bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of Delayed-Type Hypersensitivity in Mice Pretreated With Diethylstilbesterol: Involvement of Sex Hormones in Immunomodulation
Authors: Kato Kazuyuki , Chen Yu , Nakane Akio , Minagawa Tomonori , Fujieda Kenji , Kimura Takuro , Yamamoto Ken-ichi 
Published: January 2018

Abstract
Delayed-type hypersensitivity (DTH) responses were suppressed in female mice treated with diethylstilbesterol (DES), a synthetic nonsteroidal compound possessing estrogenic activity, but not in male mice. Upon analysis of this DTH-suppression in DES-treated female mice by use of the macrophage migration inhibition (MI) assay, an in vitro correlate of DTH, suppressor adherent cells (i.e., macrophages) in the peritoneal cavity were found to play an important role in this DTH suppression. On the other hand, DES-induced suppression was observed in surgically castrated male mice with depressed plasma testosterone (TS) levels, but not in TS-treated female mice or in castrated male mice, which suggests that TS inhibited the DES suppression. These results provide evidence that DTH response may be modulated by sex hormones.
Platelet Activating Factor Increases Expression of Complement Receptors on Human Neutrophils
Authors: Shalit Meir , Von Allmen Carolyn , Atkins Paul C , Zweiman Burton 
Published: January 2018

Abstract
The phospholipid inflammatory mediator platelet activating factor (PAF) has been shown to stimulate certain functions of polymorphonuclear leukocytes (PMN). However, the effect of PAF on surface complement receptors of PMN has not been described. Using monoclonal antibodies and flow cytometry, we have assessed the effects of PAF on surface expression of membrane receptors for C3bi (CR3) and C3b (CR1) in human PMN. PAF (optimal concentration of 1 × 10-8 M) increased CR3 190% and CR1 174% compared with unstimulated cells at 37°, while the PAF analogue lyso-PAF had no stimulatory effect. Both CR3 and CR1 responses to PAF reached maximum levels at 15-30 min. PAF effects were comparable to peak effects induced by LTB4 but less than induced by FMLP. A PAF receptor antagonist, SRI 63-441, blocked the increased complement receptor expression in a dose-dependent manner with maximal inhibition of 80-95% at 5 × 10-6 M. Extracellular calcium had no effect on CR1 expression but slightly enhanced and EGTA partially inhibited the PAF-induced increase in CR3 expression. Simultaneous incubation with PAF and LTB4 enhanced CR3 and CR1 expression more than either agent alone. These findings indicate that PAF, alone and in combination with LTB4, can induce altered expression of complement receptors on the surface of PMN. This effect may enhance adhesion and phagocytosis by PMN at inflammatory reaction sites.
Flow Cytometric and Histological Analysis of Mouse Thymus in Fetal Alcohol Syndrome
Authors: Ewald Sandra J , Walden Shannon M 
Published: January 2018

Abstract
Reduced thymus size and fetal weight were seen in 18-day old fetuses of C57BL/6 female mice fed a complete liquid diet containing 25% ethanol-derived calories (EDC) from gestational day 0 to 18. Thymocytes from fetuses from the 25% EDC diet group and from pair-fed and ad-lib control diet groups were compared by flow cytometry for expression of thymocyte differentiation antigens. The proportions of L3T4-positive and Lyt-2-positive thymus cells were significantly reduced in alcohol-exposed fetuses compared to controls; however, the number of Thy-l-positive cells did not differ among any of the groups. Histologically, the thymus from 25% EDC fetal mice failed to show the delineation between cortex and medulla that was seen in the thymuses of control fetuses. These results indicate that thymus immaturity is one of the accompanying features of fetal alcohol syndrome.
Decrease in Pyrogenicity of Muramyl Dipeptide After Coupling With Luteinizing Hormone-Releasing Hormone
Authors: Riveau Gilles , Hosmalin Anne , Carelli Claude , Lefrancier Pierre , Chedid Louis 
Published: January 2018

