bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of Murine Macrophage Metabolism by Glycolipids: Inhibition of LPS-Induced Metabolism by Specific Gangliosides
Authors: Ryan John L , Gobran Laurice , Morrison David C 
Published: January 2018

Abstract
We have investigated the ability of gangliosides isolated from murine brain to modulate macrophage metabolism. LPS elicits a profound increase in glucose consumption by cultured resident macrophages. When highly purified mouse brain gangliosides are added to macrophage cultures, a modest inhibition of baseline glucose utilization occurs. Both disialogangliosides and trisialogangliosides mediate this effect. In the absence of serum, these gangliosides may be toxic to cultured macrophages. GT1b is the only brain ganglioside tested that specifically inhibited LPS-induced macrophage metabolism. Sialic acid appears to be a necessary component of the gangliosides, although it is not sufficient to induce inhibition. Asialoganglioside and free sialic acid have no effect on macrophage metabolism in comparison with intact gangliosides. The inhibition of LPS-induced metabolism may be explained by the ability of LPS to form stable molecular complexes with both disialogangliosides and trisialogangliosides. These experiments also suggest that the ganglioside content of macrophages may influence functional responses of macrophages to exogenous stimuli.
Proliferative Activity of Macrophages in the Greater Omentum of the Mouse in Relation to the Early Postnatal Development of the Vascular Structures
Authors: Dux Kazimierz 
Published: January 2018

Abstract
The rudimental omentum in newborn mice presents itself as a thin, poorly vascularized membrane covering the stomach. Imprints and whole mounted preparations of the omental membrane of mice from seven different inbred strains, aged 1–10 days, were made and sequential morphological changes were described. It was found that omentum of suckling mice contains numerous foci or colonies of mononuclear phagocytes (omental macrophages).
These cells reveal a high proliferative activity when examined 1 hr after exposure of tritiated thymidine. The labeling index in the population of omental macrophages is variable, ranging in individual mice from less than 5% to 25%. This wide variation is a nonrandom phenomenon. It was found in all seven strains of mice and depends mainly on the age of the mouse. Two possible interpretations are as follows: 1) Some interrelation exists between the intensity of the proliferative activity of omental macrophages and the development of vascular and lymphoid structures that are characteristic for the omentum of adult mice. 2) Omental macrophages originate from local precursors that are not dependent on the bone marrow.
Expression of Class II-MHC Antigens by Tumor-Associated and Peritoneal Macrophages: Systemic Induction During Tumor Growth and Tumor Rejection
Authors: Evans Robert , Blake Sharon S , Saffer Jeffrey D 
Published: January 2018

Abstract
It was shown previously that combination therapy of tumor-bearing mice resulted in amplification of antitumor responses at the site of tumor rejection and involved some of the classical components of the immunological network. As a continuation of this work, we now show that amplification of immune responses involves an increase in class II-MHC antigen (Ia) expression both at the tumor site and peripherally in the peritoneal cavity. Of further interest, however, was the observation that there was also an increase in la expression by tumor-associated macrophages (TAM) and peritoneal macrophages (PMs) in mice bearing progressing tumors. In these experiments, Ia expression by TAM and PMs was assessed in C57BL/6J mice bearing the progressing syngeneic MCA/76-9 sarcoma as well as in mice that had received combination therapy consisting of an intraperitoneal injection of cyclophosphamide (CY) and an intravenous injection of tumor-sensitized T lymphocytes (immune cells). When progressing tumors were analyzed, it was seen that by the fourth day after tumor cell implantation, 45–60% TAM expressed la, a level that was sustained throughout the course of tumor growth. The treatment of tumor-bearers with CY had no effect on la expression by TAM. However, the number of la-expressing TAM increased significantly after combination therapy and, as the tumors regressed, reached a peak of up to 100% in the second week after therapy. TAM were shown by Northern blot hybridization to contain mRNA encoding for the laβ chain. When la expression by PMs was assessed, it was seen that during tumor progression there was an increased expression of la over background (from &lt; 10 to about 40%), beginning 9–12 days after tumor cell implantation and continuing for the duration of the experiments. This was not influenced by CY injection. Combination therapy significantly increased the number of PMs expressing la (up to 80%). la expression by PMs could be induced rapidly in vivo by injecting normal B6 mice intraperitoneally (ip) with T cells isolated from tumors induced to regress by combination therapy. PMs isolated up to 15 days after injection were shown to express Ia. Moreover, the ip injection of a mixture of specific MCA/76-9 tumor cells and these tumor-associated lymphocytes resulted in a more rapid rate and a higher level of Ia expression by PMs compared with the level induced by either treatment alone. In contrast to these findings, it was shown that there was little la expression by TAM and PMs from mice bearing the relatively nonimmunogenic sarcoma MCA/77-23. Overall, the data suggest that antitumor immune responses result in a widespread systemic increase in la expression by macrophages.
Phorbol Ester Circumvents the Need for Macrophages as Well as for Mitogenic Lectins in the Stimulation of Lymphocytes With Wheat Germ Agglutinin or the Calcium Ionophores A23187 or Ionomycin
Authors: Grier Charles E. , Mastro Andrea M 
Published: January 2018

