bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thromboxane A2 receptors in equine monocytes: identification of a new subclass of TXA2 receptors
Authors: Simmons T Robin , Cook James A , Moore James N , Halushka Perry V 
Published: January 2018

Abstract
Thromboxane (TX) A2 has been implicated as an important pathophysiologic mediator of a variety of cardiovascular diseases. Monocytes synthesize TXA2 and it modulates their function. This study sought to characterize monocyte TXA2 receptors. Radioligand binding studies were performed on membranes prepared from equine peripheral blood monocytes using [125I]BOP, a TXA2 receptor agonist. [125I]BOP bound to a single class of binding sites (Kd - 1.0 ± 0.3 nM and Bmax = 389 ± 191 fmol/mg protein; n = 5). Several TXA2 receptor agonists and antagonists competed for binding with [125I]BOP. I- BOP produced a concentration-dependent inhibition of endotoxin-induced tumor necrosis factor (TNF) activity (IC50 = 9.6 ± 2.5 nM; n = 5). In contrast to its effects in platelets and vascular smooth muscle, I-BOP significantly increased cAMP formation in monocytes (EC50 = 22 ± 3.6 nM; n = 4). The TXA2 receptor antagonists SQ29548 (5.6 nM) and L657925 (0.13 μM) significantly blocked I-BOP- stimulated cAMP formation but did not block 250 nM prostaglandin E2-stimulated cAMP formation. These data support the presence of a TXA2 receptor in equine peripheral blood monocytes. Activation of this receptor results in suppression of endotoxin-induced TNF formation and stimulation of cAMP production. Increased cAMP production after receptor activation suggests that this receptor may represent a unique subclass of TXA2 receptors. J. Leukoc. Biol. 53: 173–178; 1993.
Hematopoietic recovery in repeatedly irradiated mice can be enhanced by a repeatedly administered combination of diclofenac and glucan
Authors: Hofer M , Pospíšil M , Viklická š , Vacek A , Pipalovà I , Bartoničková A 
Published: January 2018

Abstract
A combination of diclofenac and glucan administered repeatedly in a protective regimen in the course of repeated gamma irradiation of mice (6 × 2 Gy during 3 weeks) enhanced granulopoiesis and other indices of hematopoietic recovery investigated from 3 to 7 days after the last radiation exposure. Repeated administration of diclofenac or glucan alone or treatment of the mice with the didofenac-glucan combination given once before the first or the last radiation exposure did not induce such effects. The protective effect of the repeatedly administered combination of the drugs was realized despite the fact that the response of the serum colony-stimulating activity to the repeated combined drug administration was decreased at the end of the treatment regimen compared to that of mice given this drug combination only once. The combined treatment is supposed to act via increased proliferation of the hematopoietic stem or progenitor cells. Additivity or even synergism of the hematostimulatory action of glucan and of the strengthening of positive control of cell proliferation achieved by removing negatively acting prostaglandins (diclofenac action) may account for the radioprotective effects observed. J. Leukoc. Biol. 53: 185–189; 1993.
Centrifugal enhancement of human immunodeficiency virus type 1 infection and human cytomegalovirus gene expression in human primary monocyte/macrophages in vitro
Authors: Ho Wen-Zhe , Cherukuri Ravi , Ge Shun-Di , Cutilli Joann R , Song Li , Whitko Stephanie , Douglas Steven D 
Published: January 2018

