bluuebunny/crossref_metadata_2025_split huggingface dataset:
A method for obtaining and culturing large numbers of purified organ-derived murine endothelial cells
Authors: MacPhee Martin J , Wiltrout Robert H , McCormick Kathryn L , Sayers Thomas J , Pilaro Anne M 
Published: January 2018

Abstract
Fibroblast growth factor 1 (FGF-1)–coated collagen-gelatin sponges were affixed to various tissues to generate vascular beds, in which the vessels originated in the tissue to which the sponges were affixed. Organ-derived endothelium was obtained from vascularized sponges implanted in or on the skin, peritoneal wall, abdominal mesentery, epimysium, spleen, and liver. Collagenase digestion yielded single-cell suspensions that were analyzed by flow cytometry. Approximately 25% of the cells were positive for the endothelial cell (EC) markers MECA-32 and Sca-1 and for uptake of diIAcLDL. Similar results were obtained when sponges were implanted in several different mouse strains, although there was some evidence of heterogeneity in the degree of vascularization and EC recovery. Long-term cultures of high purity were obtained when the ECs were grown on mitomycin C-treated L929 feeder layers, in medium supplemented with cis-hydroxyproline and FGF-1. These cells have been utilized in preliminary studies of T cell-EC binding. Thus we have developed a generalized method for the recovery and culture of organ-derived murine endothelial cells. This technique should greatly improve the feasibility of studies of the interactions between murine endothelial and immune effector cells. J. Leukoc. Biol. 55: 467–475; 1994.
Immunophenotypic and ultrastructural heterogeneity of macrophage differentiation in bone marrow and fetal hematopoiesis of mouse in vitro and in vivo
Authors: Morioka Yuki , Naito Makoto , Sato Tatsuo , Takahashi Kiyoshi 
Published: January 2018

Abstract
The present in vitro study revealed marked differences in immunophenotypic expression and ultrastructure among macrophage colony-stimulating factor (M-CSF)–derived, granulocyte-macrophage colony-stimulating factor (GM-CSF)–derived, and multi-CSF–derived macrophages. M-CSF–derived macrophages were larger and had more markedly differentiated intracellular organelles and more cytoplasmic projections than GM-CSF–or multi-CSF–derived macrophages. By the combined method of ultrastructural peroxidase cytochemistry and immunoelectron microscopy, ER-MP12 was demonstrated mainly on blastic cells; ER-MP20 on promonocytes, monocytes, and immature macrophages; and F4/80 or BM8 on immature and mature macrophages and monocytes. Macrophage heterogeneity was demonstrated to occur at the stage of macrophage precursor cells, and macrophage differentiation was different between bone marrow hematopoiesis and early fetal hematopoiesis. In vivo, F4/80- or BM8-positive (+) macrophages and ER-MP12 (+) cells developed in the yolk sac prior to the appearance of ER-MP20 (+) monocytic cell series. These results imply that CSFs are important factors for the generation of phenotypic heterogeneity of macrophage populations not only in bone marrow but also in fetal hematopoiesis, suggesting that there are different pathways of macrophage differentiation. J. Leukoc. Biol. 55: 642–651; 1994.
P-selectin-dependent leukocyte recruitment and intestinal mucosal injury induced by lactoferrin
Authors: Kurose Iwao , Yamada Tamaki , Wolf Robert , Granger D Neil 
Published: January 2018

