bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional characterization of peripheral circulating and liver recruited neutrophils in endotoxic rats
Authors: Spitzer J A , Zhang P , Mayer A M S 
Published: January 2018

Abstract
Neutrophil accumulation in tissues is a hallmark of inflammation and is associated with a variety of pathological conditions. In bacterial infection neutrophils are selectively attracted in large numbers to phagocytose and kill invading microorganisms. However, activated neutrophils can also cause injury to tissues. To investigate functional alterations in liver recruited neutrophils (PMNs), we studied the functional characteristics of circulating blood and liver sequestered PMNs in terms of host defense mechanisms, such as nitric oxide (NO) and superoxide (SO) generation, β 2 integrin expression, phagocytosis, and eicosanoid profile. Cells were isolated from rats infused with a nonlethal dose (320 μg/kg) of E. coli endotoxin (ET) or pyrogen-free saline for 90 min. Liver PMNs produced significantly more NO both in the absence and in the presence of an in vitro endotoxin challenge than did blood PMNs. No significant difference was observed in phorbol myristate acetate-stimulated SO generation. Endotoxin infusion significantly up-regulated the expression of CD11b/c in circulating and even more so in liver PMNs. Phagocytosis was significantly enhanced by in vivo ET treatment in blood PMNs, and liver PMNs showed even greater phagocytic activity than blood PMNs or Kupffer cells. The percent distribution of prostaglandins D2 and E2 of total 14C-eicosanoids was significantly higher and that of thromboxane B2 and 5-, 12-, and 15-HETEs was significantly lower in liver than in blood PMNs. Our study demonstrates several functional differences between liver-recruited and circulating PMNs in an acute endotoxic model. The implications of altered neutrophil function may extend to mechanisms of host defense and hepatotoxicity associated with sepsis and endotoxemia. J. Leukoc. Biol. 56: 166–173; 1994.
HIV infection of placental macrophages: their potential role in vertical transmission
Authors: Kesson Alison M , Fear Warwick R , Williams Lindy , Chang Joon , King Nicholas J C 
Published: January 2018

Abstract
Placental macrophages were isolated and cultured in vitro to investigate their susceptibility to HIV infection and possible role in vertical transmission of HIV. After 10 days of in vitro culture the cells were positive for nonspecific esterase and acid phosphatase and negative for myeloperoxidase and placental alkaline phosphatase. They expressed cell surface HLA-ABC, HLA-DR, CD45, as well as CD68 intracellularly, as detected by flow cytometry, confirming their macrophage lineage. Approximately 80% of cells expressed surface CD14. CD4 antigen was expressed at very low levels and was confirmed by antibody blocking experiments. Infection of placental macrophage cultures with HIV resulted in a transient peak of viral replication 3 to 7 days after infection, but no later rise in HIV was detected with culture of up to 60 days. HIV replication was not up-regulated by coculture with phytohemagglutinin-stimulated lymphocytes or by treating infected cultures with tumor necrosis factor α or granulocyte-macrophage colony-stimulating factor. J. Leukoc. Biol. 56: 241–246; 1994.
Accumulation of unintegrated circular viral DNA in monocytes and growth-arrested T cells following infection with HIV-1
Authors: Sonza Secondo , Kiernan Rosemary E , Maerz Anne L , Deacon Nicholas J , McPhee Dale A , Crowe Suzanne M 
Published: January 2018

Abstract
Cytocidal retrovirus infection is characterized by rapid accumulation of unintegrated viral DNA forms. These are thought to be generated by multiple rounds of reinfection and have been suggested to play a central role in cytopathogenesis. Here we have reviewed the work done in this area with HIV-1, mostly using acutely and chronically infected T cell and monocytic cell lines and in some cases T cells blocked at S phase of the cell cycle by aphidicolin treatment. To these studies, we have compared our findings with HIV-1 infected primary peripheral blood monocyte-derived macrophages and untreated and growth-arrested MT-2 cells, two biologically disparate cell populations. Using 1- and 2-long terminal repeat (LTR) circular forms as indicators of unintegrated viral DNA, we found similar rapid accumulation in both untreated and growth-arrested MT-2 cells. In contrast, we found much lower levels in monocyte/macrophages. Our findings suggest that accumulation of unintegrated viral DNA does not require virus production and reinfection in growth-arrested T cells. The significantly lower levels found in monocyte/macrophages may reflect superinfection resistance, allowing the maintenance of a persistent infection. J. Leukoc. Biol. 56: 289–293; 1994.
The high-output nitric oxide pathway: role and regulation
Authors: Xie Qiao-wen , Nathan Carl 
Published: January 2018

