bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of bafilomycin A1 on functional capabilities of LPS-activated alveolar macrophages
Authors: Bidani Akhil , Heming Thomas A 
Published: January 2018

Abstract
Resident alveolar macrophages (mφ) possess plasmalemmal vacuolar-type H+-ATPase (V-ATPase) that plays a crucial role in regulation of intracellular pH (pHi). To assess the importance of this V-ATPase to mφ effector functions, resident alveolar mφ from rabbits were activated with E. coli-derived lipopolysaccharide (LPS) and exposed to bafilomycin A1 a specific inhibitor of V-ATPase. Bafilomycin caused a significant cytosolic acidification in both the absence and presence of CO2-HCO3-, and in both unstimulated and activated mφ. Superoxide production and Fc receptor-mediated phagocytosis also were reduced in bafilomycin-treated mφ. Similar effects were elicited by acidifying the cytoplasm in the absence of bafilomycin, by lowering extracellular pH (pHo) from 7.4 to 6.5–6.6. Thus, the effects of bafilomycin on phagocytosis and superoxide production probably were related to cytosolic acidification, secondary to blockade of V-ATPase-mediated H+ extrusion across the plasma membrane. Conversely, bafilomycin significantly increased TNF-α release. This effect cannot be explained by a bafilomycin-induced acidosis because acidic pHo significantly reduced TNF-α release. The results demonstrate that V-ATPase activity is an important determinant of the effector functions of LPS-activated mφ. J. Leukoc. Biol. 57: 275–281; 1995.
Interleukin-9 and its receptor: involvement in mast cell differentiation and T cell oncogenesis
Authors: Renauld Jean-Christophe , Kermouni Abdenaim , Vink Anne , Louahed Jamila , Van Snick Jacques 
Published: January 2018

Abstract
Intcrleukin-9 (IL-9) is a multifunctional cytokine produced by activated TH2 clones in vitro and during TH2-like T cell responses in vivo. The IL-9 receptor is a member of the hemopoietin receptor superfamily and interacts with the γ chain of the IL-2 receptor for signal transduction. Various observations indicate that IL-9 is actively involved in mast cell responses by inducing the proliferation and differentiation of these cells. The role of IL-9 in T cell responses is less clear. Although freshly isolated normal T cells do not respond to IL-9, this cytokine induces the proliferation of murine T cell lymphomas in vitro and in vivo overexpression of IL-9 results in the development of thymic lymphomas. In the human, the existence of an IL-9-mediated autocrine loop has been suggested for some malignancies such as Hodgkin’s disease. Other potential biological targets for IL-9 include B lymphocytes, hematopoietic progenitors, and immature neuronal cell lines. J. Leukoc. Biol. 57: 353–360; 1995.
Immunocytochemical detection of lipid peroxidation in phagosomes of human neutrophils: correlation with expression of flavocytochrome b
Authors: Quinn Mark T , Linner John G , Siemsen Daniel , Dratz Edward A , Buescher E Stephen , Jesaitis Algirdas J 
Published: January 2018

