bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phagocytosis by Receptors for C3b (CR1), iC3b (CR3), and IgG (Fc) on Human Peritoneal Macrophages
Authors: Newman Simon L , Becker Susanne , Halme Jouko 
Published: January 2018

Abstract
Human peritoneal macrophages (HPM) obtained via laparoscopy were examined for the presence and functional capacity of complement and Fc receptors. Between 5 and 20 ml of peritoneal fluid containing 1–2 × 106 macrophages/ml was available for each study. Macrophages made up 80–95% of the cells in the fluid. Fc and C3 receptors on HPM were characterized by rosette formation with, and phagocytosis of, IgG- and C3-coated sheep erythrocytes (E). EIgG were bound by 82% and ingested by 63% of HPM, with 4–15 E ingested/HPM. The HPM formed rosettes with EC3b (56%) and EC3bi (71%) but not EC3d,g or EC3d. Antibodies to complement receptors type 1 (CR1) and type 3 (CR3) inhibited rosette formation with EC3b and EC3bi, respectively, indicating that HPM possessed separate and distinct receptors for the C3b and iC3b ligands. In 60% of the samples studied, HPM demonstrated the ability to ingest both EC3b and EC3bi, as well as ElgG. Because of the heterogeneous nature of the cells obtained in peritoneal fluid, due to their progressive change from monocytelike cells into mature macrophages, HPM were separated by 1 g velocity sedimentation into fractions of increasing maturity. They were then examined for phagocytosis via Fc and complement receptors. Fc receptor mediated phagocytosis occurred throughout the monocyte-to-macrophage maturation sequence, while the ability of HPM to ingest via CR1 and CR3 was maturation dependent, with ingestion via CR3 occurring before CR1, in a manner analogous to in vitro differentiation of monocyte-derived macrophages.
Monocytic Origin and Postnatal Mitosis of Intravascular Macrophages in the Porcine Lung
Authors: Winkler Gian C , Cheville Norman F 
Published: January 2018

Abstract
Ultrastructural studies of near-term to 2-month-old pigs were done to document characteristics and developmental changes of intravascular macrophages in pulmonary capillaries. Evidence is presented that blood monocytes colonize the porcine lung perinatally, replicate within capillaries postnatally, and attach to endothelium by intercellular junctions during differentiation. Major ultrastructural features of differentiated intravascular macrophages are adhesion to capillary endothelium, pseudopods, phagosomes, and tubular structures of micropinocytosis vermiformis. Ultrastructure indicates that intravascular macrophages are cells of the mononuclear phagocyte system involved in several functions (eg, blood cell sequestration) that are usually attributed to hepatolienal macrophages. In newborn and 3-day-old pigs, the majority of cells closely apposed to endothelium consisted of few differentiated monocytes, but in 7-day-old and older animals, most cells that were joined to endothelium had characteristics of differentiated intravascular macrophages.
Selectively Eliminated Blood Monocytes and Splenic Suppressor Macrophages in Mice Depleted of Bone Marrow by Strontium 89
Authors: Shibata Yoshimi , Dempsey Walla L , Morahan Page S , Volkman Alvin 
Published: January 2018

Abstract
The contribution of specific activity to the effects of the bone-seeking isotope, strontium 89 on radiosensitive components of mononuclear phagocyte populations was investigated in mice. CBA/J mice received a fixed dose of 2 μCi/g body weight of 89Sr with three different specific activities, 6 Ci, 100 μCi and 20 μCi per mg Sr. The estimated radioactivity located in the bone surface was 4,200, 3,000 and 2,400 cpm/mg bone when measured 2 days after the administration of 89Sr, and was lost with an estimated biological half-life of 27, 25, and 23 days, respectively. Bone marrow suppression was assessed by quantitation of the depletion of macrophage-colony forming cells (M-CFC) grown in vitro in the presence of macrophage growth factor. The decline in M-CFC closely paralleled the level of radioactivity in the bone. These effects were clearly reflected by the depletion of monocytes in the blood, which were reduced to 14%, 14%, and 21% of control levels corresponding to SA's of 6 Ci/mg, 100 μCi/mg and 20 μCi/mg when counted on day 10. By day 30 the respective monocyte levels were 15%, 31%, and 77%. Furthermore, the induction of prostaglandin E producing suppressor macrophages (Mø) by Corynebacterium parvum administration was found to vary inversely with the effects of radioactivity in the bone, with initial impairment followed by quantitative recovery. Resident-type Mø in peritoneal cavity, however, appear to be unaffected by 89Sr-treatment. These data suggest, as before, that the monocytes and suppressor Mø are dependent on radiosensitive marrow cells. The observations also lead to the conclusion that the specific activity of 89Sr preparations is an important determinant of the degree of suppression and of the rate of recovery of bone marrow from the effects of irradiation that follow the administration of this isotope.
Modulation of Macrophage I-A Expression: Lack of Effect of Prostaglandins and Glucocorticoids on Macrophages That Continuously Express I-A
Authors: Vespa Linda , Johnson Sarah C , Aldrich Wayne A , Zwilling Bruce S 
Published: January 2018