Abstract
Nitric oxide synthase (NOS) catalyzes the production of nitric oxide (NO), a short-lived radical gas with physiological or pathophysiological roles in nearly every organ system. The inducible NO synthase (iNOS) is a high-output isoform compared to the two constitutive NOSs. The iNOS from murine macrophages tightly binds calmodulin as a subunit, and its activity is not dependent on exogenous calmodulin or elevated calcium. This iNOS is induced at the transcriptional level by bacterial lipopolysaccharide (LPS) and interferon-γ. The promoter region of the murine iNOS gene contains at least 24 oligonucleotide motifs corresponding to elements involved in the binding of transcription factors in the promoters of other cytokine-inducible genes. Nuclear factor NF-xB/c-rel, interacting with cycloheximide-sensitive protein(s) and binding to the NF-xBd site in the iNOS promoter, controls the induction of iNOS by LPS. However, iNOS is also regulated posttranscriptionally. Complex regulation of iNOS at multiple levels may reflect the dual role of iNOS in host defense and autotoxicity. J. Leukoc. Biol. 56: 576–582; 1994.
Retention of phagocytic functions in cryopreserved human monocytes
Authors: Hansen John-Bjarne , Halvorsen Dag Seeger , Haldorsen Bjørg Christina , Olsen Randi , Sjursen Haakon , Kierulf Peter 
Published: January 2018

Abstract
Phagocytosis and respiratory burst activity were measured by flow cytometry in fresh and cryopreserved human monocytes, after ingestion of Escherichia coli and Staphylococcus aureus. Mononuclear leukocytes, isolated from 15 healthy donors, were divided into two portions, of which one was examined immediately and the other was cryopreserved for 3 weeks. Morphological characteristics and expression of receptors involved in phagocytosis were similar in fresh and cryopreserved monocytes. Furthermore, both internalization of bacteria and respiratory burst activity remained unchanged after cryopreservation. Transmission electron microscopy confirmed actual internalization of bacteria and not merely bacterial attachment to monocytes. Monocytes were demonstrated to retain integral cellular functions during cryopreservation. This may imply that the method has potential for use in basal and clinical trials. J. Leukoc. Biol. 57: 235–241; 1995.
Enhancement in accessibility to macrophages by modification of mucin-type carbohydrate chains on a tumor cell line: role of a C-type lectin of macrophages
Authors: Sakamaki Toshiyuki , Imai Yasuyuki , Irimura Tatsuro 
Published: January 2018

Abstract
We investigated the role of mucin-type (O-linked) carbohydrate chains of tumor target cells in the recognition by macrophages through a Gal/GalNAc-specific calcium-dependent lectin. Binding of a soluble form of this lectin to P815 mastocytoma cells was increased by treatment with benzyl-GalNAc, which presumably inhibited the extension of mucin-type carbohydrate chains. The levels of cell surface expression of GalNAc residues were elevated after benzyl-GalNAc treatment, as revealed by the binding of Vicia villosa agglutinin B4 and Dolichos biflorus agglutinin. Adhesion of treated P815 cells to this lectin immobilized on plastic surfaces also increased. Furthermore, the binding of P815 cells to macrophage-like RAW 264.7 cells and to peritoneal macrophages also increased after the same treatment. We concluded that elevated levels of cell surface terminal GalNAc in mucin-type carbohydrate chains increased accessibility of P815 cells to macrophages through Gal/GalNAc-specific calcium-dependent lectins. J. Leukoc. Biol. 57: 407–414; 1995.
Blood, sweat, and chemotactic cytokines
Authors: Murphy Philip M 
Published: January 2018

Abstract
Cytokine actions can be physiological, pharmacological, or toxic, depending on the concentration that is available and the cell type and host organism studied. Because they operate in vivo in complex networks, the salutary functions of any one cytokine can sometimes be difficult to pin down. Such has been the case for interleukin-8 (IL-8) and related members of the family of chemotactic cytokines or chemokines that are best known for their powerful effects on blood leukocytes [1]. Instead, considerable evidence from animal studies has incriminated IL-8 as a major mediator of acute, neutrophil-dependent inflammatory pathology [2]. Other chemokines have also been implicated in inflammatory injury, although the demonstration of guilt is thus far by association.
Differential regulation of fyn-associated protein tyrosine kinase activity by macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF)
Authors: Li Yan , Chen Ben 
Published: January 2018