Abstract
Plasma concentrations of lactoferrin relevant to an inflammatory response are known to elicit leukocyteendothelial cell adhesion in mesenteric venules. The objectives of this study were (1) to determine whether exogenously administered lactoferrin causes microvascular and mucosal injury in rat intestine and (2) to assess the contribution of adherent leukocytes to a lactoferrinmediated injury process. Mucosal myeloperoxidase (MPO) activity and vascular protein clearance were monitored in the distal intestine of male Sprague-Dawley rats. Macroscopic erosive lesions of the mucosa and increases in mucosal MPO and intestinal vascular protein were observed 2 h following the lactoferrin infusion, results consistent with granulocyte accumulation and microvascular protein leakage. These lactoferrin-induced alterations were significantly attenuated in animals pretreated with a monoclonal antibody (mAb) directed against P-selectin but not by an E-selectin-specific mAb. In another series of experiments, leukocyte adherence/emigration and leakage of fluorescein isothiocyanate (FITC)-labeled albumin were measured in rat mesenteric venules using intravital video microscopy. Lactoferrin elicited increases in both leukocyte adhesion/emigration and albumin extravasation, which were attenuated by mAbs directed against P-selectin but not E-selectin. These observations indicate that (1) the lactoferrin released by activated neutrophils may lead to significant microvascular and mucosal injury or dysfunction and (2) the lactoferrininduced injury is related to P-selectin-mediated adhesion of leukocytes to microvascular endothelium. Our results raise the possibility that neutrophil-derived lactoferrin contributes to the inflammatory response by promoting further granulocyte accumulation and activation and that mAbs to P-selectin may be therapeutically beneficial in inflammatory disorders. J. Leukoc. Biol. 55: 771–777; 1994.
Regulation of polymorphonuclear leukocyte membrane fluidity: effect of cytoskeletal modification
Authors: Wiles Marc E , Dykens James A , Wright Clifford D 
Published: January 2018

Abstract
We previously demonstrated that the f-actin cytoskeleton modulates oxygen radical production associated with polymorphonuclear leukocyte (PMN) oxidative burst activity. Given the close association of the actin and microtubule cytoskeletons with the plasma membrane and the transmembrane location of the PMN NADPH oxidase, it is likely cytoskeletal change may affect PMN membrane responses, such as cellular anisotropy. Changes in PMN membrane fluidity were therefore examined after PMN activation by the chemoattractant N-formyl-1-methionyl-1-leucyl-1-phenylalanine (fMLP) in the presence or absence of phalloidin or cytochalasin B (CB), agents that stabilize and disrupt f-actin, or taxol and vincristine, which stabilize and disrupt microtubules, respectively. Phalloidin and taxol treatment of PMN significantly decreased whereas CB and vincristine significantly increased membrane fluidity. Activation of PMN by fMLP (10-6 M) resulted in a significant increase in membrane fluidity that was attenuated by PMN pretreatment with phalloidin or taxol. CB and vincristine pretreatment of PMN did not alter the fMLP response. These data suggest that stabilization of the f-actin or microtubule cytoskdeton may prevent increases in cellular membrane fluidity associated with PMN activation.—J. Leukoc. Biol. 56: 192–199; 1994.
Biology of the mononuclear phagocyte system of the central nervous system and HIV infection
Authors: Perry V H , Lawson L J , Reid D M 
Published: January 2018

Abstract
Infection of the central nervous system by HIV-1 results in widespread neuropathology and neurological symptoms. The cells infected in the brain belong to the mononuclear phagocyte lineage. We review aspects of the biology of the macrophage populations associated with the central nervous system and consider their distribution, phenotype, and kinetics in relation to HIV pathology. J. Leukoc. Biol. 56: 399–406; 1994.
Interactions between lymphocytes, macrophages, and central nervous system cells
Authors: Couraud Pierre-Olivier 
Published: January 2018

Abstract
Brain has often been considered as an “immunologically privileged organ,” not normally accessible to leukocyte traffic, at least in part because of the presence of the blood-brain barrier, constituted by a specialized microvasculature and surrounding astrocytes, which restricts the exchanges between blood and brain. However, more recent studies have revealed that activated leukocytes can cross into the CNS, at very low levels under normal conditions, in much higher numbers during neuro-pathological disorders like multiple sclerosis or retroviral infection, and, within brain parenchyma, interact with CNS cells. The present review will thus highlight the multidirectional communication network, based on adhesion molecule expression and cytokine production, which appears in such situations between infiltrated leukocytes, brain microvessel endothelial cells, macroglia (including astrocytes and oligodendrocytes), microglial cells and neurons. J. Leukoc. Biol. 56: 407–415; 1994.
Molecular mechanism of interleukin-8 gene expression
Authors: Mukaida Naofumi , Okamoto Shu-ichi , Ishikawa Yuji , Matsushima Kouji 
Published: January 2018