Abstract
Oxidants generated by the NADPH oxidase of activated neutrophils can react with a number of tissue targets to form toxic metabolites such as 4-hydroxynonenal (4-HNE). 4-HNE is a lipid peroxidation product generated by free radical attack on ω-6 polyunsaturated fatty acids and is a marker for membrane lipid peroxidation. In this study, we examined the accumulation of 4-HNE-protein adducts in phagosomes of neutrophils obtained from a male patient with homozygous X-linked, flavocytochrome b-deficient chronic granulomatous disease (CGD), his heterozygous mother, and his normal father. Specific polyclonal antibodies recognizing 4-HNE-protein adducts and gp91-phox (flavocytochrome b large subunit) were prepared and used to immunocytochemically detect these antigens in cryofixed, molecular distillation-dried neutrophils. No 4-HNE-protein adducts were detected in flavocytochrome b-deficient cells from the homozygous patient or from the heterozygous CGD carrier. However, in gp91-phox-positive cells from both the normal and heterozygous CGD carrier, significant 4-HNE-protein adduct labeling was observed, primarily in the phagosomes. When data from single- and doublelabeled cells were combined, the frequency distribution of the labels in phagosomes supported this observation, showing that neutrophils from the heterozygous CGD carrier were 71% 4-HNE-protein adduct-positive and 56% gp91-phox-positive, while cells from the normal father were &gt;97% positive for both 4-HNE-protein adducts and gp91-phox. These results confirmed the nitroblue tetrazolium tests of 100%, 60 ± 2%, and 0% positive for the father’s, mother’s, and son’s cells, respectively, and demonstrated that 4-HNE-protein adduct antibodies are useful and accurate probes of the occurrence of lipid peroxidation in vivo. We conclude that 4-HNE and resulting 4-HNE-protein adducts are generated as a result of NADPH oxidase activity in the phagosomes of human neutrophils and that these lipid peroxidation products may contribute to microbial killing and/or damage of neutrophil phagolysosomal proteins. J. Leukoc. Biol. 57: 415–421; 1995.
Distinct actions of benzene and its metabolites on nitric oxide production by bone marrow leukocytes
Authors: Laskin Jeffrey D , Rao N R , Punjabi Chitra J , Laskin Debra L , Snyder Robert 
Published: January 2018

Abstract
Benzene is a widely used industrial solvent known to cause bone marrow depression. This is associated with increased production of reactive oxygen metabolites and nitric oxide by bone marrow phagocytes, which have been implicated in hematotoxicity. Benzene metabolism to phenolic intermediates appears to be an important factor in bone marrow toxicity. In the present studies, we compared the effects of benzene and several of its metabolites on nitric oxide production by murine bone marrow leukocytes. Bone marrow cells readily produced nitric oxide in response to the inflammatory mediators lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Treatment of mice with benzene (800 mg/kg), or its metabolites hydroquinone (100 mg/kg), 1,2,4-benzenetriol (25 mg/kg), or p-benzoquinone (2 mg/kg), at doses that impair hematopoiesis, sensitized bone marrow leukocytes to produce increased amounts of nitric oxide in response to LPS and IFN-γ. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) augmented bone marrow leukocyte production of nitric oxide induced by inflammatory mediators. Benzene, as well as its metabolites, markedly increased the sensitivity of the cells to both GM-CSF and M-CSF. Cells from hydroquinone- or 1,2,4-benzenetriol–treated mice were significantly more responsive to the inflammatory cytokines and growth factors than cells isolated from benzene- or p-benzoquinone–treated mice, suggesting that the phenolic metabolites of benzene are important biological reactive intermediates. Because nitric oxide suppresses cell growth and can be metabolized to mutagens and carcinogens, the ability of benzene and its metabolites to modulate its production in the bone marrow may be important in their mechanism of action. J. Leukoc. Biol. 57: 422–426; 1995.
Normal human sweat contains interleukin-8
Authors: Jones Anne P , Webb Louise M C , Anderson Arthur O , Leonardo Edward J , Rot Antal 
Published: January 2018

Abstract
Sweating in humans is induced by physical or emotional stress, which raises the possibility that sweating may relate to host defense. We therefore asked whether human eccrine sweat attracts leukocytes and found that it is chemotactic for human neutrophils. This activity was due to several chemoattractants, one of which was interleukin-8 (IL-8). Using immunohistochemistry and in situ hybridization IL-8 and its mRNA have been detected in sweat gland epithelium, indicating that IL-8 is produced in situ. This establishes a pattern of physiological IL-8 secretion by exocrine glands and suggests that, in addition to its role as a major inflammatory mediator, IL-8 also has physiological homeostatic functions. J. Leukoc. Biol. 57: 434–437; 1995.
LPS directly induces oxygen radical production in human monocytes via LPS binding protein and CD14
Authors: Landmann Regine , Scherer Franziska , Schumann Ralf , Link Susanne , Sansano Sebastiano , Zimmerli Werner 
Published: January 2018