Abstract
Muramyl dipeptide (MDP) and its adjuvant active derivative lysine-MDP (Lys-MDP) have been demonstrated to be pyrogenic and to induce endogenous pyrogen (EP) production in vivo and in vitro. It has recently been shown that immunologic castration can be achieved in mice by immunization with luteinizing hormone-releasing hormone (LHRH) directly conjugated by carbodilmide to Lys-MDP, termed LHRH-Lys-MDP (cdi), or with a linear monomeric MDP-linked molecule obtained by total synthesis, termed LHRH-Lys-MDP (s). These preparations were tested in the rabbit for their capacity to induce fever and were found to be devoid of pyrogenicity at dosage levels of Lys-MDP that induced fever. This decrease of pyrogenicity of Lys-MDP after coupling to LHRH seems to be related to the structure of the conjugate because the derivative LHRH-LysNH2-MDP exhibited the same pyrogenic activity as the free glycopeptide. Surprisingly, nonpyrogenic LHRH-Lys-MDP induced production of EP and interleukin-1 (IL-1) in vitro and increased in vivo modifications of metal levels attributed to the action of IL-1. Moreover, LHRH-Lys-MDP reduced the pyrogenic effect of an exogenous dose of EP.
Quantitation of Intracellular Mac-1 (CD11b/CD18) Pools in Human Neutrophils
Authors: Jones Douglas H , Anderson Donald C , Burr Bean L , Rudioff Helen E , Smith C Wayne , Krater Sharon S , Schmalstieg Frank C 
Published: January 2018

Abstract
The adhesive glycoprotein Mac-1 (CD11b/CD18) of the CD11/CD18 complex contributes to multiple neutrophil inflammatory functions. Activation of neutrophils by chemotactic stimuli results in a rapid, protein synthesis-independent increase in surface Mac-1 derived from incompletely defined intracellular compartments. Therefore, we developed a novel quantitative lectin immunoblot technique to define intracellular pools of Mac-1 in subcellular neutrophil fractions resolved on discontinuous Percoll gradients. In cavitates of unstimulated neutrophils, 30% and 26% of total Mac-1 was identified in β [1.10 gm/ml; vitamin B12 binding protein (vit B12 B.P.)-rich] or pre-γ (1.07 gm/ml; vit B12 B.P.-poor) granular fractions, respectively, whereas 24% was associated with the plasma membrane-rich γ (1.06 gm/ml) fractions. N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation (10−8 M, 15 min, 37°C) significantly diminished Mac-1 in pre-γ (-18% of total, P &lt; 0.05) but not β fractions (+6% of total). Under these conditions, the content of Mac-1 in γ fractions increased 13% in association with four- to eightfold increase in surface Mac-1 expression (OKM-1 binding). These findings suggest that chemotactic stimuli increase plasma membrane and/or surface Mac-1 on human neutrophils by mobilizing a novel intracellular granule pool.
Membrane Oxidative Metabolism of Human Eosinophilic Cell Line EoL-1 in Response to Phorbol Diester and Formyl Peptide: Synergistic Augmentation by Interferon-γ Tumor Necrosis Factor
Authors: Yoshie Osamu , Majima Toshiro , Saito Hiroshi 
Published: January 2018