Abstract
A potent leukocyte chemotactic and activating cytokine, interleukin-8 (IL-8), is produced by numerous types of cells in response to inflammatory stimuli. Accumulating evidence indicate that the transcription of IL-8 gene requires the activation of either the combination of NF-xB and AP-1 or that of NF-xB and NF-IL6, depending on the type of cells. Alternatively, the activation of NF-xB is indispensable for IL-8 gene activation in any types of cells examined. On the other hand, an immunosuppressant, FK506, and a glucocorticoid inhibit the gene transcription as well as the production of IL-8. Molecular analyses of IL-8 gene repression by these agents revealed that both affected the activity of the transcription factor(s) bound to the NF-xB site, albeit in different ways, thereby suppressing IL-8 gene transcription. Collectively, IL-8 production seems to be controlled mainly at the activation step of the transcription factor(s) bound to the NF-xB site. J. Leukoc. Biol. 56: 554–558; 1994.
Isolation of antimicrobial peptides from avian heterophils
Authors: Evans Ellen W , Beach Gwen G , Wunderlich John , Harmon Barry G 
Published: January 2018

Abstract
Five bactericidal peptides (chicken heterophil peptides CHP1 and CHP2; turkey heterophil peptides THP1, THP2, and THP3) were purified from avian heterophil granules. All peptides were cationic and rich in cysteine, arginine, and lysine. The complete amino acid sequence, consisting of 39 amino acids, was determined for CHP1. This peptide had a molecular weight of 4481 as determined by mass spectrometry. Partial NH2-terminal amino acid sequences were obtained for the remaining peptides. Both chicken peptides and THP1 shared sequence homology at 22 residues and a cysteine motif which was similar to that of bovine beta-defensins. THP2 and THP3 were homologous to each other but were not homologous to the other three and had a unique cysteine motif. Peptides CHP1, CHP2, and THP1 killed Staphylococcus aureus and Escherichia coli in vitro, whereas THP2 and THP3 killed only S. aureus in vitro. J. Leukoc. Biol. 56: 661–665; 1994.
Kinetics of macrophage subpopulations and expression of monocyte chemoattractant protein-1 (MCP-1) in bleomycin-induced lung injury of rats studied by a novel monoclonal antibody against rat MCP-1
Authors: Sakanashi Yuji , Takeya Motohiro , Yoshimura Teizo , Feng Lili , Morioka Tohru , Takahashi Kiyoshi 
Published: January 2018

Abstract
We investigated the kinetics of macrophage subpopulations and the expression of monocyte chemoattractant protein 1 (MCP-1) in a rat model of bleomycin-induced lung injury. Rat macrophage subpopulations were examined by immunohistochemistry using various anti-rat macrophage monoclonal antibodies (mAbs) and their proliferative capacity by [3H]thymidine (3HTdR) autoradiography. To detect the localization of expressed MCP-1, we generated an mAb against rat MCP-1 for immunohistochemical staining. Expression of MCP-1 messenger RNA (mRNA) was detected by Northern blot hybridization. Shortly after intratracheal instillation of bleomycin, the number of exudate macrophages recognized by mAb TRPM-3 increased in the injured lungs, peaked 3 days later, and decreased thereafter, whereas tissue macrophages identified by mAb ED2 increased slowly and peaked 2 weeks after instillation. Northern blot analysis disclosed that the expression of MCP-1 mRNA in the lung was most prominent 1 day after instillation and declined thereafter, preceding the numerical change of the TRPM-3-positive exudate macrophages. Immunohistochemistry with anti-rat MCP-1 revealed that the main sources of MCP-1 production were alveolar and interstitial macrophages and polymorphonuclear leukocytes. Based on these results, MCP-1 produced by polymorphonuclear leukocytes and by alveolar and interstitial macrophages is thought to induce the infiltration of blood monocytes, and infiltrated exudate macrophages produce MCP-1 to enhance subsequent accumulation of macrophages. In contrast, the expression of MCP-1 did not correlate with the numerical changes of the ED2-positive macrophages. J. Leukoc. Biol. 56: 741–750; 1994.
Enhancement of murine serum amyloid A3 mRNA expression by glucocorticoids and its regulation by cytokines
Authors: Ishida Tetsuya , Matsuura Keiko , Setoguchi Mihoko , Higuchi Yasunori , Yamamoto Shunsuke 
Published: January 2018