Abstract
In an effort to facilitate the efficiency of human immunodeficiency virus type 1 (HIV-1) and/or human cytomegalovirus (HCMV) infection in primary monocyte/macrophages in vitro, the effect of low-speed centrifugation was studied. The infectivity of Aree strains (Bai, Ada-M, and IIIB) of HIV-1 tested was significantly enhanced by centrifugal inoculation at a force of 1500g for 60 min. Reverse transcriptase activity and HIV-1 p24 antigen in primary monocyte/macrophages infected by a centrifugal inoculation technique were detectable 3-7 days earlier and were more than 10-fold greater in magnitude (at an early stage of the infection) than those of control cells infected by the conventional inoculation technique. Examination of the cells by indirect immunofluorescence revealed higher expression of HIV-1 p24 protein in the monocyte/macrophages infected by the centrifugal inoculation technique. These differences were directly related to centrifugal inoculation and were evident up to 3 weeks after infection. Enhancement was not observed when centrifugation was carried out before or after HIV-1 infection. Centrifugal inoculation of HCMV also enhanced its immediate-early and early gene expression up to 36- to 50-fold, although neither late nuclear antigens and glycoproteins of HCMV nor infectious virus was detected in HCMV-infected monocyte/ macrophage cultures. These results show that centrifugal inoculation is a useful technique for improving the efficiency of HCMV and HIV-1 infection in vitro. J. Leukoc. Biol. 53: 208–212; 1993.
Recombinant soluble IgA Fc receptor: generation, biochemical characterization, and functional analysis of the recombinant protein
Authors: Maliszewski Charles R , VandenBos Timothy , Shen Li , Schoenbo Michael A , Kubagawa Hiromi , Beckmann M Patricia , Monteiro Renato C 
Published: January 2018

Abstract
We previously described the cloning of a human myeloid cell surface receptor for the Fc region of immunoglobulin A (FcαR). In the present study, a soluble version of the FcαR (solFcαR) was generated by removing the transmembrane and cytoplasmic coding regions from full-length FcocR cDNA and ligating into a mammalian expression vector. COS-7 cells transfected with the solFcαR plasmid secreted a protein that inhibited both immunoglobulin A (IgA) and anti-FcaR monoclonal antibody (mAb) binding to FcαR+ U937 cells. Furthermore, the solFcαR bound specifically to and could be eluted from an anti-FcαR mAb-immunoaffinity column, retaining biological activity. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) demonstrated that the recombinant full-length FcαR migrates over a molecular mass range of approximately 40-60 kd, consistent with the reported size and heterogeneity of the naturally occurring myeloid cell surface FcocR. The solFcocR ran on SDS-PAGE as a smaller band (37-55 kd) that reduced to two bands of 23 and 25 kd following N-glycanase treatment, indicating that the FcαR is a heavily glycosylated protein. The biochemical data, coupled with flow cytometry studies showing that the recombinant FcαRs bind to five different anti-FcαR mAbs, clearly demonstrate that the cloned FcαR corresponds directly to the major FcαR species expressed on human monocytes, neutrophils, and myeloid cell lines. The generation of soluble receptor protein will permit in-vestigations of the role of FcocR in IgA-mediated im-munoregulation, effector functions, and disease. J. Leukoc. Biol. 53: 223–232; 1993.
Silica-exposed macrophages release a growth-promoting activity for type II pneumocytes
Authors: Melloni Boris , Lesur Olivier , Cantin André , Bégin Raymond 
Published: January 2018

Abstract
This study addresses the hypothesis that silica- activated alveolar macrophages could release soluble factors stimulating type II cell proliferation. Macrophages from control sheep were exposed or not in vitro to silica, aluminum-treated silica (Si-Al), or titanium dioxide (TiO2). In addition, macrophages from a model of chronic silica-exposed sheep were studied. Supernatants from unstimulated macrophages were found to double basal type II cell DNA synthesis. Alveolar macrophage-conditioned media (AMCM) collected from cells exposed in vitro to silica induced an additional growth-promoting activity for type II cells. Supernatants from Si-Al- or TiO2 dust-exposed alveolar macrophages had the same effects as unstimulated AMCM. In addition, AMCM from in vivo silicotic sheep cells also contained elevated levels of type II cell mitogenic activity. These results suggest that in vitro as in vivo, silica-activated macrophages produce a type II cell growth factor(s) for type II epithelial cells. J. Leukoc. Biol. 53: 327–335; 1993.
Human pulmonary macrophages utilize prostaglandins and transforming growth factor β1 to suppress lymphocyte activation
Authors: Roth Michael D , Golub Sidney H 
Published: January 2018