Abstract
Human eosinophilic cell line EoL-1 was studied using luminol-dependent chemiluminescence (CL) for the ability to produce a respiratory burst upon stimulation with 12-O-tetradecanoylphorbol-13-acetate (TPA) and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). TPA, a potent activator of protein kinase C, induced a biphasic CL response in EoL-1. Treatment of EoL-1 with interferon-γ (IFN-γ) for 5 days dramatically enhanced TPA-inducible CL, and IFN-αA had a similar effect. Neither IFN-γ nor IFN-αA strongly inhibited EoL-1 cell growth. Tumor necrosis factor (TNF) also enhanced TPA-inducible CL response of EoL-1 and, furthermore, was quite inhibitory to EoL-1 cell growth. The effects of IFN-γ and TNF were synergistic, whereas those of IFN-αA and TNF were additive. Superoxide dismutase completely abrogated TPA-induced CL, but sodium azide suppressed only the late phase of CL. EoL-1 pretreated with IFN-7, IFN-αA, or TNF also became capable of producing CL response to a chemotactic peptide (fMLP). The effects of IFN-γ and TNF were again synergistic. EoL-1 cells treated with IFN-γ, IFN-αA, or TNF had abundant cytoplasm, but only TNF increased cells having distinct eosinophilic granules. IFN-γ but not IFN-αA enhanced the cytological effect of TNF. It was further demonstrated that treatment of EoL-1 with IFN-γ and TNF strongly increased the binding sites for phorbol diesters and also dramatically induced the surface expression of fMLP receptors. IFN-γ had, however, little effect on the number or the ligand-binding affinity of TNF receptors on EoL-1. Thus, EoL-1 may provide a useful experimental model for the study of differentiation and regulation of human eosinophils.
Neutral Lipid Accumulation in Macrophages During Lipid-Induced Macrophage Growth
Authors: Yui Satoru , Yamazaki Masatoshi 
Published: January 2018

Abstract
We previously reported that lipids such as cholesterol esters, triglycerides, and some phospholipids that are components of cell membranes or serum lipoproteins induced the growth of mouse peritoneal macrophages in vitro. Here, we report that macrophage growth was directly induced by lipids without any soluble factors and that the continuous presence of lipids was required for their growth during culture. When macrophages were cultured with several phospholipids that stimulated macrophage growth, their triglyceride content was dramatically increased during culture, whereas their contents of phospholipids, cholesterol, and esterified cholesterols were scarcely changed. On the other hand, phosphatidylcholine and sphingomyelin, which did not stimulate macrophage growth, caused less accumulation of triglycerides in the cells. Macrophages in which triglycerides accumulated resembled foam cells, since they contained many particles that stained with oil red O. Macrophages that cultured with cholesteryl linoleate also contained many oil red O-stainable particles. These data suggest that accumulation of lipid droplets is correlated with macrophage growth induced by lipids and that foam cells in pathological states such as those in atherosclerotic or xanthoma lesions might proliferate in situ.
Differential Induction of Hematopoiesis and Immune Suppressor Cells in the Bone Marrow Versus in the Spleen by Lewis Lung Carcinoma Variants
Authors: Young M Rita , Aquino Sandy , Young Meivin E 
Published: January 2018

Abstract
Mice bearing large (≥ 3 g) metastatic and nonmetastatic Lewis lung carcinoma (LLC) tumors were studied to determine if the tumor variants differentially induced bone marrow versus splenic hematopoiesis and the appearance of hematopoiesis-associated immune suppressor cells. The metastatic LLC-C3 and nonmetastatic LLC-C8 tumors were equal in their stimulatory effects in vivo on both the number of bone marrow myeloid progenitor cells (CFU) and the appearance of bone marrow immune suppressor cells. In contrast, the tumor variants differed in their effects on the spleen, with the metastatic tumors causing a more pronounced increase in the number of nucleated cells and CFU, a reduced blastogenic responsiveness to concanavalin (Con-A), and an increased suppressor cell activity than nonmetastatic LLC-C8 tumors. The splenic suppressor cells of mice bearing large LLC-C3 tumors resembled the bone marrow suppressor cells which we previously described (Young et al.: Cancer Res. 47, 100, 1987) in that they were nonadherent to nylon wool, sensitive to treatment with L-leucine methyl ester, insensitive to treatment with complement and Thy-1.2, MG-1.2, asialo-GM1, or anti-IgM antibodies, and mediated their suppression through a mechanism which was only partially indomethacin sensitive. The stimulatory effects on hematopoiesis and suppressor cells by the LLC variant tumors may have been mediated by the tumor-derived colony stimulating factor (CSF) activities. Bone marrow cell proliferation and colony formation were stimulated in vitro by culture supernatants of metastatic LLC-C3 cells and, to a lesser degree, of nonmetastatic LLC-C8 cells. These colony-stimulating factor (CSF)-containing supernatants also induced normal bone marrow cells to become immune suppressive. In contrast, supernatants of only LLC-C3 cells, and not of LLC-C8 cells, stimulated in vitro growth of splenic CFU from LLC-C3-bearing mice; spleen cells from normal mice and from LLC-C8 bearers were unresponsive to supernatants of the LLC variants. These results suggest that CSF produced by either the metastatic LLC-C3 or the nonmetastatic LLC-C8 tumors could concurrently stimulate bone marrow hematopoiesis and the appearance of bone marrow suppressor cells. However, the metastatic LLC-C3 tumor cells, and not the nonmetastatic LLC-C8 cells, could also cause expansion of progenitor cells and hematopoiesis to the spleen and, consequently, induce the appearance in the spleen of hematopoiesis-associated immune suppressor cells.
Reversal of Virus-Induced Alveolar Macrophage Bactericidal Dysfunction by Cyclooxygenase Inhibition In Vitro
Authors: Laegreid W W , Liggitt H D , Silflow R M , Evermann J R , Taylor S M , Leid R W 
Published: January 2018