Abstract
Numerous biochemical events precede the proliferation of primary lymphocytes stimulated by mitogenic lectins in the presence of macrophages. Various compounds can activate parts of this response. Specifically the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, (TPA), can replace the requirement for macrophages, apparently by mimicking the macrophage product interleukin 1 (IL1). Wheat germ agglutinin (WGA), itself a non-mitogenic lectin, is reported to cause a calcium flux, phosphatidylinositol turnover, and enhance interleukin 2 (IL2) synthesis. In spite of these positive responses, WGA inhibits DNA synthesis caused by mitogenic lectins. Nevertheless, in this study, we tested the possibility that together TPA and WGA could complement and bring about DNA synthesis. This prediction turned out to be true. The combination of two non-mitogenic compounds resulted in lymphocyte proliferation. The TPA overcame the inhibitory effects of WGA. Moreover, macrophages were not required. The TPA also synergized with the calcium ionophores A23187 or ionomycin to cause lymphocyte proliferation in the absence of macrophages. WGA and the ionophores together did not cause proliferation, a finding which suggested that they fulfill the same roles. These observations led us to conclude that at least two signals were required for lymphocyte stimulation. One signal caused the mobilization of calcium and the other signal circumvented the need for macrophages or macrophage products possibly by mimicking diacylglycerol, the activator of protein kinase C.
Variations in Macrophage Antigen Phenotype: A Correlation Between Ia Antigen Reduction and Immune Dysfunction During Tumor Growth
Authors: Garner Ronald E , Malick Adrian P , Elgert Klaus D 
Published: January 2018

Abstract
Variable la antigen expression by macrophages (Mφ) was examined during tumor growth by measuring: i) la antigen masking and immunofluorescence by anti-la antibody, ii) accessory cell function in concanavalin A (Con A) and mixed lymphocyte reaction (MLR)-induced T cell proliferation, and iii) Mφ stimulatory function in the MLR. Tumor-induced progressive loss of la antigen expression was shown by immunofluorescence and corroborated by anti-la blockade of MLR stimulatory activity of normal but not tumor-bearing hosts (TBH) splenic Mφ. The TBH splenic Mφ supported Con A-induced proliferation of syngeneic T cells (la antigen-independent) but did not support syngeneic T cell proliferation in the MLR (la antigen-dependent). Irrespective of tissue source, normal and TBH Mφ differed in their MLR stimulatory capabilities. In general, splenic Mφ preparations were better stimulators of allogeneic T cell blastogenesis in the MLR than thioglycollate-elicited peritoneal Mφ. Kinetic studies with TBH Mφ showed a significant progressive loss in MLR stimulatory activity, which was especially pronounced with peritoneal Mφ. Expression of la antigens by normal but not TBH Mφ were diminished by 24-h in vitro plating of the peritoneal Mφ. Indomethacin treatment showed Prostaglandin E2 was not a direct in vitro factor in la antigen-mediated reduction of splenic Mφ MLR stimulatory activity. Taken together, these data delineate a loss of Mφ la antigen expression, resulting in a decrease in la antigen-mediated functional activities during tumor growth.
Changes in Splenic Macrophage Mac Antigen Expression During Tumor Growth: A Kinetic Study of Accessory Cell Function and Antigen-Defined Phenotypes
Authors: Garner Ronald E , Elgert Klaus D 
Published: January 2018