Abstract
The proliferation and differentiation of macrophages are regulated by, among others, GM-CSF and M-CSF. Treatment of bone marrow nonadherent (NA) cells with M-CSF induced a greater percentage of NA cells into adherent cells, recognized as monocyte/macrophages, than did GM-CSF. The effect of GM-CSF and M-CSF on the activation of fyn kinase, a 59-kDa src family-related protein tyrosine kinase (PTK), was studied. Control cultures of bone marrow NA cells expressed only minimal levels of fyn kinase activity. Treatment of bone marrow NA cells with M-CSF, but not GM-CSF, for 12 to 24 h greatly enhanced the levels of fyn kinase activity. The effect of M-CSF on the activation of fyn kinase was further investigated using bipotential adherent bone marrow-derived macrophages (BMDMs) that coexpress receptors for both GM-CSF and M-CSF. BMDMs can be induced by either growth factor to undergo extensive proliferation in vitro. Compared to bone marrow NA cells, BMDMs displayed higher levels of basal fyn kinase activity, which were similarly elevated by M-CSF but not GM-CSF treatment. The role of fyn kinase in regulating cell adhesion was investigated by growing BMDMs in both tissue culture and Teflon flasks. The growth of BMDMs was anchorage independent; the majority of them continued to proliferate as cell suspension in Teflon flasks. Whereas the levels of fyn kinase activity in adherent BMDMs grown in tissue culture flasks increased steadily, those in BMDMs grown in Teflon flasks diminished. To study the role of fyn kinase in growth regulation, BMDMs were treated with c-fyn sense and antisense s-oligos. In the presence of c-fyn antisense s-oligos, the proliferative response of BMDMs to M-CSF but not GM-CSF was inhibited. In contrast, the proliferation of BMDM in response to either GM-CSF or M-CSF was not influenced by c-fyn sense s-oligos. Collectively, our data suggest that the activation of fyn kinase is closely associated with the acquisition of adherent capacity in maturing macrophages. J. Leukoc. Biol. 57: 484–490; 1995.
TNF-α stimulates increased plasma membrane guanine nucleotide binding protein activity in polymorphonuclear leukocytes
Authors: Klein Jon B , Scherzer Janice A , Harding George , Jacobs Alfred A , McLeish Kenneth R 
Published: January 2018

Abstract
TNF-α enhances the response of polymorphonuclear leukocytes (PMN) to chemoattractants: however, the mechanism by which this occurs is unclear. We addressed the hypothesis that TNF-α enhances the PMN response to chemoattractants by increasing chemoattractant receptor transmembrane signaling, using fMLP as the model chemoattractant. fMLP-stimulated guanine nucleotide binding (G) protein activation was significantly increased in plasma membranes isolated from PMNs exposed to TNF-α 100 U/ml for 10 minutes (TNF-M), compared to membranes from control cells (CM). Formyl peptide receptor number and affinity were not significantly different in CM and TNF-M. Gi and G3 content were increased in TNF-M as measured by pertussis toxin and cholera toxin (CT) catalyzed ADP-ribosylation, respectively. The increased Gi was coupled to the formyl peptide receptor as shown by receptor-specific CT labeling of Gi. Immunoblot analysis showed that both Gαi2 and Gα3 were increased in TNF-M. The functional activity of the increased G protein content was demonstrated by increased NaF-stimulated phospholipase D activity in TNF-α-treated PMNs. We conclude that TNF-α rapidly stimulates increased PMN plasma membrane expression of G proteins that couple formyl peptide receptors to effector enzymes. Regulation of G protein expression may be a significant mechanism by which TNF regulates PMN function. J. Leukoc. Biol. 57: 500–506; 1995.
CD11/CD18-independent transendothelial migration of human polymorphonuclear leukocytes and monocytes: involvement of distinct and unique mechanisms
Authors: Issekutz Andrew C , Chuluyan H Eduardo , Lopes Nancy 
Published: January 2018

