bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surface Charge of Macrophages and Their Interaction With Charged Particles
Authors: Mutsaers Steven E , Papadimitriou John M 
Published: January 2018

Abstract
The distribution and concentration of surface ionogenic groups on murine peritoneal macrophages and the responses of their plasmalemma to charged markers were investigated by electron microscopy. Quantitation of the distribution of cationized ferritin (CF) as a marker for anionic groups on fixed cells revealed surface anions on invaginated parts of the plasmalemma to be fewer than those on flat or projecting segments. Cationic groups on the surface membrane, however, could not be labeled with anionized ferritin (AF). Interaction of viable macrophages with cationic particles at 37° resulted in their “internalization” within vesicles and coated pits and a closer apposition between many segments of plasmalemma than with neutral or anionic substances. The process occurred unaltered at 4° and was unaffected by cytochalasin B and colchicine, suggesting that this close apposition between segments of plasmalemma resulted from neutralization of surface negative electrostatic charges by the cationic material and did not reflect endocytosis.
Immunohistochemical Characterization of the Estrogen-Stimulated Leukocyte Influx in the Immature Rat Uterus
Authors: Zheng Yi , Zhou Zhao-Zong , Lyttle C Richard , Teuscher Cory 
Published: January 2018

Abstract
Previous studies have shown that the injection of estrogen into immature rats leads to an influx of leukocytes into the uterus. Using immunoperoxidase staining and monoclonal antibodies, we have characterized the nature of the infiltrating leukocytes in frozen sections of immature rat uteri obtained following the injection of estrogen, estrogen plus pertussigen, and the antiestrogen LY117018. Estradiol treatment for 2 days resulted in a significant increase in the number of uterine eosinophils, CD4 (W3/W25)-positive helper/inducer T lymphocytes, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells. In contrast, estradiol treatment failed to elicit a significant increase in the number of CD8 (MRC OX-8)-positive uterine cytotoxic/suppressor T lymphocytes and/or natural killer cells, as well as MAR 18.5- and/or MRC OX-12-positive B lymphocytes. The injection of LY117018 failed to elicit any changes in the number of cells expressing any of the phenotypes under investigation. The simultaneous injection of pertussigen, the major toxin responsible for the leukocytosis- and lymphocytosis-promoting activity of Bordetella pertussis, inhibited the estrogen-induced influx of eosinophils, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells but failed to prevent the influx of CD4 (W3/25) positive helper/inducer T lymphocytes. These results indicate that, in the immature rat, significant differences may exist in the susceptibility of various cell populations to the effects of estrogen, particularly with regard to uterine influx following estrogen stimulation. In addition, our observations suggest that either 1) the CD4-positive cells infiltrating the uterus following estrogen treatment may use a nonpertussigen-sensitive mechanism for chemotactic factor-receptor signal transduction or 2) a subpopulation of resident uterine cells can be induced to express the CD4 antigen following estrogen and/or estrogen plus pertussigen treatment.
SHORT COMMUNICATION: Cytokines Induce an L-Arginine-Dependent Effector System in Nonmacrophage Cells
Authors: Amber Ina J , Hibbs John B , Taintor Read R , Vavrin Zdenek 
Published: January 2018

Abstract
Treatment of EMT-6 mammary adenocarcinoma cells with gamma interferon (rMuIFNγ) plus tumor necrosis factor (rMuTNFα) and/or interleukin-1 (rHuIL-1α) causes release of iron-55 label, inhibition of DNA replication, and inhibition of aconitase activity. In addition, the same combinations of cytokines induce EMT-6 cells to synthesize L-citrulline, nitrite, and nitrate directly from L-arginine. Lipopolysaccharide (LPS) can act as a cofactor in the induction of these metabolic effects when added to EMT-6 cells in the presence of rMuIFNγ. The results show that increased levels of cytokines in the microenvironment can induce a novel effector pathway in somatic cells not specialized for host defense, resulting in specific metabolic effects as well as the inhibition of cellular proliferation.
Inhibition of Phagocytosis and Interleukin-1 Production in Pulmonary Macrophages From Rats With Sialodacryoadenitis Virus Infection
Authors: Boschert K R , Schoeb T R , Chandler D B , Dillehay D L 
Published: January 2018