Abstract
The ability to activate peripheral blood lymphocytes (PBLs) in vitro with interleukin-2 (IL-2) is suppressed by the presence of autologous human pulmonary alveolar macrophages (AMs). AMs suppress both IL-2-induced proliferation and the induction of lympho- kine-activated killer cell (LAK) activity in a dose- dependent manner (79 ±6% suppression of LAK activity at a 0.25:1 AM/PBL ratio). Increasing the IL-2 concentration increased baseline LAK activity but did not prevent AM-mediated suppression. At least two different mechanisms of suppression were observed, one diffusible in nature and the other contact dependent. Indomethacin prevented the component of inhibition that diffused across porous polycarbonate membranes, indicating prostaglandins as the diffusible inhibitor. In contrast, indomethacin had no effect when added alone into conventional AM- PBL cocultures, but a combination of indomethacin and anti-transforming growth factor β1 (TGF-β1) antibody did prevent inhibition. This result suggests that TGF-ß1 acts as an additional contact-dependent inhibitor. PBLs that were rendered unresponsive to IL-2 completely recovered their responsiveness within 4 days after removing AMs from the coculture. These features suggest that pulmonary macrophages have multiple mechanisms for locally suppressing IL-2 responses and lymphocyte activation. J. Leukoc. Biol. 53: 366–371; 1993.
Transmembrane signaling pathways involved in phagocytosis and associated activation of NADPH oxidase mediated by FcγRs in human neutrophils
Authors: Bianca Vittorina Della , Grzeskowiak Miroslawa , Dusi Stefano , Rossi Filippo 
Published: January 2018

Abstract
We have previously shown that in neutrophils classical transmembrane signaling consisting of increased [Ca2+]i and hydrolysis of phospholipids was not essential for phagocytosis mediated by more than one receptor (yeast-IgG, yeast-C3b/bi, yeast-Con A). This work deals with the role of this transmembrane signaling in phagocytosis of erythrocyte (E) IgG, which is mediated only by receptors for IgG (FcγRs). The ingestion of E-IgG was associated with an increase in [Ca+]i and production of inositol phosphates, phosphatidic acid, diacylglycerol, and arachidonic acid, via activation of phospholipases G, D and A2. Related to the same number of particles ingested, the respiratory burst and the transmembrane signaling during phagocytosis of E-IgG were much smaller than during phagocytosis of yeast-IgG. In Ca2+-depleted neutrophils, where the increase in [Ca2+]i and hydrolysis of phospholipids were lacking, the phagocytosis of E-IgG was depressed by about 60%; the respiratory burst was also depressed due to the decrease of ingestion and of stimulation of NADPH oxidase by residual phagocytosis. Pertussis toxin (PT) did not inhibit the phagocytosis of E- IgG but depressed by about 40% the stimulation of li- pidic transmembrane signaling and the respiratory burst in normal neutrophils. In Ca2+-depleted neutrophils the toxin was without effect on ingestion and respiratory burst. Staurosporine did not inhibit the ingestion of E- IgG in normal and Ca2+-depleted neutrophils but depressed by 30-40% the respiratory burst in normal and not in Ca2+-depleted neutrophils. Genistein, an inhibitor of tyrosine kinase, did not inhibit the ingestion of E-IgG but depressed by 30-40% the respiratory burst both in normal and Ca2+-depleted neutrophils. These results demonstrate the following findings in human neutrophils. (1) Contrary to the phagocytosis mediated by more than one receptor (yeast-IgG, yeast-Con A, yeast-C3b/bi), the transmembrane signaling involving increase in [Ca2+]i and hydrolysis of phospholipids plays a role in the phagocytosis and respiratory burst mediated by FcγRs alone. Thus, different signal transduction pathways can be involved in phagocytosis and associated respiratory burst depending on the receptor or combination of receptors activated. (2) FcγRs alone promote phagocytosis with two signaling pathways independent of and dependent on [Ca2+]i changes and phospholipid hydrolysis and insensitive to PT, staurosporine, and genistein. (3) The signaling pathways promoting phagocytosis triggered by FcγRs alone are in some way, or at some step, different from those that activate the respiratory burst. J. Leukoc. Biol. 53: 427–438; 1993.
Hypoxia reoxygenation-induced injury of cultured pulmonary microvessel endothelial cells
Authors: Wiles Marc E , Hechtman Herbert B , Morel Nicole ML , Shepro David 
Published: January 2018

