bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inflammatory fluids regulate TNF-α, but not IL-1β, production by human peritoneal macrophages. A study of patients on continuous ambulatory peritoneal dialysis with peritonitis
Authors: Hart Prue H , Jones Catherine A , Finlay-Jones John J 
Published: January 2018

Abstract
To gain insight into the factors regulating an inflammatory response in vivo, the activities of peritoneal macrophages and the influence of the inflammatory fluids from which they were harvested were studied in continuous ambulatory peritoneal dialysis (GAPD) patients with peritonitis. Specifically, the production of tumor necrosis factor a (TNF-α), interleukin-lβ (EL-lβ), and prostaglandin E2 (PGE2) by lipopolysaccharide-stimu- lated human peritoneal macrophages from GAPD patients with peritonitis was examined in the presence of the inflammatory dialysates from which they were isolated. When tested at a dilution of 20%, the dialysates inhibited production of TNF-α, a key monokine in the orchestration of the inflammatory response. In contrast to the effect on TNF-α, the dialysates did not affect IL-Iβ production by stimulated macrophages. The activity inhibitory for TNF-α synthesis was not fully characterized, but a number of known inhibitors were shown not to be responsible for the suppressive activity. The inhibitory activity was detected in cases of noninfective peritonitis and excluded the possibility that a bacterial product was responsible. Hyperosmolality, pH, protein levels, glucose, uremic molecules, cortisol, heparin, and antibiotics were not responsible for the inhibitory activity. The activity had some similarity to the reported actions of α-globulins (which are acute phase proteins), PGE2, TNF-α soluble receptors, and EL-6, but there was no evidence for their involvement. Whether the selective suppression of TNF-α production is a general finding in inflammatory responses will require additional studies. This study nevertheless illustrates the potential for the host to regulate tightly the development of an excessive inflammatory response and thus to limit tissue pathology. However, it is unknown whether an appropriate host defense is compromised. J. Leukoc. Biol. 53: 309–319; 1993.
Cytotoxic cell proteinase gene expression and cytolytic activity by anti-CD3-activated cytotoxic T lymphocytes is sensitive to cyclosporin A but is not dependent on interleukin-2 synthesis
Authors: Kaiser Michael , Brooks-Kaiser Jane , Fitzpatrick Lyn , Bleackley R Chris , Hoskin David W 
Published: January 2018

Abstract
We have examined the role of interleukin (IL) 2 in the expression of cytotoxic cell proteinases (CCP) 1 and 2, as well as in the induction of major histocompatibility complex (MHC)-unrestricted cytotoxic activity in murine T cell cultures following stimulation with anti- CD3 monoclonal antibody. A dramatic reduction in CCP-1 and CCP-2 gene expression and near absence of cytolytic activity was shown to occur in these cultures when the expression of IL-2 was inhibited by 10−6 M cyclosporin A (CsA). The inhibitory effect of CsA could not be eliminated by the addition to culture of recombinant IL-2 at concentrations typically present in anti- GD3-stimulated T cell culture supernatants. Furthermore, when endogenous IL-2 (45-60 U/ml) present in anti-CD3-stimulated T cell cultures was neutralized with anti-mouse IL-2 antibody there was no effect on CCP-1 and CCP-2 mRNA expression and only a slight decrease in cytolytic activity. The expression of CCP-1 and CCP-2 gene products and the induction of MHC-unrestricted cytotoxic activitv in anti-CD3-stimulated T cell cultures therefore occur independently of IL-2 synthesis but are regulated by a CsA-sensitive mechanism.
A recombinant amino terminal fragment of bactericidal/permeability-increasing protein inhibits the induction of leukocyte responses by LPS
Authors: Mészaros Károly , Parent J Brian , Gazzano-Santoro Hélène , Little Roger , Horwitz Arnold , Parsons Thomas , Theofan Georgia , Grinna Lynn , Weickmann Joachim , Elsbach Peter , Weiss Jerrold , Conlon Paul J 
Published: January 2018