Abstract
To test whether or not sialodacryoadenitis virus (SDAV) infection in rats affects pulmonary macrophage function, we intranasally inoculated pathogen-free F344 rats with SDAV and collected alveolar and interstitial macrophages 5 d later. We assessed Fc receptor-mediated attachment and phagocytosis by phase-contrast microscopic examination of monolayers of alveolar and interstitial macrophages incubated with zymosan, nonopsonized sheep erythrocytes, or erythrocytes opsonized with rabbit antisheeperythrocyte IgG. Alveolar macrophages from virus-infected rats had significantly (P ≤ .05) lower indices of attachment and phagocytosis of opsonized erythrocytes than control macrophages, but there was no difference in attachment of zymosan particles. Interstitial macrophages were not affected. Alveolar macrophages from SDAV-infected rats produced significantly less interleukin-1 than those from control rats, as assessed by testing supematants from lipopolysaccharide-stimulated macrophage cultures for induction of mouse thymocytes to take up tritiated thymidine. Effects of SDAV infection on lung macrophages could increase host susceptibility to other pathogens or complicate studies of respiratory tract immunity.
Effects of Retinoids on Macrophage Function and IL-1 Activity
Authors: Dillehay D L , Walia A S , Lamon E W 
Published: January 2018

Abstract
The effects of three retinoids, all-trans-retinoic acid (RA), 13-cis-retinoic acid (cRA), and N-(4-hydroxyphenyl) ratinamide (4-HPR), on macrophage function were evaluated. In vitro, RA, cRA, and 4-HPR caused a greater than twofold increase in phagocytosis of IgG-sensitized bovine erthrocytes (IgG-ORBC) by a mouse macrophage cell line (RAW). Significant increases in phagocytosis were produced by retinoid concentrations as low as 2 x 10-10 M. RA also significantly increased phagocytosis of IgG-sensitized ORBC by BALB/c peritoneal macrophages In vitro. The ability of RAW macrophages to bind IgG-ORBC was significantly increased by 10-6 to 10-14 M RA. The potentiation of myogenic responses of spleen cells to Con A and PWM by RA was relatively independent of macrophage function, i.e., splenocytes that were macrophage-depleted were responsive to the potentiating effects of RA. The effects of retinoids on T-cell-dependent B-cell mitogenesis induced by PWM appeared not to be dependent on their previously reported capacity to alter prostaglandin synthesis. Treatment of spleen cells with 10-6 M indomethacin did not abolish the potentiating effects of RA. However, RA in a dose-dependent fashion increased IL-1 activity at the level of the target T-cell. The greatest potentiation of IL-1 activity was at 10-8 M RA. These results show that retinoids can modulate macrophage function at two different levels: potentiation of phagocytosis and potentiation of IL-1 activity at the level of the T-cell.
Inhibition of Neutrophil Superoxide Anion Generation by Platelet Products: Role of Adenine Nucleotides
Authors: McGarrity S T , Stephenson A H , Hyers T M , Webster R O 
Published: January 2018

Abstract
Previously, we demonstrated the stimulus-specific ability of platelet lysate or release products to inhibit neutrophil functions in response to f-met-leu-phe (fMLP) or phorbol myristate acetate (PMA). The present study further characterizes these activities and identifies one of the platelet inhibitors of neutrophil superoxide anion (O) generation. Sephadex G-200 chromatography revealed two fMLP-specific inhibitory activities in platelet lysate. One component eluted with materials &lt;13 kilodaltons (kD) molecular weight, whereas the second fractionated at the void volume (Mr &gt; 200 kD). PMA-specific inhibitor(s) cofractionated at the void volume with the lysate’s fMLP-inhibitory activity. Release products of activated platelets contained low-molecular-weight (&lt;13 kD), fMLP-specific inhibitor activity but failed to demonstrate PMA-specific inhibition of neutrophil O generation. Biochemical characterization identified two distinct high-molecular-weight inhibitors in platelet lysate. Pretreatment with adenosine deaminase (ADA) completely abrogated the maximum inhibitory effect (43.8 ± 7.5%) of the high-molecular-weight, fMLP-specific lysate component but failed to reduce maximum PMA-specific inhibition (93.0 ± 2.0%) of neutrophil O generation. Likewise, while the lysate’s fMLP-specific inhibitor was heat stable, heating reduced the PMA-specific inhibition 56.5 ± 10.4%. Equal sensitivity to ADA, resistance to trypsin, and heat stability were demonstrated by the low-molecular-weight inhibitor(s) in platelet lysate and release products. Neither high- nor low-molecular-weight platelet inhibitors scavenged O. High-performance liquid chromatography (HPLC) of the low-molecular-weight inhibitory activity from both platelet lysate and release products revealed physiological levels of adenine nucleotides. Addition of pure adenine nucleotides at physiological levels (1-10 μM) mimicked the effectiveness of the platelet inhibitor. We conclude that stimulus-specific limitation of neutrophil O generation by platelet adenine nucleotides may represent a mechanism for reducing inadvertent tissue damage during inflammation.
Prostaglandin E2-Mediated Inactivation of Various Killer Lineage Cells by Tumor-Bearing Host Macrophages
Authors: Parhar Ranjit S , Lala Peeyush K 
Published: January 2018

