neutrophils (PMN) was studied. Fluorescein-conjugated C5a (FL-C5a) and FMLPL (FL-FMLPL) were used to identify C5a and formyl peptide receptors. CR1, CR3, and Fc receptors were identified with monoclonal antibodies and a Texas red-labeled goat anti-mouse immunoglobulin second step reagent The co-expression of chemotactic receptors with CR1, CR3, or Fc receptors was evaluated using two-color flow cytometry. A direct correlation between the degree of expression of receptors for FL-FMLPL and the expression of CR3, CR1, and Fc receptors on individual PMN was observed. In contrast, no correlation between the degree of C5a receptor expression and CR1, CR3, or Fc receptor expression was found. Similar results were obtained with PMN after up regulation of CR1, CR3, Fc, and FMLPL receptors by incubation at 37°C for 10 min with or without phorbol myristate acetate. These data suggest that the expression of FMLPL, CR1, CR3, and Fc receptors are regulated in a similar manner, whereas C5a receptor expression is regulated independently. Furthermore, these data indicate that within a given population of PMN, a parallel exists between the degree of CR1, CR3, FMLPL, and Fc receptor expression on individual cells.
Cytoplasmic Components of Natural Killer Cells Limit the Growth of Cryptococcus neoformans
Authors: Hidore Michelle R , Nabavi Nasrin , Reynolds Craig W , Henkart Pierre A , Murphy Juneann W 
Published: January 2018

Abstract
Murine natural killer (NK) cell-mediated inhibition of growth of a yeast-like target cell, Cryptococcus neoformans, was completely abrogated by blocking the effector cell secretory process with monensin. Therefore, further studies were performed to determine the ability of various cytoplasmic fractions of NK cells to mediate inhibition of cryptococcal growth. Percoll-fractionated homogenates of rat LGL tumor cells demonstrated that the granule-containing fractions plus three additional sets of less dense cytoplasmic fractions displayed anti-cryptococcal activity; whereas only the cytoplasmic granule-containing fractions had cytotoxic activity against YAC-1 tumor cell and sheep erythrocyte targets. Maximal cryptococcal growth inhibition induced by LGL granules occurred after a 1 h incubation, required the presence of Ca2+ (1.0 mM) or Mg2+ (0.5 mM or 5.0 mM), and was completely abrogated in the presence of rabbit anti-LGL granule IgG. Cytolysin, the granule component which mediates tumor cell and sheep erythrocyte lysis, effectively limited the growth of cryptococci. Since Percoll gradient fractionation of the LGL homogenates demonstrated three separate peaks of anti-cryptococcal activity other than the granule peak, it is possible that the cytolysin-containing granules are not the only subcellular component of NK cells playing a role in inhibition of C. neoformans growth.
Thromboxane Release by Lymphokine-Differentiated U937 Human Monocytic Cells: Response to Platelet-Activating Factor (PAF) and Chemotactic Peptide (FMLP) but Not to Low Affinity IGE-Receptor (FcεRII/CD23) Occupation
Authors: Storch Joachim , Edwards Robert J , MacDermot John 
Published: January 2018

Abstract
The primary objective of this study was to explore if the CD23 antigen is a functional low affinity IgE receptor on macrophages for the release of thromboxane B2 (TXB2). The responsiveness of U937 monocytic cells and their macrophage-like inducible forms to platelet-activating factor (Paf), the chemotactic peptide fMLP, and low affinity IgE-receptor occupation was examined. Differentiation of U937 cells by phorbol myristate acetate (PMA) and a cancer cell line (HBT 5637) conditioned medium (5637-CM), but not INFg or IL4, resulted in a macrophage-like cell line which released TXB2. A high basal release of TXB2 with no significant response to Paf or fMLP challenge was seen following culture of cells with PMA. In 5637-CM-differentiated cells, Paf and fMLP induced a rapid release of TXB2, about 10 fold above basal activity. There was a slow Ca-Independent response to short-term treatment with PMA and a rapid Ca-dependent response to the ionophore A23187. Both stimulants acted synergistically on TXB2 synthesis in 5637-CM differentiated cells. Although low affinity receptors for IgE (FcεRII/CD23) were induced by 5637-CM, no TXB2 was released in response to soluble or latex-bound IgE-antigen complexes or to anti-FcεRII/CD23-antibodies. IL4 and to a lesser extent INFg both induced FcεRII/CD23 receptor expression, but inhibited release of TXB2 in response to Paf, fMLP, or PMA. We conclude that the functional receptors for IgE on mature macrophages are most probably not FcεRII/CD23.
Flow Cytometric Study of the Activation of Polymorphonuclear Cells
Authors: Belloc Francis , Vincendeau Philippe , Freyburger Geneviève , Dumain Patrice , Boisseau Michel R 
Published: January 2018