Abstract
Three monoclonal antibodies, anti-Mac-1, -2, and -3, were used to modify accessory cell activity of whole spleen cell (WSC) or splenic adherent cell (SAC) preparations from normal or tumor-bearing hosts (TBH). Ligand activation by anti-Mac-1, -2 and -3 modified normal and TBH WSC lectin responses differentially; the most pronounced effect was with anti-Mac 1, which augmented normal WSC responsiveness, whereas anti-Mac-2 and -3 augmented TBH WSC mitogenesis. Ligand interaction with Mac-2 epitopes resulted in significantly suppressed normal host WSC responsiveness. With complement, anti-Mac-1 and -3 each reduced normal and TBH WSC proliferation. Reconstitution of blastogenesis was obtained by combining Mac-2-depleted with Macs-depleted normal host WSC or by combining Mac-1 -depleted with Mac-2-depleted TBH WSC. To evaluate the role of different types of splenic adherent cells in T cell lectin responsiveness, adherent cells were collected and depleted by antibody plus complement treatment and added back to normal T cells. Removal of TBH SAC indicated the number of Mac-1+ SAC susceptible to lysis increased during tumor growth, whereas those susceptible to anti-Mac-2 and-3 treatment decreased. Removal of Mac-1 + normal host SAC stimulated the supportive accessory function of the remaining SAC. Enhancing accessory cell function diminished after removal of Mac-2+ or Mac-1 + normal and TBH SAC, respectively. T cell responsiveness was increased by adding back combinations of normal host SAC, Mac-1-depleted with Mac-3-depleted SAC or Mac-1-depleted with Mac-2-depleted SAC but not by Mac-2-depleted with Macs-depleted SAC. In contrast, none of the TBH SAC combinations were completely restored in accessory activity. In summary, SAC from normal host demonstrated an accesssory cell function corresponding to a Mac-1- phenotype, which was either replaced or obscured by the predominance of a Mac-1+ phenotype in TBH.
Differences in Fc Receptor Expression Between Small and Large Guinea Pig Monocytes
Authors: Noga Stephen J , Normann Sigurd J , Weiner Roy S 
Published: January 2018

Abstract
Guinea pig monocytes have been separated into subpopulations differing in size, morphology, and cytochemistry. We report now that these peripheral blood monocyte subpopulations differ also in native Fc receptor expression. All freshly isolated small monocytes formed Fc rosettes with sensitized sheep erythrocytes, whereas Fc receptor expression was not detectable on large monocytes. However, Fc receptor expression developed rapidly in culture such that by 48 hours all monocytes were positive. This phenomenon was inhibited by 2-deoxy-D-glucose and cycloheximide, suggesting that Fc receptor expression depended upon glycolysis and protein synthesis. Large monocytes participated in antibody-dependent lysis of sheep erythrocyte targets. That large monocytes lacking Fc receptors were cytolytic in this assay was concordant with expression of Fc receptors during the 16-hour test period. We believe that the large number of lymphocytes present in the Fc receptor-positive small monocyte fraction interfered with their measurement of antibody-dependent cytotoxicity. We conclude that Fc receptor expression on guinea pig monocytes is heterogeneous within the peripheral circulation. These differences quickly diminish in vitro with the expression of Fc receptors by all monocytes. Additionally, antibody-dependent lysis of sensitized erythrocytes by guinea pig mononuclear cells is due to monocytes and not lymphocytes or Kurloff cells.
A New Monoclonal Antibody, TRPM-3, Binds Specifically to Certain Rat Macrophage Populations: Immunohistochemical and Immunoelectron Microscopic Analysis
Authors: Takeya Motohiro , Hsiao Lily , Takahashi Kiyoshi 
Published: January 2018

Abstract
An anti-macrophage monoclonal antibody designated TRPM-3 was produced using thioglycollate-elicited rat peritoneal macrophages as immunogen. By the immunoper-oxidase method, TRPM-3 was found to be specific for certain macrophage populations, such as marginal zone macrophages and marginal metallophils of the spleen, sinus macrophages of the lymph nodes, and omentum macrophages. No epithelial cells, peripheral blood monocytes, granulocytes, or lymphocytes had reacted with TRPM-3. Immunoelectron microscopically, reaction to TRPM-3 was clearly demonstrated on the plasma membrane of splenic marginal zone macrophages, lymphatic sinus macrophages, omentum macrophages, and peritoneal macrophages. Accordingly, TRPM-3 was considered to have recognized the particular membrane antigen expressed by restricted macrophage populations.
Experimental Histoplasmosis in the Beige Mouse
Authors: Patiño Maria Mercedes , Williams Dwight , Ahrens Joan , Graybill John R 
Published: January 2018

