bluuebunny/crossref_metadata_2025_split huggingface dataset:
BCG, in Contrast to C. parvum, Does Not Induce Increased Sensitivity to the Toxic Effects of Indomethacin in Mice
Authors: Hart David A 
Published: January 2018

Abstract
Treatment of mice with killed Corynebacterium parvum (also designated Propionibacterium acnes, P. acnes) or Bacille Calmette Guerin (BCG) leads to modification of several of the same host systems. However, BCG, in contrast to C. parvum, did not induce increased sensitivity to the toxic effects of indomethacin in BALB/c or C57B1/6 mice. In addition, treatment of mice with BCG did not interfere with the induction of sensitivity by C. parvum. Therefore C. parvum must uniquely induce changes in host systems which alter the sensitivity to this anti-inflammatory drug. Additional experiments with splenectomized animals revealed that the presence of this organ, which undergoes hypertrophy following C. parvum treatment, was not necessary for the induction of indomethacin sensitivity. Presentation of C. parvum via the subcutaneous route versus the intraperitoneal route revealed that the two routes were equally efficient in inducing sensitivity in C57B1/6 mice but the former route was less effective (50% deaths) than the intraperitoneal route (95% deaths) in BALB/c mice. These results indicate that host related factors (genetic) may be important in the generation of enhanced sensitivity to the toxic effects of indomethacin.
Human Monocyte-Released Cytotoxic Factor: Effect on Various Cellular Functions, and Dependency of Cytolysis on Various Metabolic Processes
Authors: Nissen-Meyer Jon , Kildahl-Andersen Odd , Austgulen Rigmor 
Published: January 2018

Abstract
The ability of the human monocyte-released cytotoxic protein factor(s) (CF) to mediate cytolysis when various metabolic processes in target cells were inhibited, and its effect on various cell functions have been studied. Cytolysis was reduced when target cells were exposed to either chloroquine or colchicine, indicating that lysosome function and the formation of microtubule are of importance with respect to the interaction between CF and target cells, possibly by effecting internalization and processing CF and its receptor. A decrease in the energy charge of the target cells did not affect the ability of CF to mediate cytolysis, since the 60-70% reduction of the cellular ATP content by uncoupling oxidative phosphorylation had little effect on CF-induced lysis. It was unnecessary for target cells to be actively growing and dividing for CF to induce lysis because inhibition of cellular protein, RNA, and DNA synthesis potentiated the cytolytic effect of CF.
CF-induced cell lysis of Walter and Eliza Hall Institute (WEHI) 164 target cells was first detected between 3.0 and 4.5 hr after addition of CF. Target cell DNA synthesis nearly terminated within 3-4 hr, about the time of first cell lysis detection. Compared to the effect on DNA synthesis, the CF effect on protein synthesis was negligible and only a slight reduction was detected in the RNA synthesis and in the cellular ATP content. The results indicated that the DNA-synthesizing machinery may either be a primary target site of CF or a rapid influence of CF action on its primary target site; however, neither the protein- or RNA-synthesizing machinery nor the cellular ATP generating systems are likely to be primary target sites.
Prostaglandin E2 Content of Regressing and Progressing Moloney Sarcomas
Authors: Wechsler Sally J , Eurell Thomas E , Russell Stephen W 
Published: January 2018

Abstract
Regressing mouse Moloney sarcomas contain macrophages that are activated for tumor cell killing, while those found in progressively growing sarcomas either cannot kill or do so very poorly. Prostaglandin E2 (PGE2) has been shown to down-regulate macrophage activation in vitro. The study described here was designed, therefore, to ascertain and compare the concentrations of PGE2 in regressing and progressing Moloney sarcomas. Tumors were harvested for extraction and analyzed using conditions that minimized artifactual increases in PGE2 levels attributable to de novo synthesis. Concentrations of PGE2 were higher in progressing, compared to regressing, Moloney sarcomas during the early stages of tumor development. At nearly all time points, however, whether the neoplasms were of regressing or progressing type, the estimated concentrations of PGE2 in tumors exceeded the level that completely inhibits macrophage activation for tumor cell killing in vitro, that is, 10−8 M. These data suggest either that PGE2 is not responsible for down-regulating activation in Moloney sarcomas or that, if PGE2 is responsible for the negative regulation of activation in progressing Moloney sarcomas, there must be something in regressing sarcomas that prevents the hormone from having its inhibitory effect.
Phagocytic Rabbit Cell Lines Expressing Class II MHC Products: Establishment of Cell Lines by Viral Transformation
Authors: Kulaga Henrietta , Kindt Thomas J , Sogn John A 
Published: January 2018