Abstract
The activation of human polymorphonuclear cells (PMN) by the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP), or the protein kinase C activator, phorbol myristate acetate (PMA), was studied using flow cytometry. Two probes were used to evaluate PMN activation: 1) a monoclonal antibody (MoF11) directed against an antigen (Ag) expressed on the membrane of monocytes and of activated PMN; 2) rhodamine phalloidin was used at the cytoplasmic level to measure the F-actin content. The expression of MoF11 antigen was found to be 3 to 5 times greater on the membrane of PMN activated by either FMLP or PMN as compared with membrane expression of the same Ag on resting PMN. This increase was found to be dose dependent for the two activators. Kinetic studies showed that a maximum response was observed in 1 to 2 min at 37° when FMLP was used, whilst a similar response required 10 min when PMA was used. The same discrepancy with activators was observed when actin polymerization was measured by labelling with rhodamine phalloidin. However, pretreatment of PMN with cytochalasin B inhibited actin polymerization whilst MoF11 antigen expression was increased, suggesting that the MoF11 antigen could be stored in granules of resting PMN. The study of actin polymerization and of MoF11 antigen expression, separately or in combination, could be a useful tool for the detection of activated PMN in biological samples.
Interactions Between Epithelial Cells and T Lymphocytes: Role of Adhesion Molecules
Authors: Singer Kay H 
Published: January 2018

Abstract
Cell-cell interaction is critical for normal T cell development and function. A number of adhesion molecules important in T cell interactions with other cell types have been defined. This paper reviews the role of two adhesion pathways, CD2/LFA-3 and LFA-1/ICAM-1, in T cell interactions with epithelial cells of the thymus and skin. While thymic epithelium-T cell interactions are mediated by both the LFA-1/ICAM-1 pathway and the CD2/LFA-3 pathway, epidermal-T cell interactions are mediated primarily by the LFA-1/ICAM-1 pathway. Although ICAM-1 is not expressed in vivo on epidermal keratinocytes in normal skin, ICAM-1 is expressed by epidermal keratinocytes at the site of T cell infiltration in inflammatory dermatitis. ICAM-1 is expressed in vivo on thymic epithelium. These antigen independent adhesion molecules play an important role in the cell-cell interactions associated with T cell differentiation and function.
Gene Regulation in Macrophage Activation: Differential Regulation of Genes Encoding for Tumor Necrosis Factor, Interleukin-1, JE, and KC by interferon-γ and Lipopolysaccharide
Authors: Yu Sheau-Fung , Koerner T J , Adams Dolph O 
Published: January 2018