Abstract
Macrophages are regulated by hormones, cytokines, and other substances. We examined the effects of glucocorticoids (GC) on serum amyloid A (SAA) mRNA expression using an antisense SAA3 probe, and found that dexamethasone (DEX) and triamcinolone (TC) increased SAA3 mRNA expression by macrophage cell lines in a time- and concentration-dependent manner. Both an RNA polymerase II antagonist, α-amanitin, and a specific GC antagonist, RU38486, inhibited the enhancement of SAA3 mRNA expression by DEX. These results show that GC lead to enhanced SAA3 mRNA transcription. Nuclear run-on experiments supported these results. Enhanced expression of SAA3 mRNA by DEX was accompanied by production of SAA3 protein. Interferon-γ (IFN-γ) alone showed any effect on SAA3 mRNA expression. Enhanced SAA3 expression by DEX was inhibited by treatment with IFN-γ in a dose-dependent manner. Either transforming growth factor (TGF)-β1 or interleukin (IL)-4 alone showed no effect on SAA3 mRNA expression, but suppressed DEX-induced SAA3 expression. The timing of the effects of IFN-γ and TGF-βl on DEX- induced SAA3 expression differed: IFN-γ showed its effect between 30 h before and 18 h after DEX administration, whereas TGF-β1 showed an effect when administered concomitantly with DEX and in the late stages after DEX administration. IL-4 mildly suppressed DEX-induced SAA3 expression when given 12 h before and after DEX administration. J. Leukoc. Biol. 56: 797–806; 1994.
Comparative ultrastructure and immunolabeling of MHC-II antigens of alveolar macrophages obtained from patients with paracoccidioidomycosis and other lung diseases
Authors: Bretañ;a Antonio , Goihman-Yahr Mauricio , Tapia Felix J , Istúriz Guillermo , Viloria Nora , Carrasquero Mercedes , Saavedra Nelly , de Albornoz María C , Pereira José , de Román Ana , de Gómez Maria H 
Published: January 2018

Abstract
Samples of alveolar macrophages (AM) obtained by bronchoalveolar lavage from patients with either paracoccidioidomycosis, silicosis, sarcoidosis, or allergic alveolitis were investigated by electron microscopy and immunocytochemistry to compare cellular ultrastructure and expression of MHC-II antigens in the AM cell surface. All samples of AM obtained from patients with these pathologies showed heterogeneous structural features. Although, this morphological diversity is also present in AM of healthy donors, our observations seem to indicate that in the diseases studied this morphofunctional diversity is associated with additional ultrastructural characteristics inherent to each disease. In paracoccidioidomycosis the proportion of vacuolated macrophages is significantly lower than in other diseases; this might indicate that in paracoccidioidomycosis the proportion of activated AM is smaller. We observed significant differences in the expression of MHC-II antigens. Silicosis, sarcoidosis, and allergic alveolitis do not differ significantly in the quantity of immunolabeled AM or in the distribution of the label. The percentage of AM from paracoccidioidomycosis that exhibit the MHC-II molecule is very low with poor immunolabeling. In this disease the low expression of the MHC-II molecule could be related to a decrease of the antigen presenting function by AM. J. Leukoc. Biol. 57: 101–109; 1995.
Inactivation of interleukin-8 by aminopeptidase N (CD13)
Authors: Kanayama Naohiro , Kajiwara Yayoi , Goto Junko , El Maradny Emad , Maehara Kayoko , Andou Katuaki , Terao Toshihiko 
Published: January 2018