Abstract
Monocytes and polymorphonuclear leukocytes (PMNLs) migrate across cytokine (interleukin-1, tumor necrosis factor) activated endothelium or unstimulatcd endothelium in response to chemotactic factors in vitro and in vivo utilizing the CD11/CD18 (i.e., β 2 integrin) adhesion molecule complex. However, in vivo studies have suggested that under some conditions and/or in certain tissues, leukocyte migration can also proceed via CD11/CD18-independent mechanisms. Here we com pared adhesion mechanisms involved in the migration of 51Cr-Iabeled blood monocytcs and PMNLs across human umbilical vein endothelium (HUVE) monolayers. We ob served that monocyte transendothelial migration was not inhibited by monoclonal antibody (mAb) to CD18, when the HUVE was activated with IL-1 and the chemotactic factor C5a induced the migration. This CD18-independent monocyte migration was blocked by treatment of the monocyte with mAb to β 1, orα 4 integrin, suggesting that very late activation antigen 4 (VLA-4) on the monocyte served as the alternative migration mechanism. In con trast to monocytes, mAb to CD18 inhibited PMNL migration to C5a across IL-l-aetivated HUVE, but only by 66%, significantly less than with C5a alone (84%) or IL-l-aetivated HUVE alone (95%). The migration of anti-CD18 mAb-treated PMNLs was not inhibited by function-blocking mAbs to sialyl Lewis*, L’Selectin, β 1 or of4 integrin, the β 3-related leukocyte response integrin, IL-8, or platelet-activating factor (PAF) antagonists, alone or in combination. Antibody-blocking studies of the ligands on HUVE indicated that E-selectin may be partially involved in this CD18-independent PMNL migration but that ICAM-1, VCAM-1, PECAM-1, and P-sclectin are not involved. Of several chemotactic factors tested, C5a and C5adesArg in activated plasma were the most active in inducing CD18-independent migration of PMNLs across IL-l-aetivated HUVE. These results demonstrate that (1) monocytes can utilize VLA-4 for op timal transendothelial migration and (2) PMNLs may have a novel CDl8-independent migration mechanism that is activated by C5a in conjunction with one or more ligands on cytokine-activated endothelium. This may in volve, in part, E-selectin interacting with a yet to be identified counterreceptor on PMNLs. J. Lcukoc. Biol. 57: 553–561; 1995.
Selective responses (actin polymerization, shape changes, locomotion, pinocytosis) to the PKC inhibitor Ro 31-8220 suggest that PKC discriminately regulates functions of human blood lymphocytes
Authors: Trachsel S , Keller H U 
Published: January 2018

Abstract
The results suggest that protein kinase C (PKC) plays a pivotal role in the control of F-actin levels, locomotion, pinocytosis, and cell shape in lymphocytes. The PKC inhibitor Ro 31-8220 elicits a high proportion of polarized (ED50 = 1,5 10-6 M) and locomoting cells and reduces the relative amount of F-actin (by 29% at 10-5 M) in initially resting cells. Phorbol myristate ace tate (PMA) counterbalances the polarizing effect of Ro 31-8220. This indicates that the spherical shape and the F-actin content of resting cells are maintained by con stitutive PKC activity. PMA-induced increases in fluid pinocytosis, F-actin content, and formation of nonpolar cells with surface protrusion are suppressed by Ro 31-8220 (IC50 = 2–4 10-7 M). Spherical cells and, at higher concentrations (ED50 = 13 10-6 M), polarized cells are formed instead. As a result, lymphocyte function switches from fluid pinocytosis to cell polarity and locomotion. The data indicate that PKC is instrumental in selectively switching lymphocyte function between resting state, locomotor activity, and fluid pinocytosis. Ro 31-8220 is extremely potent in stimulating lymphocyte polarity and locomotion (B and T cells). It acts faster and/or produces a higher proportion of polarized lymphocytes than other available agonists. It may thus be used as a tool in further experiments requiring locomoting lymphocytes.J. Leukoc. Biol. 57: 587–591; 1995.
Role of C-X-C chemokines as regulators of angiogenesis in lung cancer
Authors: Strieter Robert M , Polverini Peter J , Arenberg Douglas A , Walz Alfred , Opdenakker Ghislain , Van Damme Jo , Kunkel Steven L 
Published: January 2018

Abstract
Lung cancer is the leading cause of malignancy-related mortality in the U.S. and is predicted to increase over the remainder of this decade. Despite attempts to advance early diagnosis and use combination therapies, the clinical response of this cancer yields an overall 5-year survival rate of less than 15%. Clearly, new strategies for therapy are indicated. Although carcinogenesis is complex, tumor growth beyond 1–2 mm3 is dependent on angiogenesis. One of the potential mechanisms that allows for tumorigenesis is dysregulation of the balance of angiogenic and angiostatic factors that favors net neovascularization within the primary tumor. Numerous studies have investigated the role of a variety of molecules in the regulation of angiogenesis. Recently, interleukin-8 (IL-8), a member of the C-X-C chemokine family, has been found to be an angiogenic factor. In contrast, platelet factor 4 (PF4), another C-X-C chemokine, has been shown to have angiostatic properties. It is interesting that the major structural difference between IL-8 and PF4 is the presence of the NH2-terminal ELR (Glu-Leu-Arg) motif that precedes the first cysteine amino acid residue of IL-8 and is important in ligand/receptor interactions. We hypothesize that angiogenesis associated with tumorigenesis is dependent on members of the C-X-C chemokine family acting as either angiogenic or angiostatic factors. This paradigm predicts that the biological balance in the expression of these C-X-C chemokines dictates whether the neoplasm grows and develops metastatic potential or regresses. In this review we discuss our recent laboratory findings that support this contention and suggest that further elucidation of the biology of C-X-C chemokines in the context of neovascularization of nonsmall cell lung cancer will permit novel targeted therapy aimed specifically at attenuating tumor growth and metastasis. J. Leukoc. Biol. 57: 752–762; 1995.
Interleukin-3, granulocyte-macrophage colony-stimulating factor, and interleukin-5 transduce signals through two forms of STAT5
Authors: Mui Alice L-F , Wakao Hiroshi , Harada Nobuyuki , O’Farrell Anne-Marie , Miyajima Atsushi 
Published: January 2018