Abstract
We have previously reported that natural killer (NK) lineage cells are progressively inactivated during tumor development by prostaglandin E2 (PGE2) secreted by host macrophages; that this facilitates spontaneous tumor metastases, which can be prevented by chronic indomethacin therapy (CIT); and that CIT combined with multiple rounds of interleukin 2 (IL-2) can cure experimental metastases and activate all killer lineage cells in situ including NK cells, lymphokine-activated killer (LAK) cells, and tumoricidal macrophages. The present study tested whether PGE2 secreted by tumor-bearing host macrophages exerts pansuppressor effects against the activation of T cells, NK cells, LAK cells, and tumoricidal macrophages from normal splenic cell populations. Macrophages isolated from CBA mice bearing 21-day intraperitoneal Ehrlich ascites tumors (EAT) or C3H/HeJ mice bearing 21-day subcutaneous T58 mammary adenocarcinomas were added (± 10−5 M indomethacin, or a monoclonal anti-PGE2 ab) to syngeneic splenic lymphocytes to examine the effects on 1) polyclonal activation (3-d 3H-thymidine [3H-TdR] uptake) with concanavalin A (Con A); 2) one-way (CBA α BALB/C or C3H α BALBC) MLR (5-d 3H-TdR uptake) and subsequent CTL generation (tested against 51Cr-labeled Con A blasts of the stimulator phenotype); 3) NK activity (after 24-h co-culture) against YAC-1 targets; 4) generation of LAK cell activity (in the presence of 200 or 2,000 units recombinant IL-2 for 3 or 5 days), tested against NK-sensitive and NK-resistant targets. Similar effects were also noted on the generation of tumoricidal activity in normal splenic macrophages cultured for 3 days in the presence of LPS. Normal splenic macrophages added under the same conditions served as controls. Effects of pure PGE2 or PGF2 (10−6M) were also examined on these activation events. Results revealed that tumor-host-derived macrophages (but not normal macrophages) markedly suppressed all these activation events and this suppression was abrogated nearly totally by indomethacin and totally by anti-PGE2 ab, indicating its mediation by PGE2. This finding ran parallel with high levels of PGE2 production by tumor-host-derived but not normal splenic macrophages. Pure PGE2 but not PGF2α mimicked these suppressor effects. While tumoricidal activity was generated in normal macrophages in the presence of LPS, IL-2, or IFN-γ or their various combinations (which led to further augmentation), these agents required the presence of indomethacin to generate significant killer activity in tumor-host-derived macrophages. These results indicate that macrophages in tumor-bearing hosts exert pansuppressor effects against the activation of all tumoricidal effector lineages inclusive of T, NK, LAK cells, and killer macrophages.
Enhancement of the Expression of Activation Markers on Human Peripheral Blood Mononuclear Cells by In Vitro Culture With Retinoids and Carotenoids
Authors: Prabhala Rao H , Maxey Vada , Hicks Mary J , Watson Ronald R 
Published: January 2018

Abstract
Retinoids (retinol, retinal, retinoic acid, retinyl beta-glucuronide, and 13-cis retinoic acid) and carotenoids (beta-carotene and canthaxanthin) were evaluated for their immunomodulatory effects on human peripheral blood T-lymphocyte subpopulations and natural killer (NK) cells. Peripheral blood mononuclear cells (PBMC) from healthy young volunteers were isolated and incubated for 72 hours at various levels of retinoids and carotenoids including a physiological concentration (10-8 M). Expression of surface antigens for total T cells, T-helper and T-suppressor cells, and activation markers (transferrin receptor, HLA-Dr antigen, and interleukin 2 receptor) were analyzed with an EPICS V flow cytometer. Retinoic acid and 13-cis retinoic acid (13-cRA) produced significant increases in the percentage of cells with markers for total T-helper cells, with a minimal effect on percentage of lymphocytes with markers for NK cells. However, beta-carotene (BC), canthaxanthin (CTX), and retinyl beta-glucuronide (RBG) dramatically increased the percentage of PBMC with markers for NK cells and produced a smaller increase in lymphocytes with surface antigens identifying them as T-helper cells. Furthermore, retinol and retinal did not show significant change either in the percentage of lymphocytes with markers for T-helper cells or in the helper/suppressor ratio. An increase in the expression of HLA-Dr antigen and transferrin receptors was greater when cells were incubated with 13-cRA than with either BC, CTX, or RBG, while carotenoids produced a greater increase in the expression of IL-2 receptors than 13-cRA. Our study indicates that both retinoids and carotenoids might be activating different subpopulations of immune cells.
Regulation of Monokine Gene Expression: Prostaglandin E2 Suppresses Tumor Necrosis Factor but Not Interleukin-1α or β-mRNA and Cell-Associated Bioactivity
Authors: Scales W E , Chensue S W , Otterness I , Kunkel S L 
Published: January 2018