Abstract
Continuous rabbit macrophage-like cell lines were established after in vitro infection of spleen cells with either Simian virus 40, lymphotropic papovavirus or herpesvirus sylvilagus. These cell lines are characterized as morphologically similar to mature macrophages, esterase positive, and have unrearranged immunoglobulin genes. They possess macrophage functionality because they are highly phagocytic and are able to mediate an antibody dependent cell mediated cytotoxicity assay on chicken red blood cells. Northern blot analysis of total cellular RNA with a DQα probe indicates that the cell lines constitutively express message for class II gene products. In addition, cell sorter analysis indicates that two of these lines display class II antigen at the cell surface.
Extracellular Calcium Is not an Absolute Requirement for Tumoricidal Activation of RAW-264 Macrophage-Like Cell Line
Authors: Gorecka-Tisera Alicja M , McCulloch Mary Ann 
Published: January 2018

Abstract
The purpose of these studies was to establish whether extracellular calcium (Cao 2+) plays a role in the process of activation of RAW-264 macrophages for tumor cell killing. We found that these cells were capable of developing a significant level of cytolytic activity under treatment with lymphokine (LK) and lipopolysaccharide (LPS), in the absence of Cao 2+ and that responses developed in Ca2+-free media were only 6–18% lower in comparison with the responses developed in the presence of Cao 2+. The determination of 45calcium uptake in RAW-264 cells treated with LK and LPS showed that the rate of 45calcium uptake has displayed no increase during either the course of activation or in activated, highly cytolytic cells. Finally, three calcium channel blockers examined here: verapamil, diltiazem and flunarizine, with concentrations ranging from 1 × 10-7 M – 2.5 × 10-5 M, showed no inhibitory effect on the process of activation. Nifedipine, another calcium channel blocker, inhibited the development of cytolytic activity with concentrations ranging from 1 × 10-6 M – 2.5 × 10-5 M. It could be argued, however, that this inhibition was nonspecific, since this agent was 13 times more potent with regard to the calcium ionophore A23187-induced release of β-glucuronidase, the function which is entirely dependent on Cao 2+. Taken together, these results suggest that Cao 2+ is not an absolute requirement for the process of tumoricidal activation of RAW-264 macrophages but it may play some supportive role in this process.
Effect of Bacterial Flora and Mouse Genotype (Euthymic or Athymic) on Scrapie Pathogenesis
Authors: Wade W F , Dees C , German T L , Marsh R F 
Published: January 2018

Abstract
Euthymic and athymic female BALB/c mice, reared under either germfree or defined flora conditions, were used to investigate the pathogenesis of scrapie after intracerebral or intraperitoneal inoculation. Time in days to onset of clinical signs (Stage I), to endstage (Stage II), and the time interval between Stage I and Stage II were compared among groups. In addition, scrapie agent titers in spleen were determined at 28 and 90 days after infection, as were agent titers in spleen and brain at Stage II. Three-way analysis of variance indicated that the bacterial flora, the presence or absence of a thymus, and the route of agent inoculation interact to produce significant differences in the pathogenesis of disease. The three factors in the experimental design also influenced the spleen titers of scrapie infectivity. The variation in scrapie pathogenesis among the groups of mice is likely to be mediated by differences in their reticuloendothelial systems. These differences may alter the agent's adsorption in spleen and/or route of transport from spleen to brain.
Size and Filterability of Human and Hamster Pulmonary Macrophages Exposed to Cigarette Smoke
Authors: Smith Clark M. , Tukey David P , Boyd Ruth , Garlich Dawn J , Hoidal John , Clawson C C 
Published: January 2018