Abstract
In human monocytes, superoxide (O2-) generation accompanies phagocytosis and is important for bactericidal activity. It also contributes to tissue damage in inflammation. In the present study we investigated, whether lipopolysaccharide (LPS) directly stimulates monocyte O2- production with kinetics known for other LPS effects and, if so, by which mechanism. LPS caused a time- and dose-dependent O2- release in nonadherent purified monocytes. The effect appeared after 5 min, peaked at 30 min, and disappeared after 2 h. It was maximal with 10 ng/ml lipid A (+148 ± 22%, P &lt; .001), 1 ng/ml LPS Escherichia coli Re (+226 ± 68%, P &lt; .001), and 100 ng/ml LPS Salmonella abortus equi sm (+272 ± 52%, P &lt; .001), respectively. The effect was not observed in buffer, even when using 10 üg/ml LPS. It was dependent on the presence of heat-inactivated AB serum, with a maximal effect at ≥;0.5%. Serum could be replaced by LPS-binding protein (LBP). Polymyxin B and anti-LBP antiserum, respectively, blocked the LPS effect. LPS-induced O2- generation was also completely blocked by anti-CD14 antibodies (3C10 and 63D3) and by their corresponding F(ab’)2 fragments. Monocytes treated with phosphoinositol-specific phospholipase C and monocytes from patients with paroxysmal nocturnal hemoglobinuria, lacking the phosphatidylinositol-anchored CD14, did not respond to LPS stimulation with O2- production. Similarly to LPS, E. coli caused stronger O2- production with heat-inactivated serum than without, and this effect was blocked by anti-CD14 antibodies. In conclusion, these data indicate that LPS directly stimulates O2- production in human monocytes via CD14 depending on LBP. J. Leukoc. Biol. 57: 440–449; 1995.
A mouse monoclonal antibody specific for the Vβ5.3 chain of the human TcR recognizes a subgroup of the mouse TcR Vβ8.2 chains
Authors: Bleux C , Lacoste-Eleaume A S , Cabaniols J P , Carrière D , Poncelet P , Kanellopoulos-Langevin C 
Published: January 2018

Abstract
We have analyzed the reactivity of a mouse monoclonal antibody directed against the human T cell receptor for antigen (TCR). This antibody (111-427) of immunoglobulin G1 isotype has been produced in a BALB/c mouse immunized with HPB-ALL cells and normal human peripheral blood leukocytes. It reacts specifically with the HPB-ALL lymphoma and 2 to 7% of normal human blood lymphocytes, on which it has a mitogenic effect in vitro. We have shown that it immunoprecipitates the αβ TCR of HPB-ALL and that it is specific for the Vβ5.3 chain of the human TCR. In addition, we have observed that this antibody stains a minor fraction of T lymphocytes in different strains of mice. We have screened a number of murine T cell clones or hybridomas and have found that the T cell hybrid line D0.11.10.S4.4 is positive. We have been unable to immunoprecipitate reproducibly the molecule recognized by 111-427 after 125I cell surface labeling and cell lysis in NP-40 or digitonin, probably because of low-affinity binding. On Western blotting, 111-427 revealed one band that has an apparent molecular mass of 89 kDa in nonreducing conditions and disappears after reduction. Similar results were obtained in parallel with the F23.1 and F23.2 antibodies. Thus, this antibody appears to recognize an epitope present primarily on the Vβ8.2 chain of the mouse TCR. We have assayed its capacity to stimulate splenic T lymphocytes in vitro. We have observed that it is capable of triggering, to a minor degree in soluble form and very effectively when coupled to Sepharose beads, the proliferation of spleen T lymphocytes from mice chronically infected with the blood parasite Trypanosoma cruzi. J. Leukoc. Biol. 57: 491–499; 1995.
Phenotypic and functional heterogeneity of the murine alveolar macrophage-derived cell line MH-S
Authors: Sankaran Kumaresan , Herscowitz Herbert B 
Published: January 2018