Abstract
Virus infection of alveolar macrophages (AM) both in vivo and in vitro has been associated with a decreased ability of these cells to kill bacteria, together with enhanced production of metabolites of arachidonic acid. These metabolites, especially PGE2, may be inhibitory to some phagocyte functions. Primary cultures of bovine AM obtained by bronchoalveolar lavage of normal cattle were infected in vitro with parainfluenza-3 (PI3 virus) virus. Killing of Staphylococcus epidermidis by AM was determined on days 1-4 post-infection (p.i.) PI3 virus-infected AM killed significantly fewer bacteria on day 4 p.i. compared to uninfected controls (12.1 ± 1.3% infected vs. 52.7 ± 7.2% controls, P ≤ 0.05). Bacterial killing by virus-infected AM, but not control AM, was significantly enhanced on day 4 p.i. by addition of cyclooxygenase inhibitors 1 hr prior to bactericidal assay (28.0 ± 4.5% indomethacin, 36.0 ± 4.1% mefenamic acid, 38.6 ± 7.3% piroxicam, 37.0 ± 6.4% NDGA, 44.9 ± 7.7% ETYA, P ≤ 0.05). Phagocytosis of opsonized sheep erythrocytes and superoxide generation by virus-infected AM were not significantly increased by cyclooxygenase inhibition. Phagosome-lysosome fusion was severely impaired in virus-infected AM. Pretreatment of virus-infected AM with indomethacin significantly enhanced the percentage of cell expressing fusion activity. This data suggests that in vitro bactericidal dysfunction associated with virus infection of AM is partially the result of enhanced production of prostaglandins or thromboxane by AM and/or an abnormal response to normal levels of endogenously produced cyclooxygenase metabolites. The data further indicate the presence of cyclooxygenase sensitive (phagosome-lysosome fusion) and insensitive (phagocytic) components of virus-induced bactericidal dysfunction in AM.
Formalin-Fixed Macrophages Bind Tumor Targets Similarly to Viable Macrophages
Authors: Chapes Stephen Keith 
Published: January 2018

Abstract
Macrophages (MPs) fixed with 1% formalin in PBS bound targets similarly to viable MPs. Like binding between viable MPs and tumor cells, the process was temperature and calcium dependent. Fixed MPs discriminated targets similarly to viable MPs. Targets not bound by viable MPs were not bound by fixed MPs. The lectin Bandeiraea simplicifolia (ASI-B4) was able to enhance MP binding to tumor cells regardless of whether MPs were fixed or viable. However, it did not appear that ASI-B4–like molecules were involved in the direct recognition of F5b tumor cells by MPs. Target cells could not be fixed in 1% formalin for binding to occur. These data suggest that the receptor on the MP for tumor cell binding is functional in the absence of active physiological processes. In contrast, tumor cell processes that are dependent upon target cell viability are required for binding.
Differential Production of Tumor Necrosis Factor, Macrophage Colony Stimulating Factor, and Interleukin 1 by Human Alveolar Macrophages
Authors: Becker Susanne , Devlin Robert B , Haskill J Stephen 
Published: January 2018