Abstract
Polymorphonuclear leukocyte (PMN) sequestration within the pulmonary microvasculature is known to occur in association with ischemia/reoxygenation (I/R). This sequestration is dependent on eicosanoids and reactive oxygen species. PMN sequestration within the lungs suggests that pulmonary microvascular endothelial cells (MECs) may in part regulate the I/R response. Simulating I/R, we examined the effect of hypoxia/reoxy- genation (H/R) on pulmonary MECs in vitro, with and without PMNs. Significant cellular injury, assessed by 51Cr release, occurred upon reoxygenation of MECs (P &lt; .01). Addition of PMNs to the H/R-injured monolayers did not increase MEC injury. Reoxygenation of MECs also resulted in increased thromboxane (Tx) B2 production compared to controls (P &lt; .01). Inhibition of Tx secretion by aspirin reduced H/R-induced PMN adhesion to MECs (P&lt; .01). Furthermore, H/R-induced increases in PMN-MEC adhesion were prevented by al- lopurinol and superoxide dismutase (P&lt; .01). These data suggest that the pulmonary response to H/R is mediated by MEC generation of reactive oxygen radical species and Tx, which promotes increased PMN adhesion. J. Leukoc. Biol. 53: 490–497; 1993.
Separation of alveolar macrophages and dendritic cells via autofluorescence: phenotypical and functional characterizatior
Authors: Havenith Carin EG , Breedijk Annette J , van Miert Paula PMC , Blijleven Nico , Calame Wim , Beelen Robert HJ , Hoefsmit Elisabeth CM 
Published: January 2018

Abstract
In a previous study we demonstrated that an increase of monocytes and dendritic cells (MDC) was found in the bronchoalveolar lavage fluid (BAL) after intratracheal instillation of a bacillus Calmette-Guérin suspension. In the current study, the bright autofluorescence of alveolar macrophages (AMs) was used to separate them efficiently from the MDC. Sorting of freshly isolated BAL cells resulted in a high-autofluorescent fraction, consisting predominantly of AMs, and a low-autofluorescent fraction containing the MDC, lymphocytes, and granulocytes. Thus, a clear separation between suppressive (AM) and stimulating (MDC) activity was obtained as shown in antigen-specific T cell responses. Flow cytometric parameters, density fractionation, and a series of ED monoclonal antibodies raised against rat macrophage antigens showed that both AMs and MDC were diverse populations. After overnight culture, more than 80% of an MDC population with a density range of 1.065-1.079 changed to a lower density (&lt; 1.056) and morphologically developed into DCs with many processes. Concomitantly, monoclonal antibody EDI expression changed from a granular pattern to a discrete juxtanuclear spot localization. J. Leukoc. Biol. 53: 504–510; 1993.
A lipopolysaccharide-inducible macrophage gene (D3) is a new member of an interferon-inducible gene cluster and is selectively expressed in mononuclear phagocytes
Authors: Tannenbaum Charles S , Major Jennifer , Ohmori Yoshihiro , Hamilton Thomas A 
Published: January 2018