Abstract
Pulmonary alveolar macrophages (PAM) obtained from healthy human cigarette smokers generated greater pressure in filtration through small cylindrical pores than PAM from nonsmoking controls. A well standardized hamster smoking model was employed to study the structural basis for the impaired PAM filtration acompanying cigarette smoke exposure. Hamsters also demonstrated increased PAM filtration pressure through cylindrical pores less than half a cell diameter in size after inhalation of cigarette smoke, but not after exposure to vapor phase smoke that had been strained through a particle filter. Cigarette smoker PAM were equally filterable as control through larger diameter channels, and showed comparable improvements in filterability with cytochalasin B treatment. Altered PAM filtration was associated with the formation of characteristic cytoplasmic smoker inclusions, an increase in cell size, and loss of redundant, ruffled surface membrane. The study of smoker and control PAM separated into different sizes on the basis of variations in cell density suggested that discrepancies in cell size were insufficient to explain the filtration disparity. A loss of availability of surface membrane for deformation appeared to be the most important factor responsible for the impaired filtration.
Immunohistochemical Analysis of the Involvement of F4/80 and Ia-Positive Macrophages in Mouse Liver Infected With Lymphocytic Choriomeningitis Virus
Authors: Dixon Jane E , Allan Jane E , Doherty Peter C , Hume David A 
Published: January 2018

Abstract
The distribution of cells bearing the F4/80 macrophage marker and class II MHC glycoproteins has been analyzed in the livers of mice infected with viscerotropic LCMV. The number of F4/80+ macrophages in the liver increases greatly during infection. Much of this is due to the localization of F4/80+ Ia+ monocytes, large numbers of which attach to the walls of the sinuses and the central and hepatic veins. Numerous lymphocytes are also observed in the sinusoids, frequently in close association with macrophages. The lymphocytes tend to move on from this intravascular location, while the macrophages remain. Foci of F4/80− Ia− mononuclear cells (probably T lymphocytes) are found both in the liver parenchyma and in locations that are obviously perivascular. The most prominent of these lymphocyte cuffs are located in the region of the portal triad. Infiltration of the lymphocyte foci with F4/80+ Ia+ elements occurs late, concurrent with evidence of cell death within the lesion. The dissociation in the focal accumulations of lymphocytes and monocyte/macrophages early in the disease process is both striking and unforeseen.
Enhanced Superoxide Production by Rat Alveolar Macrophages Stimulated In Vitro With Biological Response Modifiers
Authors: Badger Alison M 
Published: January 2018

Abstract
The kinetics of superoxide release and the effects of several biological response modifiers (BRM) on superoxide release from rat pulmonary alveolar macrophages (AM) have been studied. These cells produced superoxide anion both spontaneously and in repsonse to phorbol myristate acetate (PMA) in a dose-related manner. The response to PMA peaked in approximately 2 hr and maintained plateau levels for an additional 2-3 hr before subsiding. Pretreatment of the macrophages in vitro with a number of immunostimulants enhanced the production of superoxide above that of controls. The release of superoxide in response to the immunostimulants was a slow phenomenon that took place over a 3-5 hr time period. Lymphokine-containing supematants from concanavalin A (con A)-stimulated rat spleen cells (LK-Sup), murine recombinant gamma interferon (rMuIFN-γ), nigeran, and muramyl dipeptide (MDP) enhanced this response in a dose-related manner. Poly I:C and Salmonella typhosa lipopolysaccharide (LPS) stimulated rat alveolar macrophages at low but not high concentrations. In contrast to the alveolar macrophages, rat peritoneal exudate cells were not activated by immunostimulants to produce increased amounts of superoxide.
Enhancement of Human Peripheral Blood Monocyte Respiratory Burst Activity by Aggregated C-Reactive Protein
Authors: Zeller Janice M , Landay Alan L , Lint Thomas F , Gewurz Henry 
Published: January 2018