Abstract
Mice carrying the beige mutation (bg/bg) on a C57BI/6 background were challenged with Histoplasma capsulatum. bg/bg mice had higher mortality and higher lung tissue fungal counts in their lungs than either bg/ + or C57BI/6 mice challenged with equal inocula. Immunologic studies showed that bg/bg mice developed normal delayed-type hypersensitivity (DTH) reactions to histoplasmin, but had deficient NK cell cytotoxic activity against YAC-1 target cells. Studies of macrophage killing of H. capsulatum in vitro showed that T lymphocytes of either bg/ + or bg/bg mice were able to activate fungal killing by bg/ + but not by bg/bg macrophages. These studies, while not excluding a role for the NK cell, suggest that macrophage dysfunction may be critical in the greater susceptibility of the bglbg mouse and, by extension, that macrophage function is of major importance in host defense against H. capsulatum.
Neutrophils from burn patients are unable to increase the expression of CD11b/CD18 in response to inflammatory stimuli
Authors: Rodeberg David A , Bass Robert C , Alexander J Wesley , Warden Glenn D , Babcock George F 
Published: January 2018

Abstract
Neutrophils (PMNs) from patients with thermal injury are dysfunctional for the CD11b/CD18-dependent functions of diapedesis, chemotaxis, and phagocytosis. The expression of CD11b/CD18 on normal PMNs is increased after an inflammatory stimulus. We proposed that CD11b/CD18 expression on burn patient PMNs would respond abnormally to inflammatory stimuli. PMNs were obtained from nonseptic burn patients during the second week after thermal injury. PMNs from burn patients incubated with lipopolysaccharide (LPS), N-formyl-methionyl-leucyl-phenylalanine, phorbol myristate acetate, or A23187 did not increase the expression of CD11b/CD18 to the same degree exhibited by normal PMNs. This inability to increase CD11b/CD18 was not due to differences in CD14 receptor expression, LPS binding, or factors present in the serum of burn patients. The upregulation of CD35 also was decreased on burn patient PMNs. Western blot analysis revealed decreased quantities of CD11b protein in burn patient PMNs compared with normal control PMNs. The deficiency in CD11b/ CD18 expression after inflammatory stimuli may explain some of the abnormalities observed in burn PMN function.
Leukosialin (CD43) behavior during adhesion of human monocytic THP-1 cells to red blood cells
Authors: Soler M , Merant C , Servant C , Fraterno M , Allasia C , Lissitzky J C , Bongrand P , Foa C 
Published: January 2018

Abstract
To understand the modulation and the behavior of glycocalyx elements during adhesion, we explored one of its components, the CD43 molecule, on human monocytic THP-1 cells exposed to cytokine stimulation and its redistribution during heterotypic adhesion to opsonized erythrocytes. First we demonstrated by immunofluorescence and immunoprecipitation that CD43 is dys-sialylated in monocytic THP-1 cells stimulated by interferon-γ (IFN-γ) and tumor necrosis factor α (TNF-α) and stimulation increased correlated to heterotypic adhesion. CD43 anti-adhesive effect seemed to be related to sialic acid moeties because an increase in adhesion was also induced by sialidase treatment and by monoclonal antibodies recognizing sialic acid-dependent epitopes on CD43. Second, a redistribution of CD43 molecules was observed after adhesion, resulting in the exclusion of CD43 molecules from contact areas as demonstrated by immunofluorescence and by ultrastructural immunogold localization. We therefore demonstrated in monocytic THP-1 cells that some glycocalyx molecules can be modulated by cytokines and redistributed during adhesion. These results support the concept that CD43 can regulate cell interactions.
Effect of neutrophil serine proteinases and defensins on lung epithelial cells: modulation of cytotoxicity and IL-8 production
Authors: Van Watering Sandra , Mannesse-Lazeroms Sylvia P G , Dijkman Joop H , Hiemstra Pieter S 
Published: January 2018