Abstract
We previously reported the isolation and characterization of cDNA clones encoding novel lipopolysac- charide (LPS)-inducible mRNAs from murine peritoneal macrophages. We now present the complete coding sequence of a cDNA previously termed D3. Analysis of multiple clones from a murine macrophage cDNA library provided a complete cDNA sequence of approximately 1.6 kb. The corresponding RNA contains a single open reading frame encoding a hydrophilic protein composed of 425 amino acids and is characterized by a region including three perfect and two imperfect repeats of a seven- amino-acid sequence. Based on nucleotide and deduced amino acid sequence, this mRNA is a new member of a previously described multigene cluster of interferon- inducible genes termed the Mouse 200 series genes. This new sequence most closely resembles gene 204 because both D3 and 204 genes have segments containing the seven-amino-acid repeat sequence. The Mouse 202 and 204 genes, however, have an approximately 200-amino- acid carboxyl-terminal domain that is absent in the LPS- inducible macrophage-derived cDNA. In addition, D3, 202, and 204 can all be distinguished from one another by virtue of unique 3′ noncoding regions 200-300 base pairs in length. The D3 unique sequence is largely restricted to the smallest of the three size classes of this gene family expressed in macrophages and is not detected in interferon- or platelet-derived growth factor-stimulated fibroblasts. Overall, three separate mRNAs have now been described, each of which has three or more of a possible seven nucleotide sequence domains. Although the functions) of the members of this gene family remains unknown, the multiple forms inducible by diverse stimuli and their restricted cell type expression suggest diverse and important physiologic roles for their products in inflammation. J. Leukoc. Biol. 53: 563–568; 1993.
Evidence for integrins other than β2 on polymorphonuclear neutrophils: expression of α6β1 heterodimer
Authors: Rieu Philippe , Lesavre Philippe , Halbwachs-Mecarelli Lise 
Published: January 2018

Abstract
The expression of non-β2 integrins on polymorphonuclear neutrophils (PMNs) was analyzed by im- munoprecipitation and flow cytometry using platelet-free PMN preparations and anti-FcγR blocking mAbs. No β3 integrin was detected with six anti-β3 mAbs. Conversely, integrin β1 chain was present on PMNs, although at low level, and could be distinguished from platelet β1 by SDS-PAGE. The MW differences disappeared after N- glycanase treatment. PMNs express only 2500 molecules of β1 per cell and this expression is not modulated by agonists such as phorbol myristate acetate, formylmethionyl- leucyl-phenylalanine, granulocyte-macrophage colony- stimulating factor, or tumor necrosis factor α, which enhance CDllb expression, or by interferon-7 or transforming growth factor α. PMNs were found to express α6 associated with β1, and no reactivity was observed with various anti-α1, anti-α2, anti-α3, anti-α4, anti-α5 or anti-αv mAbs. In conclusion, although other leukocytes express various β1 integrins, which mediate cell interactions with ECM proteins, PMNs appear to express only the laminin receptor α6β1 PMN interactions with nonlaminin ECM ligands thus seem to be mediated either exclusively by β2 integrins or by nonintegrin molecules. J. Leukoc. Biol. 53: 576–582; 1993.
Multiple pathways of interferon-induced gene expression in murine macrophages
Authors: Politis Alexander D , Sivo Judit , Vogel Stefanie N 
Published: January 2018