Abstract
The ability of prostaglandins, glucocorticoids and lipopolysaccharide to modulate I-A expression on macrophages that continuously or transiently express I-A was compared. We found that neither prostaglandins nor glucocorticoids affected I-A expression by macrophages that continuously expressed I-A. In contrast, prostaglandin E2 (PGE2) inhibited the lymphokine-induced maintenance of I-A on macrophages that transiently expressed I-A while glucocorticoids inhibited both the induction and expression of I-A. Lipopolysaccharide caused a loss in the expression of Class II molecules on macrophages that continuously expressed l-A by a prostaglandin-independent mechanism. The lack of effect of PGE2 and glucocorticoids may be related to our observation that continuous expression of I-A does not require its continued synthesis.
Alveolar Macrophage Phagocytic Kinetics Following Pulmonary Parainfluenza-3 Virus Infection
Authors: Slauson David O , Lay John C , Castleman William L , Neilsen Nancy R 
Published: January 2018

Abstract
Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza-3 virus pneumonitis and control calves were made. Calves were exposed to 109 TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected calves, and the percentage of neutrophils was elevated (P &lt; 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P &lt; 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 × 106beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM β-glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI-3 virus-inflamed lungs relative to controls. In concert with virus-induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.
The Effect of a Protein Kinase C Inhibitor, H-7, on Human Neutrophil Oxidative Burst and Degranulation
Authors: Berkow Roger L , Dodson Robert W , Kraft Andrew S 
Published: January 2018

Abstract
The role of C-kinase in the activation of human polymorphonuclear leukocytes has been examined using H-7, a recently described C-kinase inhibitor. We found that H-7 will inhibit PMN superoxide anion release in response to the tumor promotor phorbol myristate acetate and the calcium ionophore A23187. In contrast, no inhibition by H-7 was seen for PMN superoxide release stimulated by the chemotactic peptide FMLP. H-7 did not inhibit PMN NADPH oxidase activity or PMN degranulation by any stimulant, but it reversed a phorbol ester-induced inhibition of granule release by FMLP. The results show that H-7 differentially affects the PMN functional events of secretion and superoxide release and suggests that an H-7 inhibitable C-kinase 1) is not involved in chemotactic peptide induced activation of PMN and 2) may not regulate stimulus induced PMN degranulation.
Neutrophil Dysfunction in the Rabbit Model of Spur Cell Anemia
Authors: Lichtenstein Israel H , Zaleski Ellen M , MacGregor Rob Roy 
Published: January 2018

Abstract
In the rabbit model for spur cell anemia, animals fed a 5% cholesterol diet develop marked hypercholesterolemia and hemolytic spur cell anemia after several weeks on the diet. In vitro tests of granulocytes showed a 15% increase in cholesterol: phospholipid ratio, and decreased membrane fluidity measured with a fluorescent probe. Function tests revealed impairment of adherence, phagocytosis, and chemotaxis. Both a plasma factor and an intrinsic cellular defect appeared to contribute to the abnormal adherence. Bactericidal activity was normal. In vivo demargination in response to epinephrine was increased in animals on the diet, but exudation of granulocytes into sterile peritonitis fluid was diminished to 39.4% of control at 8 hours. Therefore, rabbits with experimental spur cell anemia have impaired in vitro and in vivo granulocyte function. The clinical significance of these findings for patients with spur cell anemia and less severe alcoholic liver disease is uncertain.
Effects of Adherence, Activation and Distinct Serum Proteins on the In Vitro Human Monocyte Maturation Process
Authors: Akiyama Yukio , Griffith Richard , Miller Paul , Stevenson G W , Lund Stacy , Kanapa D J , Stevenson Henry C 
Published: January 2018