Abstract
We have previously reported that MH-S, an established murine alveolar macrophage-derived cell line, mediated profound inhibition of in vitro antibody production, as did their freshly isolated alveolar macro phage (AM) counterparts. In this communication we show that like freshly recovered AMs, the MH-S cell line also displays phenotypic and functional heterogeneity. Sorting of parental MH-S cells by flow cytometry based on reactivity with anti-Mac-1 antibody yielded two sub sets. Further analysis by staining with monoclonal anti bodies against well-characterized murine macrophage cell surface markers revealed that both Mac-1+ and Mac-1-subsets expressed the mature murine macrophage antigen (F4/80) and class II major histocompatibility complex molecules, but with different intensity. In contrast, the two subsets stained equivalently with antibody against the FCγII receptor, whereas neither subset stained with anti-CD4 antibody. Examination by light microscopy revealed pleomorphism in the Mac-1+ population with many of the cells appearing spindle shaped and having elongated processes, whereas a majority of the cells in the Mac-1- population were spherical in shape. Functionally, cells from the Mac-1+ population were less inhibitory of in vitro antibody production and produced significantly more nitric oxide in response to stimulation with lipopolysaccharide than were cells in the Mac-1- population. Essentially similar results were obtained using cloned Mac-1+ and Mac-1- MH-S cells. The finding of het erogeneity in an established cell line that displays functions similar to those of freshly recovered AMs suggests that distinct subsets of AMs may be involved in the pathogenesis of disease processes in the lung. J. Leukoc. Biol. 57: 562–568; 1995.
Effects of myristate phorbol ester on V-ATPase activity and Na+-H+ exchange in alveolar macrophages
Authors: Heming Thomas A , Bidani Akhil 
Published: January 2018

Abstract
The roles of protein kinase G (PKC) in regulation of the plasmalemmal vacuolar-type H+-ATPase (V-ATPase) and Na+-H+ exchanger (NHE) of rabbit alveolar macro phages (mφ) were investigated using phorbol 12-myristate 13-acetate (PMA). At an extracellular pH (pHo) of 7.4 (nominal absence of CO2-HCO- 3), PMA caused a dose-dependent increase in the rate of cellular H+ extrusion with little change in intracellular pH (pHi). PMA caused a prolonged cytosolic acidification at pHo &lt; 6.8. PMA-induced changes in pHi were sensitive to bafilomycin A1, but were insensitive to amiloride. Studies of pHi recovery following intracellular acid challenge showed that both V-ATPase and the NHE were up-regulated by PMA. An inactive analog, 4α-phorbol, had no detectable effects on pHi homeostasis. These data indicate that (a) PKC is involved in regulation of V-ATPase and the NHE of resident alveolar mφ and (b) V-ATPase is the predominant mechanism for pHi homeostasis in unstimulated and PMA-activated mφ. J. Leukoc. Biol. 57: 600–608; 1995.
IFN-γ increases cathepsin H mRNA levels in mouse macrophages
Authors: Lafuse William P , Brown David , Castle Lynn , Zwilling Bruce S 
Published: January 2018