Abstract
Prostaglandin E2 (PGE2)-mediated suppression of macrophage interleukin-1α,β and tumor necrosis factor-α synthesis was examined at the cellular and molecular levels. Treatment of lipopolysaccharide (LPS)-stimulated adjuvant-elicited murine macrophages with 5 × 10-7M PGE2 caused a 70% reduction in cell-associated TNF but had no suppressive effect on cell-associated interleukln-1 (IL-1) activity. Consistent with this result, Northern blot and nuclear transcription analyses demonstrated suppression of TNF mRNA but PGE2 had no effect on IL-1α and IL-1β mRNA accumulation, as compared to LPS controls. Immunoperoxidase staining for cell-associated TNFα, IL-1α, and IL-1β demonstrated that PGE2 suppressed TNF, but not IL-1α or -β expression, supporting the bioassay data. These results imply that PGE2-mediated regulation of IL-1α,β and TNFα is quite distinct. Synthesis of TNF appears to be regulated at least at the level of transcription, whereas that for IL-1α and -β is regulated post-transcriptionally.
Characterization of the Luminol-Amplified Light-Generating Reaction Induced in Human Monocytes
Authors: Johansson Agneta , Dahlgren Claes 
Published: January 2018

Abstract
Increased production of oxidative metabolites following interaction between mononuclear phagocytes and soluble stimuli can be measured as luminol-amplified chemiluminescence (CL). The effects of superoxide dismutase (SOD), catalase, and azide on the monocyte CL response were investigated. Azide, a myeloperoxidase (MPO) inhibitor, reduced the CL reaction by more than 80%, which indicates that the CL reaction is dependent on the granule enzyme MPO. Because SOD and catatase only partly inhibited the monocyte CL response, the authors propose that part of the monocyte CL response is of intracellular origin. This conclusion is further supported by the effects on the CL response obtained by adding extra peroxidase and the lack of correlation with techniques measuring only extracellular generated metabolites. However, it should be pointed out that the relation between extracellular and intracellular activity is stimulus dependent. Furthermore, even if quantitative differences exist between monocyte and granulocyte CL, the mechanism for the light-generating reaction seems to be the same in both cell types.
Selective Depletion of Rat Neutrophils by In Vivo Administration of a Monoclonal Antibody
Authors: Sekiya Sakae , Gotoh Seiji , Yamashita Takao , Watanabe Tadashi , Saitoh Susumu , Sendo Fujiro 
Published: January 2018

Abstract
A monoclonal antibody (RP-3) that depletes rat neutrophils selectively in vivo was developed by hybridization of mouse myeloma cells (P3-X63.Ag8.653) and spleen cells of BALB/c mice sensitized with peritoneal neutrophils of WKA/Hok rats. RP-3 reacted with rat neutrophils but not with lymphocytes, macrophages, natural killer cells, basophils, eosinophils, or tissues of various organs. The mitogenic responsiveness to concanavalin A (ConA), phytohemagglutinin (PHA), and lipopolysaccharide (LPS) of rats given RP-3 was not significantly different from that of normal rats.
Administration of RP-3 into the peritoneal cavity of rats that had been kept under specific pathogen-free (SPF) or clean conditions induced selective depletion of circulating neutrophils to under 100/mm3 (0.5% WBC). The numbers of monocytes, lymphocytes, and platelets were not changed. Administration of 2 ml of RP-3 reduced blood neutrophils to under 100/mm3 for approximately 24 h, and administration of 1 ml caused depletion for approximately 12 h.
Regulation of Systemic Macrophage IL-1 Gene Transcription: The Involvement of Tumor-Derived Macrophage Growth Factor, CSF-1
Authors: Evans Robert , Duffy Theodore M , Blake Sharon S , Lin Hsiu-San 
Published: January 2018