Abstract
We had previously demonstrated that C-reactive protein (CRP), an acute phase reactant, when aggregated or coupled to a ligand, interacts with monocytes and certain human peripheral blood lymphocytes. The purpose of the present study, after further characterizing the binding interaction of CRP with human monocytes, was to focus on the biological response of monocytes to CRP binding. Flow cytometric analysis of human mononuclear leukocytes, following incubation with fluoresceinated heat-aggregated CRP (Agg-CRP), revealed that while greater than 70% of monocytes bound Agg-CRP, only 8% of lymphocytes demonstrated positive fluorescence. Furthermore, mean channel fluorescence values indicated that monocytes bound greater amounts of Agg-CRP per cell than did lymphocytes. Luminol-enhanced chemiluminescence (CL) was used as a measure of monocyte respiratory burst activity. Monocytes were stimulated only minimally by Agg-CRP alone; however, Agg-CRP substantially enhanced the CL response to heat-aggregated IgG. This Agg-CRP enhancing effect was selective for IgG-initiated monocyte activation, as no augmentation in CL was observed following cell stimulation with phorbol myristate acetate or serum-opsonized zymosan. These results demonstrate that aggregated CRP binds to the major proportion of human monocytes and selectively augments Fc receptor-mediated stimulation of monocyte oxidative metabolism.
Natural Killer Cell Activity in the Rat. VI. Characterization of Rat Large Granular Lymphocytes as Effector Cells in Natural Killer and Antibody-Dependent Cellular Cytotoxic Activities
Authors: Fukui Hiroyasu , Overton W Roy , Herberman Ronald B , Reynolds Craig W 
Published: January 2018

Abstract
The present study examined rat natural killer (NK) celts, which mediate not only NK activity but also anitibody-dependent cellular cytotoxicity (ADCC). NK and ADCC activities were compared with regard to 1) organ distribution, 2) strain distribution, 3) Percoli fractionation of the effector cells, 4) effects of aging, and 5) potential to be augmented by biological response modifiers (BRM). Like NK activity, appreciable ADCC activity was observed in peripheral blood leukocytes (PBL), splenic leukocytes (SPL), and peritoneal exudate cells (PEC), but not in cell preparations from the peripheral lymph nodes (PLN), mesenteric lymph nodes (MLN), bone marrow (BM), and thymus (THY). ADCC activity, when compared with NK activity, was significantly higher in PBL but the same or lower in SPL and PEC. In terms of strain distribution, a high NK/AOCC strain (mu/mu), four intermediate NK and high ADCC strains (PVG/RTLRL, Lewis, PVG/OLA, and F344), an intermediate NK/ADCC strain (WF/N), and a low NK/ADCC strafa (Buffato) were observed.
Fractionation of effector cells on discontinuous Percoli gradients revealed that both NK and ADCC activities were associated with relatively high-density large granular lymphocytes (LGL). In contrast, ADCC but little or no NK activity was associated with tower density LGL. However, the NK activity of this tower-density LGL population could be elicited following the in vitro incubation with a number of BRM, including rat interferon (IFN) and OK-432, but not rat interteukin-2 (IL-2). In general, the ADCC activity of both higher and tower density LGL enriched celi populations correlated with both the frequency of FC7R+ LGL and the percentage of LGL binders to antibody-coated P815 target cells.
The present study also has shown that in contrast to NK activity, which remained relatively stable with age, ADCC activity from F344 but not WF/N rats increased until 30-50 wk of age. This increase of ADCC activity in older F344 rats was accompanied by an increase in the percentage and absolute number of lower density FCγR+ LGL.
This study demonstrates a number of similarities and differences between NK and ADCC activities in the rat. These findings should be useful for further examining and comparing the in vivo development and biological role of these two effector arms of the immune system.
1,25-Dihydroxyvitamin D3 Stimulates Interieukin-2 Production by a T Cell Lymphoma Line (MLA-144) Cultured in Vitamin D-Deficient Rat Serum
Authors: Haverty Thomas , Haddad John G , Neilson Eric G 
Published: January 2018

Abstract
A lymphocyte T celt line (MLA-144), which constitutively secretes interieulin-2 (IL-2), was shown to express receptors for 1,25-diydroxyvitamin D3 (1,25(OH)2 D3). The proliferation of an IL-2-dopondent cell line (HT-2) in response to supernatant! from MLA-144 cells was employed as an index of IL-2 production by MLA-144 cells. IL-2 production was two fold higher from MLA-144 cells cultured in 2% vitamin D-deficient rat serum compared to 10% fetal calf serum (FCS). The addition of 1,25(OH)2D3 at 10-15 Mor 10-11 M augmented IL-2 production by MLA-144 cells in vitamin D-deflcient rat serum, but not in fetal calf serum. At 10-7 M 1,25(OH)2D3 there was inhibition of IL-2 production by MLA-144 cells In either vitamin D-deflcient serum or FCS. There was no effect of 1,25(OH)2D3, added directly to HT-2 celis. Monoclonal antibody to the IL-2 receptor competitively inhibited the proliferation of HT-2 cells in response to MLA-144 supernatants, suggesting that it was IL-2 from the MLA-144 supernatants which influenced HT-2 proliferation. Our findings demonstrate biphasic does effects of 1,25(OH)2D3 on rymphokine secretion. The use of vitamin D deficient rat serum allowed us to demonstrate the effects of 1,25(OH)2D3 in the physiologic and subphysiologic range.
Metabolic Characterization of Mouse Bone Marrow Cells Responsive to Estrogenic Inhibition: Hexose Monophosphate Shunt Enzyme Activity in Enriched Populations of Mature Cells and Progenitor Cells
Authors: Dieter M P , French J E , Boorman G A , Luster M I 
Published: January 2018