Abstract
Although macrophage activation is induced in a complex manner by signals such as Interferon-γ(IFNγ) and bacterial lipopolysaccharide (LPS) and depends on alterations in levels of specific proteins due to differences in gene expression, the complexity of gene regulation during macrophage activation in regard to multiple signals is not fully appreciated. To probe this question, we selected four model genes encoding for tumor necrosis factor (TNF), interleukin-1 (IL-1), and the immediate early genes JE and KC. After analyses of Northern blots for specific mRNA, LPS was found to enhance levels of mRNA for IL-1, TNF, JE, and KC. IFNγ initialed heightened mRNA levels for JE but did not alter specific mRNA for IL-1, TNF, or KC. When IFNγ and LPS were combined, additive effects on levels of specific mRNA for JE, enhancement of mRNA for TNF, suppressed mRNA for KC, and no effect on mRNA for IL-1 were observed. When transcription of these genes was assessed by nuclear “run on” experiments, LPS increased transcription of KC and TNF but not of IL-1 or JE, implying that the increased levels of mRNA for JE and IL-1 were attributable to increased stability of mRNA. Likewise, IFNγ did not initiate transcription of JE. When IFNγ and LPS were given together, IFNγ enhanced the LPS-induced transcription of TNF and KC, suggesting decreased stability of mRNA for KC. A distinct pattern of regulation for each of the four genes was thus observed. Taken together, the data suggest that gene regulation in macrophage activation represents a complex response of enhanced and suppressed transcription and mRNA stability, the precise pattern of which depends on the stimuli given to the macrophages and the gene examined.
Relationship Between Chemical Composition and Biological Function of Pseudomonas aeruginosa Lipopolysaccharide: Effect on Human Neutrophil Chemotaxis and Oxidative Burst
Authors: Kharazmi Arsalan , Fomsgaard Anders , Conrad Robert S , Galanos Chris , Høiby Niels 
Published: January 2018

Abstract
There are conflicting data on the effect of bacterial lipopolysaccharides (LPS) on the function of human neutrophils. The present study was designed to examine the relationship between chemical composition and the modulatory effect of LPS on human neutrohpil function. LPS was extracted from five strains of Pseudomonas aeruginosa isolated from cystic fibrosis patients by the hot phenol–water method. Chemical characterization included neutral sugars, amino components, and fatty acids. Neutrophils isolated from peripheral blood of healthy individuals were preincubated with different concentrations of LPS. After preincubation, the chemotaxis and chemiluminescence of neutrophils to various stimuli were determined. It was shown that LPS from different strains did not exert the same degree of regulatory effect on neutrophil functions. LPS from strain 174-O:9 exerted the most pronounced effect on neutrophil function seen as inhibition of neutrophil chemotaxis toward the chemotactic peptide f-Met-Leu-Phe and zymosan-activated serum (ZAS) and priming of the cells for ≤8-fold enhancement of chemiluminescence response to f-Met-Leu-Phe. Conversely, LPS from strain 1118-O:3 had no effect on neutrophil chemotaxis and a slight effect on chemiluminescence. The major differences in chemical composition of the LPS from these two strains are in the rhamnose and heptose content of the O side chain and in the alanine content of the core region. These data indicate that chemical composition of the LPS molecule may play an important role in biological activity of LPS.
Priming and Stimulation of Bovine Neutrophils by Recombinant Human interleukin-1 Alpha and Tumor Necrosis Factor Alpha
Authors: Sample Allen K , Czuprynski Charles J 
Published: January 2018

Abstract
We have examined the in vitro effects of two recombinant human monokines, interleukin-1 alpha (rHulL-1α) and tumor necrosis factor alpha (rHuTNFα), on bovine neutrophil functions. Both rHulL-1α (10 to 1,000 ng/ml) and rHuTNFα (5 to 50 ng/ml) directly stimulated the oxidative burst of bovine neutrophils as measured by Luminol-dependent chemiluminescence, superoxide anion generation, and hydrogen peroxide production. In addition, both rHulL-1α (1 to 1,000 ng/ml) and rHuTNFα (0.5 to 50 ng/ml) primed bovine neutrophils for an enhanced oxidative burst to subsequent stimulation with opsonized zymosan. Neutrophils pretreated with either monokine exhibited an earlier, as well as stronger, zymosan-stimulated Luminol-dependent chemiluminescence response, as compared to untreated neutrophils. Exposure of bovine neutrophils to combinations of suboptimal doses of rHulL-1α (10 and 100 ng/ml) and rHuTNFα (0.5 and 5 ng/ml) resulted in a synergistic stimulation of Luminol-dependent chemiluminescence, whereas, no synergism was observed when using optimal doses of each monokine. Pre-incubation of bovine neutrophils with an optimal concentration of recombinant bovine interferon gamma (100 U/ml), and either rHulL-1α or rHuTNFα further augmented the maximal oxidative response of neutrophils stimulated with opsonized zymosan. Bovine neutrophils released both primary and secondary granules in response to rHulL-1α and rHuTNFα, and also exhibited enhanced adherence in the presence of either monokine.
Granule Changes of Human Skin Mast Cells Characteristic of Piecemeal Degranulation and Associated With Recovery During Wound Healing In Situ
Authors: Dvorak Ann M , Kissell Susan 
Published: January 2018