Abstract
Elutriator-purified human monocytes were cultured in a serum-free (SF) medium, and various serum proteins and functional activating agents were assessed for their effects on the in vitro maturation of human monocytes to macrophages. Following 3 days of suspension culture in Teflon labware, 60% of the monocytes were easily recovered. When varying concentrations of human AB serum (HuAB) were employed, human monocyte maturation progressed rapidly; the kinetics of this maturation process during cell suspension culture were very similar to the pattern observed following adherence culture. In contrast, when SF medium was employed, a marked retardation of the monocyte maturation process was observed; this could not be attributed to any changes in cell recovery and/or viability. Thus, cells could be maintained in their monocytoid form for 3 days when cultured in SF medium. When HuAB was added after 3 days of culture, human monocyte maturation into macrophages proceeded at a normal rate.
We attempted to characterize certain of the serum protein(s) found in HuAB which promoted the monocyte maturation process. Human immunoglobulin G (IgG) was found to be the most potent serum protein in increasing 5′-N activity and decreasing peroxidase activity of suspension cultured monocytes. Immunoglobulin M (IgM) and albumin (Alb) were shown not to have significant monocyte maturation activity. Heat-treated human gamma globulin and IgG purified by high-performance liquid chromatography (HPLC) were shown to have patterns identical with that of untreated HGG and IgG with regard to promoting monocyte maturation; F(ab′)2 was not an active maturation promoter, indicating the need for an intact Fc portion of the IgG molecule. Fibrinogen and fibronectin also had maturation promoting activity.
Finally, addition of the potent monocyte functional activators, muramyl dipeptide (MDP), polyriboinosinic:polyribocytidilic acid (Poly I:C), and lipopolysaccharide (LPS) had no effect on the monocyte maturation process. Thus, neither cell adherence or activation appear to be critical for the monocyte to macrophage maturation process. Instead, we hypothesize that in addition to proper nutritional support, a group of serum proteins (unified mainly by their ability to interact with monocyte membrane receptors) appear to be the principal promoters of this process.
Bacterial Lipopolysaccharide Enhances Chemoattractant-Induced Elastase Secretion by Human Neutrophils
Authors: Fittschen C , Sandhaus R A , Worthen G S , Henson P M 
Published: January 2018

Abstract
Bacterial lipopolysaccharide (LPS) has previously been shown to enhance a number of chemoattractant-induced responses by human neutrophils. The possible role of elastase, a neutral protease with broad substrate specificity, in neutrophil-mediated vascular injury of a variety of diseases prompted us to examine a) whether or not LPS enhances the direct chemoattractant-induced secretion of elastase, b) the quantitative requirements of LPS and chemotactic factors, and c) some structural requirements of LPS for this effect. Our results show that LPS at 10 ng/ml and above, enhanced formyl-methionyl-leucyl-phenylalanine-induced neutrophil secretion of elastase, as well as secretion of myeloperoxidase and vitamin B12-binding protein. This effect was independent of cytochalasins or surface stimulation, and thus may occur during chemotactic factor stimulation in vivo. LPS also enhanced neutrophil secretory responses to the complement fragments C5a, C5a des arg, and, to a lesser degree, to leukotriene B4 and platelet-activating factor. This enhancement effect appeared to require the presence of the lipid A moiety and/or parts of the core polysaccharide but not the O-antigen portion of the LPS molecule. Our findings identify a possible LPS-dependent mechanism of neutrophil elastase-mediated tissue injury in Gram-negative infections.
Differences in the Ability of Neutrophils and Monocytes to Traverse Epithelial Occluding Junctions
Authors: Migliorisi Grace , Folkes Edmund , Cramer Eva B 
Published: January 2018