Abstract
Aminopeptidase (APN) was found to degrade interleukin-8 (IL-8) and inactivate its chemotactic activity. The chemotactic activity of IL-8 was decreased by APN or neutrophil plasma membranes dose- and time-dependently. The chemotactic activity was not inactivated in the presence of bestatin or WM15 monoclonal antibody. The expression of IL-8 was measured by flow cytometry. On lipopolysaccharide (LPS) stimulation, IL-8 expression increased for 60 min and then decreased markedly. In contrast, on treatment with LPS and bestatin, the expression of IL-8 increased continuously for at least 120 min. These results suggest that the expression and release of IL-8 from phagocytic cells are regulated by the proteolytic effect of APN on IL-8. J. Leukoc. Biol. 57: 129–134; 1995.
Mycoplasma stimulates the production of oxidative radicals by murine peritoneal macrophages
Authors: Avron Ann , Gallily Ruth 
Published: January 2018

Abstract
Mycoplasmas and mycoplasma membranes have been shown to induce the production of inflammatory cytokines, including tumor necrosis factor α and interleukin-6, as well as nitric oxide, by mouse macrophages and rat brain astrocytes. Luminol-enhanced chemiluminescence was used as a sensitive method to show that Mycoplasma capricolum membranes induce mouse peritoneal macrophages to produce reactive oxygen radicals. Coincubation of the mycoplasma with a secondary stimulus, namely macrophage-activating factor or interferon-γ, increased the chemiluminescence. The augmentation was abolished by the nitric oxide synthase inhibitor NG-methyl-l-arginine, indicating the involvement of nitric oxide. The coproduction of superoxide and nitric oxide by the same cell allows the formation of the powerful oxidant peroxynitrite, which could be responsible for the increased chemiluminescence. Induction of oxidizing radicals by mycoplasmas may contribute to the clinical pathology seen in mycoplasma infections. J. Leukoc. Biol. 57: 264–268; 1995.
Activation of multiple protein kinases induced by cross-linking of FcγRII in human neutrophils
Authors: Liang Li , Huang Chi-Kuang 
Published: January 2018

Abstract
Several neutrophil protein kinases that undergo changes in activity during FCγRII activation have been investigated. These kinases include calcium/calmodulin-dependent protein kinase II (CAMPKII), mitogen-activated protein kinase (MAPK), and histone H4 protein kinase (PKH4). They are rapidly and transiently activated in a dose-dependent manner by the cross-linking of FCγRII. The activation of CAMPKII but neither PKH4 nor MAPK was inhibited by treating the cells with either a tyrosine kinase inhibitor, genistein, or an intracellular calcium chelator, BAPTA/AM. The superoxide production induced by cross-linking FCγRII can be inhibited partially by various protein kinase inhibitors: 33% by protein kinase C inhibitor calphostin C, 30% by CAMPKII inhibitor KN-62, and 62% by tyrosine kinase inhibitor genistein. These results indicate that cross-linking of FCγRII induces multiple signaling pathways that lead to the activation of various protein kinases. The activation of these kinases may be involved directly or indirectly in the regulation of superoxide production. J. Leukoc. Biol. 57: 326–331; 1995.
Evidence for LFA-1/ICAM-1 dependent stimulation of protein tyrosine phosphorylation in human B lymphoid cell lines during homotypic adhesion
Authors: Wang Shirley C-T , Kanner Steven B , Ledbetter Jeffrey A , Gupta Shalini , Kumar Gita , Nel André E 
Published: January 2018