Abstract
Human alveolar macrophages (AMO) have been investigated for their ability to produce three monokines, tumor necrosis factor-alpha (TNF), macrophage colony stimulating factor (CSF-1), and interleukin 1-beta (IL-1). No TNF activity was found in supematants of unstimulated AMO cultured for 20 h, although TNF mRNA was detected in the cells by Northern blot analysis. Stimulation of the cells with lipopolysaccharide (LPS) Induced production and release of high levels of TNF into the culture supernatant. Increased levels of TNF mRNA were detectable at 90 min after LPS stimulation by dot blot analysis, reaching maximum expression between 4 and 8 h and declining thereafter. TNF activity peaked at approximately 8 h in the AMO supematants. After 24 h TNF production had ended. Compared to autologous monocytes the AMO produced 5.7 times more TNF on a per cell basis (activity accumulated in 20 h supematants). Uncultured AMO expressed CSF-1 mRNA which was translated into active protein recovered in supematants upon culture in the absence of stimulus. The addition of LPS to AMO slightly reduced both mRNA levels and amount of factor in the supematants. In contrast to the AMO, monocyte production of CSF-1 was enhanced by LPS. CSF-1 production by AMO continued for at least 48 h of culture. Spontaneous production of low amounts of IL-1 was found in one-third of the AMO samples, while low levels of IL-1 mRNA were present in all tested preparations. LPS stimulation induced increase in IL-1 mRNA within 90 min; mRNA levels peaked between 12 and 20 h and stayed high for at least 42 h. However, while all LPS-stimulated AMO expressed high levels of IL-1 mRNA biologically active IL-1 was again detected only in a fraction of the AMO supematants. These results show that the production of monokines CSF-1, TNF, and IL-1 is differentially regulated by LPS in alveolar macrophages and has different responses as compared to monocytes. The longevity of the messages for each of the factors is possible indicators of the relative contribution of these factors to the response to endotoxin-induced injury and repair processes in the lung.
Thrombin-Treated Endothelium Primes Neutrophil Functions: Inhibition by Platelet-Activating Factor Receptor Antagonists
Authors: Vercellotti G M , Wickham N W R , Gustafson K S , Yin H Q , Hebert Mary , Jacob H S 
Published: January 2018

Abstract
We have shown previously that fluid phase platelet-activating factor (PAF) can enhance or “prime” polymorphonuclear (PMN) responses to subsequent stimulation with agonists such as formyl-methionine-leucine-phenylalanine (FMLP). Since thrombin induces PAF production in endothelial cells, we tested whether this thrombin-provoked endothelial PAF primes responses of marginateci PMNs. Monolayers of human umbilical vein endothelial cells were exposed to either thrombin (0.5-5.0 units/ml) or buffer for up to 5 min and then PMNs were layered on top of the endothelial cells. After a further 5 min incubation, the PMNs were stimulated with a suboptimal concentration of FMLP (10-7 M), and their superoxide production, elastase release, adhesion to endothelium, and capacity to cause endothelial cell lysis and detachment were assessed. Thrombin pretreatment significantly enhanced each of these FMLP-stimulated neutrophil responses. The extent of this enhancement correlated with both the dose and duration of thrombin treatment of endothelial cells and also the duration of PMN incubation with thrombin-exposed endothelium. Evidence that the augmentation was due to endothelial-derived PAF was obtained as follows: (1) thrombin induced [3H]acetate incorporation into endothelial PAF (assayed in lipid extracts); (2) antithrombin III conjointly inhibited this [3H]acetate uptake and prevented the priming effect of thrombin-treated endothelium on PMN responses; and (3) the PAF receptor antagonist BN52021. when preincubated with PMNs, also effectively blocked the enhancement of PMN responses. We conclude that thrombin stimulation of endothelial cells initiates a sequence of events culminating in the production of PAF—a membrane phospholipid capable of priming marginated PMNs. We suggest that this coagulation-fostered endothelial PMN interaction may underlie a paracrine response that may potentiate PMN-mediated endothelial injury during sepsis and other thrombin-generating disorders.
Monokine Secretion in Aging and Protein Malnutrition
Authors: Bradley Suzanne F , Vibhagool Asda , Kunkel Steven L , Kauffman Carol A 
Published: January 2018