Abstract
This study examines the effect of epithelial permeability on 1) the passage of the chemoattractant tritiated formyl methionyl-leucyl-phenylalanine (3H-fMLP; m.w. 437) and 2) the migration of leukocytes. In addition, it also compares the kinetics of neutrophil and monocyte transepithelial migration. As we had demonstrated with neutrophils (Milks et al.: Journal of Cell Biology 96:1241, 1983), when the permeability of the epithelium decreased, the accumulation of 3H-fMLP and the emigration of monocytes also decreased. When neutrophils and monocytes traversed epithelia with similar permeability, neutrophil accumulation was at least ninefold greater than that of monocytes at 30, 60, and 90 min. During the same time intervals, the number of neutrophil invasion sites/mm epithelium exceeded the number of monocyte invasion sites by at least fivefold, with approximately twice as many neutrophils as monocytes traversing each invasion site. These studies demonstrate that epithelial permeability affects the passage of the chemoattractant and the emigration of leukocytes. In addition, the enhanced ability with which neutrophils traverse occluding junctions compared to monocytes helps to explain, at least in part, the more rapid accumulation of neutrophils at inflammatory lesions.
Characterization of Murine Bronchoalveolar Macrophage Respiratory Burst: Comparison of Soluble and Particulate Stimuli
Authors: Sugar Alan M , Field Keith G 
Published: January 2018

Abstract
Stimulation of the respiratory burst of murine bronchoalveolar macrophages obtained by lung lavage was studied using four different stimuli and different assay conditions. One soluble stimulus, phorbol myristate acetate (PMA), two intracellular particles, zymosan and Blastomyces dermatitidis conida, and one extracellular particle, B. dermatitidis yeast, were incubated with either freshly obtained macrophages in suspension or 2- and 48-hour macrophage monolayers. Suspension cultures were incubated with stimuli for 90 minutes and monolayers for 10 minutes before O2− was assayed. PMA did not elicit O2−production in macrophage suspensions or 2-hour macrophage monolayers, but 48-hour macrophage monolayers exhibited a 13-fold increase above control values (P = .0001). On the other hand, zymosan elicited an increase in O2− production in both suspensions and monolayers, although monolayers incubated for 48 hours produced almost fourfold more O2− than the other systems (P = .025). Opsonization had no effect on the ability of zymosan to elicit respiratory burst B. dermatitidis conidia resulted in a two- to threefold increase in O2− production in macrophage suspensions and a five- to eightfold increase in 48-hour monolayers, representing significantly less respiratory burst stimulation than with either zymosan or PMA. Similarly, B. dermatitidis yeasts demonstrated similar submaximal stimulation of O2−, 3–4 times that over control values, and again this was less than zymosan and PMA. We conclude that 1) freshly obtained murine bronchoalveolar macrophages do not respond to PMA with an increase in O2− production, but that responsiveness is evident after 48 hours of incubation in monolayers; 2) B. dermatitidis conidia and yeasts do not stimulate respiratory burst activity to the same degree as zymosan or PMA; and 3) opsonization of zymosan is not necessary for stimulation of the murine bronchoalveolar macrophage oxidative burst, confirming previous data that functional complement receptors are not present on these cells.
Electron Spin Resonance Spectroscopy Does Not Reveal Hydroxyl Radical Production in Activated Natural Killer Lymphocytes
Authors: Gibboney James J , Haak Richard A , Kleinhans Frederick W , Brahmi Zacharie 
Published: January 2018