Abstract
JK32.1 and SKW6.4 are Epstein-Barr virus (EBV)-positive human B cell lines that undergo spontaneous, lymphocyte function-associated antigen 1 (LFA-1) dependent homotypic adhesion in culture. This process is associated with induction of tyrosine phosphoproteins of molecular mass 90, 106, and 120 kDa and could be reproduced when these cells were centrifugationally aggregated. Antibodies to the β 2 (CD18) chain of LFA-1 interfered with induction of p120, p106, and p90 during cellular aggregation. Response induction was abrogated when cells were incubated with protein tyrosine kinase (PTK) inhibitors (erbstatin, genistein, and geldanomycin) or cytochalasin B prior to aggregation. An in vitro kinase assay did not reveal activation of focal adhesion kinase. Although the role of LFA-1-dependent tyrosine phosphorylation in B cells is uncertain, patients with the leukocyte adhesion defect (LAD) exhibit humoral abnormalities. Moreover, aggregation did not induce specific tyrosine phosphoproteins in an EBV-transformed B cell line from a LAD patient. These results suggest that an LFA-1-dependent PTK pathway may play an important role in human B cell function. J. Leukoc. Biol. 57: 343–351; 1995.
Effects of oxidized LDL on mononuclear phagocytes: inhibition of induction of four inflammatory cytokine gene RNAs, release of NO, and cytolysis of tumor cells
Authors: Thai S-F , Lewis J G , Williams R B , Johnson S P , Adams D O 
Published: January 2018

Abstract
A critical step in development of atherosclerosis is the interaction of oxidized low-density lipoprotein (LDL) with mononuclear phagocytes. Oxidized LDL, as well as acetyl-LDL, is rapidly taken up into macrophages via a family of scavenger receptors. We report that macrophages treated with oxidized LDL have markedly lower levels of mRNA specific for the genes MCP-1, TNF-α, IL-1α, and KC as measured by Northern blot analyses of lipopolysaccharide (LPS)-stimulated macrophages. By contrast, acetyl-LDL does not inhibit these genes at the doses at which oxidized-LDL is effective. Similar effects are observed whether the LDL is oxidized in the presence of Cu2+ or of Fe2+. Such inhibition also occurs when maleylated bovine serum albumin (BSA), which also clears by one or more scavenger receptors on macrophages, is used as the stimulant. Fe2+ or Cu2+ oxidized LDL inhibits release of nitric oxide when triggered by LPS and direct cytolysis of tumor cells when triggered by maleylated BSA or LPS. Taken together, the data presented indicate that oxidized LDL inhibits induction of several important gene RNAs as well as functional markers that characterize the development of inflammatory and fully activated macrophages. J. Leukoc. Biol. 57: 427–433; 1995.
Na+-H+ exchange in resident alveolar macrophages: activation by osmotic cell shrinkage
Authors: Heming Thomas A , Bidani Akhil 
Published: January 2018

Abstract
Intracellular pH (pH;) homeostasis in resident alveolar macrophages (mφ) under nominally CO2-free conditions is mediated primarily by the activity of plasmalemmal H+-ATPase, The mφ also possess an Na+-H+ exchanger (NHE) but this mechanism has no de tectable role in pHi regulation in the physiologic range. To further explore the physiological significance of the NHE in this cell type, resident alveolar mφ from rabbits were subjected to a hyperosmotic challenge (620 mOsm/kg) in the nominal absence of C02-HCO3-. Os motic cell shrinkage was accompanied by an amiloridesensitive increase in baseline pHi The NHE-mediated rate of pH; recovery from intracellular acid loads also in creased under hyperosmotic conditions. Cell shrinkage caused an alkaline shift in the pHi set point of the NHE without altering the exchanger’s affinity for extracellular Na+. The results indicate that Na+-H+ exchange in resi dent alveolar mφ is activated by osmotic cell shrinkage and imply that the NHE may be involved in volume regulatory responses of the cell. J. Leukoc. Biol. 57: 609–616; 1995.