Abstract
Recently, JAK2 kinase was found to be one of the tyrosine kinases activated by interleukin-3 (IL-3) in target cells. JAK2 belongs to a family of kinases that act upstream of transcription factors called STATs. STATs exist in the cytoplasm as latent, transcriptionally inactive forms until, in response to extracellular signals, they become phosphorylated on tyrosine residues, translocate to the nucleus, and bind to specific DNA elements. Because IL-3 activates JAK2, we searched for the STAT(s) that might transduce IL-3 signals. Several lines of evidence suggest that IL-3 uses the murine homologue of STAT5, a factor originally purified from sheep. Unexpectedly, during isolation of the murine homologue, we found two highly related molecules that we have designated STAT5A and STAT5B. J. Leukoc. Biol. 57: 799–803; 1995.
Recombinant human IL-7 administration in mice affects colony-forming units-spleen and lymphoid precursor cell localization and accelerates engraftment of bone marrow transplants
Authors: Boerman Otto C , Gregorio Theresa A , Grzegorzewski Krzysztof J , Faltynek Connie R , Kenny James J , Wiltrout Robert H , Komschlies Kristin L 
Published: January 2018

Abstract
Murine reconstitution assays were used to investigate the effects of recombinant human interleukin-7 (rhIL-7) on myeloid and lymphoid precursors and on bone marrow engraftment. Reconstitution with bone marrow from rhIL-7-treated mice results in a 3.4-fold decrease in total colony-forming unit-spleen (CFU-S) activity (day 9) and an 18.1- and 11.9-fold decrease in its ability to generate thymocytes and splenic B lineage cells, respectively. In contrast, after reconstitution with splenocytes from rhIL-7-treated mice, CFU-S activity increased 23.6-fold (day 9) and the thymocyte and splenic B lineage cell regenerative capacity increased by 4.0- and 3.2-fold, respectively. In addition, CD43low+, B220low+ cells that contain pre-pro-B cells and pro-B cells were expanded two- to threefold and Igμ-, B220+, CD2- and Igμ-, B220+, CD2+ B lineage cells were expanded approximately 10-fold and 10- to 45-fold (depending on the tissue examined), respectively, after rhIL-7 treatment Administration of rhIL-7 to irradiated mice transplanted with bone marrow resulted in accelerated T cell and B cell reconstitution by up to 2–4 weeks. Thus, rhIL-7 administration affects the distribution of myeloid and lymphoid precursors. Moreover, rhIL-7 administration accelerates murine bone marrow cell engraftment and therefore may be useful in reducing the engraftment time in bone marrow transplant patients. J. Leukoc. Biol. 58: 151–158; 1995.
Enhanced expression of novel CD57+CD8+ LAK cells from cats infected with feline immunodeficiency virus
Authors: Zhao Y , Gebhard D , English R , Sellon R , Tompkins M , Tompkins W 
Published: January 2018

Abstract
As a model for lymphokine-activated killer (LAK) function in HIV infection, we studied LAK cells in cats infected with feline immunodeficiency virus (FIV), which causes an acquired immunodeficiency syndrome. Peripheral blood mononuclear cells cultured in concanavalin A and interleukin-2 developed LAK cytotoxicity against chronically FIV-infected CrFK cells and acutely infected CD4+ lymphocytes but not uninfected cells. LAK cells from FIV+ cats were more cytotoxic than LAK cells from uninfected cats. Enhanced FIV+ LAK cytotoxicity against feline leukemia virus–infected cells (FL74) suggested that the cytotoxicity was not antigen specific. Two-color fluorescence-activated cell sorter analysis and antibody depletion studies demonstrated that the majority of LAK cells and their progenitors were positive for both CD8 and CD57. The in vitro induction of dual positive CD8+CD57+ LAK cells was enhanced in FIV+ cats, as reported for HIV+ patients. These CD8+CD57+ LAK cells may play a role in maintaining the long asymptomatic stage of infection in FIV+ cats.