Abstract
Previous data indicated that progressive growth of the C57BL/6J sarcoma, MCA/76-9, was associated with a systemic increase in the level of IL-1 activity in peritoneal and tumor-associated macrophages. In this paper, the hypothesis was tested that macrophage IL-1 alpha and beta gene expression was regulated by the specific macrophage growth factor, CSF-1, produced by tumor cells. The data indicated that all of the nine C57BL/6J, BALB/cJ, and C3H/HeJ sarcomas tested transcribed the CSF-1 gene. The tumor cell culture supernates induced proliferation of bone marrow cells that differentiated into macrophages. Moreover, proliferative activity of conditioned medium and the ability to induce macrophage differentiation were abrograted by neutralization with the 5A1, rat-anti-mouse monoclonal anti-CSF-1 antibody. Conditioned medium from tumor cell cultures, as well as recombinant CSF-1 and L cell-conditioned medium, induced transcription of the IL-1 alpha and beta genes, the latter being more strongly expressed. IL-1 gene transcription was not induced after neutralization of the culture supernates by the monoclonal antibody, 5A1. The overall data would support the hypothesis that the pathway in vivo leading to the increased IL-1 expression by macrophages is regulated by at least one tumor cell product, CSF-1.
Morphological and Functional Changes During Cytomegalovirus Replication in Murine Macrophages
Authors: van Bruggen I , Price P , Robertson T A , Papadimitriou J M 
Published: January 2018

Abstract
Structural and functional changes were studied in murine peritoneal macrophages infected with murine cytomegalovirus by using centrifugal enhancement to achieve a high-level (&gt; 90%) pulsed infection. During 3 d of culture the infected cells became enlarged and rounded with smooth surface contours. Transmission electron microscopy demonstrated various stages of viral maturation in the nucleus and cytoplasm. Intracellular organization was generally retained, apart from the development of large, irregular, intracytoplasmic vacuoles, in which enveloped virions and cell debris accumulated. The infected macrophages lost most surface markers tested (F4/80, Mac-1, FcR, and the receptor for gluteraldehyde-fixed sheep red blood cells), but H-2 expression was increased. Moreover, ingestion of colloidal gold or horseradish peroxidase was depressed, and the levels of acid phosphatase activity, lymphocytostatic activity, and interleukin 1 production were also decreased. The latter may explain the observed loss of accessory cell function.
Human Neutrophil Degranulation Stimulated by Aspergillus fumigatus
Authors: Levitz Stuart M , Farrell Timothy P 
Published: January 2018

Abstract
Previous studies have established that human neutrophils (PMN) are unable to kill resting conidia (RC) of Aspergillus fumigatus but can kill conidia that have been preincubated in culture medium until swollen but not yet germinated. Compared with swollen conidia (SC), RC stimulate a relatively weak PMN respiratory burst In the present study, we further examined the mechanisms of resistance of RC to neutrophil killing by comparing neutrophil degranulation and phagocytosis following stimulation by RC and SC opsonized in pooled human serum. RC, compared with SC, stimulated significantly less release of both the primary granule marker β-glucuronidase and the secondary granule marker lactoferrin. PMN also phagocytosed significantly greater numbers of SC, although the differences in phagocytosis were not great enough to account for the differences in degranulation. Suboptimal stimulation of degranulation and phagocytosis may thus contribute to the inability of neutrophils to kill RC. Moreover, reagent lactoferrin bound avidly to both RC and SC, raising the possibility that PMN-released lactoferrin may contribute to antifungal activity at the conidial surface by competing for iron or catalyzing the formation of oxygen radicals.
Kupffer Cell Proliferation and Glucan-Induced Granuloma Formation in Mice Depleted of Blood Monocytes by Strontium-89
Authors: Yamada Masahiko , Naito Makoto , Takahashi Kiyoshi 
Published: January 2018

Abstract
In mice with prolonged severe monocytopenia induced by selective irradiation of the bone marrow with the bone-seeking isotope 89Sr, the proliferative capacity of Kupffer cells was studied by immunohistochemistry with an anti-mouse macrophage monoclonal antibody, F4/80, ultrastructural peroxidase (PO) cytochemistry, and tritiated thymidine (3HTdR) autoradiography. The number and 3HTdR uptake of Kupffer cells were significantly increased in the splenectomized mice after severe monocytopenia had continued for more than 4 wk, and almost all the Kupffer cells showed a localization pattern of PO activity similar to that of resident macrophages in the liver of normal mice. In the glucan-induced granuloma formation in similar mortocytopenic mice, Kupffer cells proliferated. conglomerated, and transformed into epithelioid cells, which fused together to become multinuclear giant cells. These results suggest that Kupffer cells are a self-renewing population by their own cell division and can participate actively in granulomatous inflammations in severely monocytopenic and intact mice.