Abstract
Expression of major histocompatibility complex (MHC) class II molecules and ability to present anti gen to T lymphocytes is acquired upon activation of the macrophage by intcrfcron-γ (IFN-γ). Little information is available concerning immune regulation of protease gene expression in mouse macrophages. We have isolated a eDNA clone for cathepsin H, a lysosomal cysteine pro teinase from a cDNA subtraction library of mouse macro phage genes induced by IFN-γ, and have characterized its expression. The level of cathepsin H mRNA increased in mouse peritoneal macrophages following addition of IFN-γ. Cathepsin H mRNA levels began to increase 8 h after the addition of IFN-γ and was maximal at 24–48 h. This increase was concordant in time with appearance of MHC class II Eβ mRNA and Ia invariant chain mRNA. The increase in cathepsin H mRNA levels by IFN-γ was dose dependent. Cycloheximide treatment of peritoneal macrophages inhibited the increase in cathepsin H mRNA levels induced by IFN-γ, suggesting that the in crease in cathepsin mRNA levels requires de novo protein synthesis. Lipopolysaccharide and cytokines interleukin-2 (IL-2), IL-4, IL-10, and tumor necrosis factor α were found to have no effect on cathepsin H mRNA levels in mouse peritoneal macrophages. J. Leukoc. Biol. 57: 663–669; 1995.
Contribution of mannose receptor to signal transduction in Fcγ receptor-mediated phagocytosis of mouse peritoneal macrophages induced by liposomes
Authors: Murai Makoto , Aramaki Yukihiko , Tsuchiya Seishi 
Published: January 2018

Abstract
The contribution of mannose receptors on the cell surface of mouse peritoneal macrophages to the pro cess of liposome-induced phagocytosis of immunoglobu lin G-opsonized sheep red blood cells (SRBCs) through Fcγ receptor has been investigated. Fcγ receptor-mediated phagocytosis of opsonized SRBCs was activated by modified α 2-macroglobulin, which was produced in the incubation mixture of α 2-macroglobulin and liposometreated splenic B cells. The phagocytosis was specifically inhibited by the addition of D-mannose, and the inhibition was dependent on the D-mannose concentration. The binding of modified α 2-macroglobulin to macro phages was also reduced by the addition of D-mannose. The activation effect of modified α 2-macroglobulin was not inhibited when in the presence of α 2-macroglobulintrypsin and -methylamine complexes. In the presence of cydoheximide, activated phagocytosis was reduced to the control level. By Scatchard plot analysis of IgG binding studies, the number of Fcγ receptors of a macrophage had been increased to 4.6-fold that of a control macrophage by treatment with modified α 2-macroglobulin. These findings suggest that macrophage mannose receptors are involved in activating the process of FCγ receptor-mcdiatcd phagocytosis of opsonized SRBCs induced by modified a α 2-macro globulin. Lectins may participate in a signal transduction in macrophage activation by lipo somes, J, Lcukoc, Biol. 57: 687–691; 1995.
CD4 T cell development and cytokine polarization: an overview
Authors: Swain Susan L 
Published: January 2018

Abstract
We have studied two key stages of CD4 development that serve as important checkpoints in determining whether a response will occur, how big it will be, and how long it will last. The response of naive CD4 cells is strictly regulated by the requirement for interaction of the potential precursor with an antigen-presenting cell-expressing multiple costimulatory molecules such as B7 family and intercellular adhesion molecule-1. The extent of naive cell proliferation is critically dependent on interleukin-2, whose autocrine production is similarly regulated. We show that effector CD4 cells can either die, expand, and/or generate memory. Antigen stimulation accelerates death or promotes expansion dependent on the presence of cytokines. Interleukin-2 and transforming growth factor-β synergize to block apoptosis and favor extensive effector expansion. J. Leukoc. Biol. 57: 795–798; 1995.
Regulatory effect of aminopeptidase inhibitor (bestatin) on the cervix during induction of ripening by interleukin-8
Authors: El Maradny Emad , Kanayama Naohiro , Halim Abdul , Maehara Kayoko , Sumimoto Kazuhiro , Terao Toshihiko 
Published: January 2018