Abstract
Aged and protein-malnourished hosta have diminished febrile responses and increased morbidity and mortality from infection that could be due to deficiencies in the production of certain monokines. In this study, the ability of peritoneal macrophages from aged and protein-malnourished rats to produce IL-1 and TNF was explored. Aged rats fed a standard diet produced less IL-1 and TNF, as measured by the thymocyte proliferation and L929 cytotoxicity assays, than young and middle-aged rats. Monokine production was not diminished by protein malnutrition in any age group. No synergistic decline in IL-1 or TNF production was seen with increasing age in malnourished rats. Diminished IL-1 and TNF production may partially explain the severity of infection seen in the elderly patient, but not the malnourished host. The role of other cytokines such as IL-6 and cytokine inhibitors in aging and malnutrition should be explored.
Selective Potentiation of Lymphocyte-Derived Macrophage Chemotactic Factor Release in Complete Freund’s Adjuvant-Treated Guinea Pigs
Authors: Sakata Ken-mei , Muramoto Kazuhiro , Hirashima Mitsuomi , Hayashi Hideo 
Published: January 2018

Abstract
Dinitrophenol (DNP)-ovalbumin(OA)-induced tissue macrophage reaction in sensitized guinea pigs is enhanced by treatment with complete Freund’s adjuvant (CFA). The enhancement of the reaction may be due to the increased production of a T-lymphocyte-derived macrophage chemotactic factor (LDMCF) because treatment of animals with CFA potentiates antigen- and concanavalin A(ConA)-induced release of LDMCF activity from spleen cells of the CFA-treated animals in vitro. This potentiating effect by CFA seems to be ascribed to the release of an adherent-cell-derived soluble factor from the CFA-treated animals. The adherent cell-derived factor, LDMCF-potentiating factor (LDMCF-PF), preferentially potentiates the release of LDMCF activity but not of eosinophil chemotactic activity from antigen- or Con-A-stimulated T lymphocytes. Protein synthesis is required for release of LDMCF-PF. Molecular weight of LDMCF-PF activity is assumed to be about 10,000-20,000. LDMCF-PF activity is sensitive to trypsin, to neuraminidase, and also to alkalinity at pH 11, suggesting that LDMCF-PF is a glycoprotein. The present study provides one explanation for the enhanced macrophage reaction in delayed-type hypersensitivity reactions.
Human Neutrophils Activated by Interferon-γ and Tumour Necrosis Factor-α Kill Entamoeba histolytica Trophozoites In Vitro
Authors: Denis Michel , Chadee Kris 
Published: January 2018

Abstract
The interaction between cytokine-activated human neutrophils and Entamoeba histolytica trophozoites was studied as well as the mechanism(s) involved. Treatment of neutrophils with rlFN-γ alone allowed them to kill 30% of E. histolytica trophozoites; however, rlFN-γ and rTNF-α pretreatments in combination increased neutrophil killing to 70%. In the absence of direct contact between neutrophils and amebae, rlFN-γ-treated neutrophils were shown to kill 70% of amebae, and rlFN-γ- and rTNF-α-treated neutrophils killed 97% of amebae. Neutrophil enhancement of amebicidal activity following cytokine treatments was correlated with Increased neutrophil resistance to amebic contact-dependent killing and was shown to be 73% H2O2 dependent.