Abstract
Neutrophil accumulation in the lung may contribute to tissue injury as observed in inflammatory diseases. Both oxidative and non-oxidative mechanisms are involved in neutrophil-mediated tissue injury. Non-oxidative mechanisms include the release of neutrophil granule proteins such as the serine proteinases elastase and cathepsin G, and the non-enzymatic defensins. Because stimulated neutrophils are thought to release their products simultaneously, we investigated possible interactions between purified defensins and serine proteinases with respect to induction of cellular injury and their ability to induce interleukin-8 (IL-8) synthesis in cells of the lung epithelial cell line A549. Whereas defensins induced cell lysis, elastase and cathepsin G induced detachment of A549 cells. Co-incubation of elastase and cathepsin G revealed an additive effect on detachment, whereas defensins inhibited serine proteinase-induced detachment. Vice versa, both serine proteinases reduced defensin-induced cell lysis. Furthermore, elastase and cathepsin G prevented defensin-induced IL-8 synthesis. In contrast, no inhibitory interaction between cathepsin G and defensins was observed with respect to their antibacterial activity. The results from this study indicate that, at sites of inflammation, neutrophil-mediated injury might be regulated by interactions between released defensins and serine proteinases.
Human monocyte ATP-induced IL-1β posttranslational processing is a dynamic process dependent on in vitro growth conditions
Authors: Laliberte Ronald E , Perregaux David G , McNiff Patricia , Gabel Christopher A 
Published: January 2018

Abstract
Despite a large production capacity, freshly isolated lipopolysaccharide (LPS)-activated human monocytes release only a small percentage of their newly synthesized interleukin (IL)-1β into the medium. Extracellular ATP, acting via surface P2z-type purinoreceptors, increases cytokine posttranslational processing. To explore whether this ATP response was affected by culture conditions, monocytes were maintained for different time periods in the absence and presence of various media components including fetal bovine and human sera and recombinant human cytokines. The ability of monocytes to produce radiolabeled pro-IL-1β in response to LPS and to posttranslationally process the procytokine after ATP stimulation was affected both by time in culture and by the presence of specific media components. These observations indicate that ATP's ability to promote human monocyte IL-1β posttranslational processing is a dynamic process that is subject to regulation by cytokines and/or growth factors. Changes in monocyte/macrophage ATP responsiveness may provide an important regulatory mechanism for the control of IL-1 biological activity in vivo.
Endogenous PMN-derived reactive oxygen intermediates provide feedback regulation on respiratory burst signal transduction
Authors: Derevianko Alexandre , D'Amico Ronald , Graeber Thomas , Keeping Hugh , Simms H Hank 
Published: January 2018

Abstract
The role of polymorphonuclear leukocytes (PMN) in stemming systemic infection is executed mainly by the utilization of molecular O2 leading to the production of reactive oxygen intermediates (ROI). PMN-derived ROI also serve as intra- and extracellular second messengers providing both positive and negative feedback on cellular autoregulation. We investigated the effect of endogenous ROI on two signal transducing pathways: the receptor (R)-G-protein-phospholipase D (PLD) and receptor (R)-G-protein-phospholipase C pathways responsible for the subsequent interleukin-8 (IL-8)-induced PMN respiratory burst. Purified human PMN were primed with LPS adhered to plastic surfaces and stimulated with IL-8 with or without the presence of each of five different selective ROI scavengers/antioxidants: DMSO, NaN3, L-alanine, catalase, or superoxide dismutase. Total IL-8 surface receptor expression was assessed by 125I-IL-8 125I-labeled mAbs against IL-8R type A and B binding assays; PLD activation was assessed by measuring formation of phosphatidyl ethanol (PEt) in the presence of ethanol; PLC activation was measured by quantitative conversion of [32P]ATP-labeled phosphatidic acid (PA) into diacylglycerol (DAG); expression of Gα-inhibitory subunit was assessed by SDS-PAGE and immunoblotting with polyclonal Abs against this subunit. Production of O2–, H2O2, HClO, and myeloperoxidase (MPO) in the experimental model was confirmed in a separate set of experiments. The overall impact of antioxidants on each component of the transducing tripartite complex was stimulatory; however, NaN3 and SOD exhibited the most ubiquitous effect with consistent upregulation by NaN3 of IL-8R expression, whereas even trace amounts of externally added authentic MPO significantly down-regulated the functional activity of both effector enzymes. These results demonstrate a multiple site-specific targeting of the signal-transducing complex by endogenous PMN-derived ROI and an overall protective effect of ROI scavengers/antioxidants.