Abstract
Bestatin is an immunomodulatory peptide that stimulates the humoral and cell-mediated immune system. It also has an inhibitory effect on multiple aminopeptidases. Recently we found that aminopeptidase N inactivates interleukin-8 in vitro. Bestatin successfully suppresses the effect of aminopeptidase N on interleukin-8. During cervical maturation many biochemical changes occur including decrease in collagen concentration and increase in collagenase and elastase activities. Interleukin-8, which has a potent neutrophil chemotactic effect, was found to induce cervical ripening in rabbits. The combination of interleukin-8 with bestatin also induced cervical ripening by providing approximately regular levels of neutrophil numbers, collagenase, and elastase activities. We therefore suggest that this regulatory mechanism also takes place in vivo through the inhibitory effect of bestatin on aminopeptidase N. J. Leukoc. Biol. 57: 832–836; 1995.
Ultraviolet radiation reduces phagocytosis and intracellular killing of mycobacteria and inhibits nitric oxide production by macrophages in mice
Authors: Jeevan Amminikutty , Bucana Corazon D , Dong Zhongyun , Dizon Victor V , Thomas Stephanne L , Lloyd Thomas E , Kripke Margaret L 
Published: January 2018

Abstract
Exposure of mice to a single or multiple low doses of ultraviolet radiation (UVR) decreases the induction of the delayed-type hypersensitivity (DTH) response to Mycobacterium bovis BCG and Mycobacterium lepraemurium (MLM) and impairs the clearance of bacteria from the lymphoid organs. This study is an attempt to address the mechanism by which UV radiation impairs the clearance of bacteria from the lymphoid organs by determining whether alterations in macrophage function such as ingestion and intracellular killing of mycobacteria or production of reactive nitrogen intermediates might be responsible for these effects. BALB/c or C3H/HeN mice were exposed to a single dose of UVB (280–320 nm) radiation ranging from 0.35 to 45 kJ/m2, and at regular intervals after irradiation, the peritoneal and splenic macrophages were collected, cultured, and infected with live BCG or MLM. Phagocytosis was assessed at 6 h by counting the number of acid-fast bacteria per macrophage after Ziehl-Neelsen staining. The rate of intracellular killing was assessed by lysing the macrophages at 6, 12, 24, and 48 h after BCG infection, plating the suspension on 7H11 agar, and counting the number of colony-forming units 21 days later. Similarly, the nitric oxide production, as measured by nitrite, by macrophages obtained from UVB-irradiated and nonirradiated mice in response to BCG was assessed. There was a significant reduction in the uptake of organisms by both peritoneal and splenic macrophages collected from UV-irradiated mice. The intracellular killing of organisms was also significantly reduced, as was the production of nitric oxide by peritoneal macrophages infected with BCG in vitro. These results indicate that UVR affects macrophage functions and are consistent with our hypothesis that impaired clearance of bacteria in vivo results from an alteration in macrophage function. J. Leukoc. Biol. 57: 883–890; 1995.
Influence of serum on zinc, toxic shock syndrome toxin-1, and lipopolysaccharide-induced production of IFN-γ and IL-1β by human mononuclear cells
Authors: Driessen Christoph , Hirv Kaimo , Wellinghausen Nele , Kirchner Holger , Rink Lothar 
Published: January 2018

Abstract
Measurement of cytokine secretion in vitro is usually performed in culture medium supplemented with human serum. We compared the secretion of interferon-γ and interleukin-1β as a parameter for lymphocyte and monocyte activation in RPMI 1640 medium supplemented with fetal calf or autologous serum in serum-free medium and protein-free medium. Four different stimulatory mechanisms were tested: phytohemagglutinin, toxic shock syndrome toxin-1 (TSST-1), lipopolysaccharide (LPS), and zinc ions. We found that the optimal stimulatory zinc concentration depended on the total protein content of the medium, whereas the monokine levels were dependent on the concentration of transport proteins such as transferrin. Monokine induction by LPS or TSST-1 were each influenced by the protein and serum composition in a specific manner. Our results show that the differing mechanisms of cytokine induction are influenced by the medium and serum composition in a diverse but specific manner. Serum- or protein-free medium are especially suitable after superantigen challenge when LPS activity needs to be ruled out or after activation by agents with only a weak stimulatory capacity. J. Leukoc. Biol. 57: 904–908; 1995.