Abstract
Steady-state levels of mRNAs that encode specific FcyR and la antigen genes have been measured in macrophages treated with interferons (IFNs) to examine the induction of these markers at the molecular level. Our previous studies suggested requirement for protein kinase C (PKC) in the IFN induction of these macrophage surface markers, although a difference in PKC dependence was found between IFN-α/β- and IFN-γ-induced FcγR expression. The protein kinase antagonist H 7, used previously to distinguish between the surface induction of FcyR by IFN-α/β and IFN-γ, also distinguishes between the IFN-γ and IFN-γ in the induction of FcyRI mRNA and FcyRI surface expression. Protein kinase inhibitors blocked the IFN-γ induction of la mRNA in a manner similar to that reported previously for cell surface la expression. It is concluded that FcyRI is induced by both IFN-γ and IFN-γ through distinct biochemical pathways, whereas IFN-γ utilizes distinct pathways to induce the two macrophage activation markers, la antigen and FcyRI. J. Leukoc. Biol. 53: 583–590; 1993.
Respective role of polymorphonuclear leukocytes and their integrins (CD-11/18) in the local or systemic toxicity of lipopolysaccharide
Authors: Chang Hernán R , Vesin C , Grau Georges E , Pointaire R , Arsenijevic Denis , Strath Malcolm , Pechdre Jean-Claude , Piguet Pierre-Frangois 
Published: January 2018

Abstract
The role of neutrophils (PMNs) and leukocyte integrins was investigated in two models of lipopolysac- charide (LPS)-induced toxicity: the systemic lethality assay in D-galactosamine-sensitized mice and the local reaction elicited by intradermal injection of LPS and tumor necrosis factor (TNF) at 24-h intervals. In the local reaction, depletion of PMNs with an anti-PMN monoclonal antibody (mAb) and mAbs against CD-11a (or LFA1) and CD-llb (or CR3) completely prevented the hemorrhagic necrosis. Evaluation of histological sections and myeloperoxidase levels suggested different mechanism of protection because PMNs were abundant in anti- CD-11- and absent in anti-PMN-treated mice. In the systemic assay, depletion of PMNs ensured 100% survival, whereas after administration of anti-CD-1 la or b mAb, the percentages of survivors were 6 and 59%, respectively. One hour after LPS injection, the serum TNF-α level was higher in PMN-depleted mice than in controls. These studies provide evidence that neutrophils are essential for the expression of local or systemic LPS-induced injury, whereas the requirement for their leukocytic integrins is obvious only in the local reaction. J. Leukoc. Biol. 53: 636–639; 1993.
The in vivo effects of PIXY321 therapy on human monocyte activity
Authors: Hamilton Raymond F , Vadhan-Raj Saroj , Uthman Margaret , Grey Marjorie , Holian Andrij 
Published: January 2018

Abstract
In this report we describe the time-dependent effects of PIXY321 (a synthetic hybrid cytokine) treatment (500 and 750 μg/m2/day for 14 days) on six sarcoma patients. Blood was taken prior to PIXY321 injection (day 0), on days 1, 7, and 14 of treatment, and 7 days posttreatment (day 21). The number of isolated monocytes quadrupuled by day 7 and sustained a significant increase through day 14. There were significant increases in the percentage of circulating monocytes relative to total mononuclear cells on days 1 and 7 of therapy. There were no significant changes in monocyte cell surface antigens (15 checked), suggesting that the increase in monocyte numbers was not due to increased numbers of immature monocytes. The basal activity of the monocytes was not markedly altered during treatment; however, they were primed for significantly increased phorbol 12,13- dibutyrate-stimulated superoxide anion production and endotoxin-stimulated release of interleukin-1 β (IL-lβ) and tumor necrosis factor-α (TNF-α) on days of 1 and 7 of therapy. There was a significant increase of IL-β mRNA levels (unstimulated cells) on days 1 and 7, but TNF-α mRNA levels increased significantly on day 1 only. Consistent with the increase in superoxide anion production, there were increases in monocyte protein kinase C (PKC) levels on all days of therapy. There was a significant increase in PKCIIβ mRNA only on the first day of treatment. All significant changes in monocyte number and function produced by PIXY321 infusion were reversible, as there were no sustained effects on day 21 (7 days after therapy). These results indicate that the effects of PIXY321 may be mediated through up-regulation of PKC resulting in monocytes primed for increased functional activity in response to an appropriate second stimulus. J. Leukoc. Biol. 53: 640–650; 1993.