Abstract
We investigated hydroxyl radical (OH) production by human natural killer (NK) cells, using electron spin resonance (ESR) spectroscopy and 5,5 dimethyl-1-pyrroline-N-oxide (DMPO), a spin trap specific for OH production. We confirmed that hydroxyl radical scavengers, n-propyl gallate and catechin, inhibited NK cell-mediated cytotoxicity (NK-CMC) in a dose-dependent manner and demonstrated that DMPO also inhibited NK-CMC. Polymorphonuclear leukocytes (PMNL) activated by opsonized zymosan (2.4 mg/ml) and mixed with DMPO (0.14 M) showed an early increase in hydroxyl radical production, leading to a net production of free radical of almost 400 pMol/106 cells. We then mixed NK cells with K562, an NK-sensitive tumor cell, at a 1:1 ratio and added DMPO (0.14 M). We pelleted the cells to increase EC to TC binding before taking the sample readings. Activated NK cells showed no increase in OH production, leading to a net production of free radicals less than 1% that of activated PMNL. These data strongly suggest that hydroxyl radical production does not play a role in the early events of NK cell activation; they indicate a need to reevaluate the mechanism of inhibition of NK-CMC by OH scavengers.
Activated Langerhans Cells Release Tumor Necrosis Factor
Authors: Larrick James W , Morhenn Vera , Chiang Yawen L , Shi Tim 
Published: January 2018

Abstract
Langerhans cells act as antigen-presenting cells in immune reactions in the skin. What other roles they may play in inflammation is less well defined. We have tested whether these cells can produce TNF-alpha, an important mediator of inflammation. Resting Langerhans cells produce less than 0.1 U TNF-alpha/ml. Langerhans cells stimulated with phorbol myristate acetate (PMA) and lipopolysaccharide (LPS) release 4-5 U TNF-alpha/ml. Specificity of the released TNF-alpha in an L929 cytotoxicity assay was confirmed by using neutralizing anti-TNF-alpha monoclonal antibodies, and the identity of TNF-alpha was further confirmed by Northern blot hybridization with an TNF-alpha oligomer DNA probe. Activated Langerhans cells may contribute to inflammation in the skin by releasing TNF-alpha, which is known to effect fibroblast growth, endothelial cell activation, and lymphocyte function.
Germinal Center B Cells and Mixed Leukocyte Reactions
Authors: Monfalcone Alan P , Kosco Marie H , Szakal Andras K , Tew John G 
Published: January 2018

Abstract
The present study was undertaken to determine if germinal center (GC) B cells are sufficiently activated to stimulate mixed leukocyte reactions (MLR). Percoll density fractionation and a panning technique with peanut agglutinin (PNA) were used to isolate GC B cells from the lymph nodes of immune mice. The GC B cells were treated with mitomycin C or irradiation and used to stimulate allogeneic or syngeneic splenic T cells in the MLR. Controls included high-density (HD) B cells prepared from spleens of the same mice and HD B cells activated with lipopolysaccharide (LPS) and dextran sulfate. GC B cells bound high amounts of PNA (i.e., PNAhi). Similarly, the LPS-dextran sulfate-activated B cells were PNAhl. Treatment with neuraminidase rendered the PNA HD B cells PNAhl. GC B cells and the LPS-dextran sulfate-activated HD B cells stimulated a potent MLR, while the untreated HD B cells did not. However, following neuraminidase treatment, the resulting PNAhl HD B cell population was able to induce an MLR. The PNA marker appeared to be an indicator of stimulatory activity, but incubating the cells with PNA to bind the cell surface ligand did not interfere with the MLR. GC B cells were also capable of stimulating a syngeneic MLR in most experiments although this was not consistently obtained. It appears that germinal centers represent a unique in vivo microenvironment that provides the necessary signals for B cells to become highly effective antigen-presenting cells.
Macrophage-Parasite Interactions in Leishmania Infections
Authors: Mauël Jacques 
Published: January 2018

Abstract
Macrophages have different roles in Leishmania infections. They function as host-cells to the parasite, they present parasite antigens to the immune system, and they also act as effector cells responsible for parasite killing in the healing stages of the infection. Protein and carbohydrate Uganda on the parasite surface, which interact with receptors on the macrophage membrane during phagocytosis, have been identified. Survival of Lelshmania in its host cell requires a metabolic adaptation to the intracellular environment The nutritional requirements of the microorganism must be satisfied and the deleterious effect of oxygen metabolites and of lysosomal hydrolases must be adequately counteracted. When a successful immune response develops, macrophages become activated and acquire the capacity to destroy the microorganism. Possible reasons why these mechanisms fail in certain individuals or experimental host-parasite combinations are discussed.