Abstract
Human skin mast cells (HSMC) in situ were examined by electron microscopy of surgical biopsy specimens obtained from a wide variety of circumstances. From these studies, it is apparent that the general ultrastructural morphology of normal HSMC is similar to that of human mast cells from other sites, except that the most prevalent granule pattern is that of crystal granules. Scroll granules, particle granules, and mixed granules can also occur in HSMC. Cytoplasmic lipid bodies occur in HSMC extremely rarely, unlike mast cells from lung and gut. Circumstances in which piecemeal degranulation (PMD) of HSMC occurs, such as bullous pemphigoid, examined at high magnifications, revealed typical, focal geographic losses from cytoplasmic granules, often leaving completely empty granule containers in the cytoplasm. Crystal portions of mixed granules were uniquely susceptible to granule losses typified by PMD. Cytoplasmic smooth vesicles were prominent in PMD. These structures were either empty or contained granule-like dense materials and were free in the cytoplasm or attached to granules. HSMC present in wound healing revealed recovery from PMD losses. Typically these granules contained numerous irregular foci of markedly dense new granule products within empty or partially empty granule containers. The morphology of PMD and recovery of HSMC in vivo is contrasted with the morphology of anaphylactic degranulation (AND) and recovery of human mast cells ex vivo.
Effect of Soluble Aminated β-1,3-D-Polyglucose on Human Monocytes: Stimulation of Cytokine and Prostaglandin E2 Production but Not Antigen-Presenting Function
Authors: Doita Minoru , Rasmussen Lill-Tove , Seljelid Rolf , Lipsky Peter E 
Published: January 2018

Abstract
Glucans are insoluble polymers of β-1,3-linked glucose derived from yeast cell walls that effectively activate macrophages. Recently, aminated derivatives of β-1,3-D-polyglucose have been developed that are soluble but also activate murine macrophages. The current studies were undertaken to determine whether soluble aminated β-1,3-D-polyglucose (AG) would also stimulate human monocytes. The AG employed contained &lt;2 ng endotoxin/mg. AG induced the production of intracellular, membrane-associated, and secreted forms of interleukin 1 (IL1) in a dose-dependent manner, with 50 µg/ml yielding maximal responses. AG also induced tumor necrosis factor-α (TNFα) secretion by human monocytes. Prostaglandin E2 (PGE2) production was also stimulated in a concentration-dependent manner. Quantitatively, optimal stimulatory concentrations of AG were comparable to endotoxin in the capacity to induce production of these various mediators. In contrast to its capacity to induce production of IL1, TNFα, and PGE2, AG did not stimulate monocytes to become more effective antigen presenting cells. These results indicate that AG is a potent inducer of proinflammatory mediators from human monocytes but does not enhance their capacity to initiate immune responses.
Role of Natural Killer Cells in Resistance to Systemic Cryptococcosis
Authors: Salkowski Cindy A , Balish Edward 
Published: January 2018

Abstract
These studies demonstrate that Cryptococccus neoformans infection induced a dose-dependent augmentation of splenic natural killer (NK) cell activity by bg/+, but not bg/bg mice. To directly assess the role of NK cells in resistance to C. neoformans, bg/+ and bg/bg mice were treated with anti-NK-1.1 monoclonal antibody (mAb). Anti-NK-1.1-treatment abrogated the augmented NK cell activity observed during C. neoformans infection in bg/+ mice. Anti-NK-1.1-treated bg/+ mice had higher C. neoformans colony forming units (CFU) in their lungs on days 3 and 7 after intravenous (i.v.) challenge than control bg/+ mice. Moreover, the number of C. neoformans CFU in the lungs of anti-NK-1.1-treated bg/+ mice on days 3 and 7 were similar to those observed for infected bg/bg mice. By day 14, however, no differences in C. neoformans CFU were evident in the lungs of anti-NK-1.1-treated and control bg/+ mice. Anti-NK-1.1-treatment did not alter either the growth of C. neoformans in the spleens, livers, kidneys, or brain of bg/+ mice or the susceptibility of bg/bg mice to systemic cryptococcosis. These studies suggest that NK cells do not play a role in resistance to systemic cryptococcosis in the spleen, but do appear to play an early, but transient role in resistance to C. neoformans in the lungs. Overall, congenital defects in polymorphonuclear neutrophils (PMNs) and macrophages (Mφs), in addition to defects in NK cells, contribute to the enhanced susceptibility of bg/bg mice to systemic cryptococcosis.
Independence of the Pattern of Early Cytokine Release From Autoregulation by Nitric Oxide
Authors: Tucker Stanley D , Sivaramakrishnan Mathoor R , Klostergaard Jim , Lopez-Berestein Gabriel 
Published: January 2018