Abstract
Compounds with estrogenic activity cause initial toxic responses in the bone marrow characterized by hypocellularity and stem cell myelotoxicity. To elucidate the biochemical nature of these toxic responses, bone marrow cells were collected from mice treated with pharmacological doses of estrogenic chemicals, separated into enriched cell populations, and the enzymatic responses of the individual cell types characterized. Female B6C3F1 mice were injected s.c. with five daily doses of 0.07-5.6 μmoles diethylstilbestrol (DES) or 17-β estradiol. At 4 days posttreatment body and organ weights were recorded and bone marrow was collected for enumeration and assay of stem cell proliferative responses and enzyme analyses. Treatment with higher dose levels of either estrogenic chemical caused equivalent thymic atrophy, but DES resulted in greater liver and spleen hypertrophy than estradiol. Hexose monophosphate shunt dehydrogenase enzymes in unfractionated bone marrow cells were more sensitive to inhibition by lower estrogen doses than representative enzymes from glycolysis of the Kreb's Cycle, and on an equimolar basis were inhibited to a greater extent by DES than by estradiol. Enzyme analyses after density gradient cell separation indicated that 70-80% of the hexose monophosphate shunt enzyme activity in bone marrow from untreated mice occurred in the enriched band of cells containing predominantly granulocyte-macrophages. The majority of the enzyme inhibition induced by DES treatment could also be ascribed to this cellular population. Furthermore, it was shown that DES had a greater inhibitory effect on the proliferative capacity of the committed stem cells than on the multipotential stem cell population, and the main response was again expressed in the enriched band of cells containing predominantly granulocyte-macrophage precursors. Preliminary endocrine ablation experiments indicated estrogen inhibition of hexose monophosphate shunt enzyme activity was independent of the adrenal and the ovary, but was mediated through the thymus at lower estrogen concentrations.
L-Fucose, D-Mannose, L-Galactose, and Their BSA Conjugates Stimulate Macrophage Migration
Authors: Takata I , Chida K , Gordon M R , Myrvik Q N , Ricardo M J , Kucera L S 
Published: January 2018

Abstract
The effect of selected monosaccharides on the random migration of normal adult rabbit alveolar macrophages (AM) was investigated. It was observed that 10 mM of L-fucose, L-galactose, or D-mannose stimulated AM migration 1.5-2.0 times. In addition, derivatives of L-fucose and D-mannose occupying the carbon-6 position such as L-fucosyl-lactose, D-mannose-6-phosphate, D-mannitol, and mannan enhanced the migration of AM, whereas derivatives of L-fucose and D-mannose in the carbon-1 position produced no migration enhancement. Macrophage migration enhancement activity that was produced spontaneously by spleen cell cultures from normal young rabbits was destroyed by treatment with L-fucosidase. Accordingly, the migration enhancement factor (MEF) found in spleen cell culture supernatants appeared to depend on L-fucose conjugated to some protein carrier because MEF was non-dialyzable. When normal adult AM were treated with L-fucosidase, they lost their responsiveness to migration inhibitory factor (MIF) but retained their responsiveness to MEF. We have interpreted this to mean that the MIF and MEF receptors are distinct. Synthetic MEFs were prepared by conjugating L-fucose, D-mannose, of L-galactose to bovine serum albumin (BSA). It was noted that these sugar-BSA conjugates were about 200 times more effective than the corresponding free sugars in producing migration enhancement. In addition, these sugar-BSA conjugates neutralized MIF activity in a migration inhibition test.