Abstract
The L-arginine-dependent tumor cell cytotoxicity produced by activated macrophages (Mφ) may be mediated either directly by production of nitric oxide (NO), or by induction of NO synthesis in the tumor cell. The influence of Mφ NO synthesis on the release of soluble cytotoxic mediators was investigated in this study. The synthesis of Mφ NO, measured as nitrite, was detected 6 h after lipopolysaccharide (LPS)-triggering and reached a peak level by 44 h. A concurrent decrease in Mφ viability beginning at 18 h after triggering was detected during a period of 72 h in culture. Both the production of NO and loss of viability correlated with the presence of L-arginine in the incubation media and was inhibited by NG-monomethyl-L-arginine (NMA). The medium in which LPS-triggered adherent peritoneal exudate cells were incubated was examined for the presence of tumor necrosis factor (TNF), gamma interferon (IFN-γ), and the soluble mediators that induce mitochondrial respiratory inhibition in tumor cells. All of these effector molecules were released at peak levels into the conditioned supernatants within 12 h after LPS-triggering. The peak level obtained for each effector molecule was influenced by the media in which the Mφ was incubated; however, no correlation was detected between the level of cytokines produced and the synthesis of nitrite by the Mφ indicating that NO synthesis has no inhibiting effect on the initial burst of cytotoxic factors released.
Characterization of immunosuppressive functions of murine peritoneal macrophages induced with various agents
Authors: Tomioka Haruaki , Saito Hajime 
Published: January 2018

Abstract
Murine peritoneal macrophages (Møs), induced with stimuli such as thioglycollate, zymosan A, OK-432, bacille Calmette-Guérin (BCG), or live Mycobacterium intracellulare, showed varying levels of inhibitory activity against the concanavalin A (Con A) blastogenic response of splenic T cells. All test Møs significantly inhibited the interleukin 2 (IL-2)–producing ability of T cells but this inhibition was not enough to explain the observed reduction in T cell Con A mitogenesis. In contrast, they markedly inhibited IL-2–reactive T cell generation, and the inhibition was sufficient to cause the reduction in T cell mitogenesis. A general relationship was observed between immunosuppressive activity of a given Mø and its active oxygen-producing ability (measured in terms of chemiluminescence) in response to phorbol myristate acetate triggering (r = .84, P &lt; .005). However, the suppressor activity of test Møs was not reduced by superoxide dismutase and catalase, indicating that active oxygen radicals themselves did not mediate the expression of the immunosuppressive activity of these Møs. On the other hand, indomethacin (an inhibitor of prostaglandin synthesis) caused a partial reduction in their immunosuppressive activity. The suppressor activity of Møs induced with intraperitoneal injection of recombinant interferon γ (IFN-γ) was markedly reduced in the presence of myoglobin, a scavenger for nitric oxide radical (NO·). Tumor necrosis factor α (TNF α) failed to affect Con A mitogenesis of splenic T cells, even in combination with IFN-γ. On the other hand, unsaturated long-chain fatty acids including oleic, linoleic, linolenic, and arachidonic acids markedly reduced the T cell function. These findings suggest some important roles of prostaglandins, NO·, and long-chain unsaturated fatty acids as mediators of the expression of immunosuppressive function of the peritoneal Møs.