Abstract
Bactericidal/permeability-increasing protein (BPI) is a major component of the granules of polymorphonuclear neutrophils (PMNs) and is involved in the killing of gram-negative bacteria. A 23-kd recombinant protein, corresponding to the NH2-terminal fragment of human BPI (rBPI23), has been shown to bind lipid A and antagonize some lipopolysaccharide (LPS)-mediated effects. In this study the ability of rBPI23 to prevent a wide range of cellular responses to LPS was investigated. In vitro assays were carried out using human blood to more closely approximate in vivo conditions. The release of proinflammatory cytokines [tumor necrosis factor (TNF), interleukin-1β (IL-1β), IL-6, IL-8], induced by E. coli 0113 LPS, was markedly reduced by rBPl23 in a concentration-dependent fashion. The production of the anti-inflammatory protein IL-lra (IL-1 receptor antagonist) was triggered by lower LPS concentrations than those necessary for the other cytokines. Furthermore, prevention of IL-lra release required higher rBPl23 concentrations than for other cytokines. The LPS-induced production of oxygen-derived free radicals by phagocytic cells (resulting in chemiluminescence) was also prevented by rBPl23· The inhibition was specific for LPS because the activation of leukocytes by phorbol myristate acetate, zymosan, or TNF was unaffected by BPI. The ability of rBPl23 to antagonize specifically the effects of endotoxin in the complex environment of human blood along with its bactericidal activity suggests that rBPI23 may be a novel therapeutic agent in the treatment of gram-negative infections.
CD18 integrin-dependent endothelial injury: effects of opsonized zymosan and phorbol ester activation
Authors: Lum Hazel , Gibbs Lester , Lai Linda , Malik Asrar B 
Published: January 2018

Abstract
We examined the hypothesis that neutrophil (PMN)-mediated injury of the vascular endothelium is dependent on adhesion of PMNs to endothelial cells via the leukocyte adhesion glycoprotein CD11/CD18. We compared the PMN activation responses [i.e. adhesion to cultured endothelial cells, superoxide (O2-) production, degranulation, and cytosolic [Ca2+] ([Ca2+]i)] and endothelial injury elicited by opsonized zymosan (OZ, which is phagocytosed by PMNs) or phorbol 12-myristate 13-acetate (PMA, a protein kinase C activator). The basal adherence of nonstimulated PMNs to bovine pulmonary artery endothelial cells (BPAEC) was 9.0 ± 1.1 PMN/field. PMA and OZ increased PMN adherence to BPAEC (to 31.1 ± 1.4 and 39.8 ± 3.8 PMN/field, respectively), which in both cases was inhibited by anti-GDI 8 monoclonal antibody (mAb) IB4. Stimulation of PMNs with PMA or OZ produced injury to 73% and 53% of BPAEC examined, respectively, which corresponded to 6.8-fold and 3.5-fold increases in transendothelial 125I-albumin permeability from baseline. Pretreatment of PMNs with mAb IB4 prevented endothelial injury in both cases. Both PMA and OZ increased the production of O2- (by 7.6-fold and 3.1-fold over control, respectively) and promoted the release of myeloperoxidase (5.2-fold and 9.1-fold over control, respectively) (P &lt; .01). IB4 did not inhibit the PMA- or OZ-induced increases in O2-. IB4 did not inhibit the PMA-induced myeloperoxidase release but reduced by 29% the OZ-induced myeloperoxidase release. Stimulation of PMNs layered on BPAEC with OZ (0.5 mg/ml) caused an 7-fold increase in PMN [Ca2+]i over baseline, which decayed to a steady-state level above baseline at 10 min. IB4 (10 μg/ml) alone did not alter baseline [Ca2+]i and did not inhibit the OZ-induced increase in [Ca2+]i. In contrast to OZ, stimulation of PMNs with PMA did not increase [Ca2+]i. The results indicate that the protective effects of the anti-CD18 mAb IB4 were associated predominantly with its antiadherence property. Therefore, CD18 integrin-mediated PMN adhesion to the endothelium is a critical determinant of endothelial injury irrespective of the PMN-activating stimulus. J. Leukoc. Biol. 55: 58–63; 1994.
Induction of osteopontin mRNA expression during activation of murine NK cells
Authors: Pollack Sylvia B , Linnemeyer Paul A , Gill Santokh 
Published: January 2018

Abstract
Osteopontin (OPN) is an extracellular phosphorylated glycoprotein expressed in bone, kidney, nervous tissue, bone marrow, and granulated metrial gland (GMG) cells in murine decidua. We recently demonstrated that GMG cells are differentiated natural killer (NK) lineage cells that share phenotypic, functional, and morphologic characteristics with adherent interleukin-2 (IL-2)-activated NK cells. We now show that conditions that induce resting splenic NK cells to develop into adherent, activated cells induce the expression of opn mRNA. Nonstimulated NK cells did not express opn mRNA detectable by Northern analysis. However, expression was evident by day 1–2 of culture of NK cells with IL-2, increased to high levels by day 4, and was maintained at high levels thereafter. Thus, expression of mRNA for OPN, a secreted protein associated with cell adhesion, embryonic development, tissue remodeling, and immune regulation, is up-regulated during the activation of NK cells. J. Leukoc. Biol. 55: 398–400; 1994.
Macrophages and angiogenesis
Authors: Sunderkötter Cord , Steinbrink Kerstin , Goebeler Matthias , Bhardwaj Ranjit , Sorg Clemens 
Published: January 2018

Abstract
Macrophages are supposed to play a key role in inflammatory and tumor angiogenesis. Their importance derives from (1) their ubiquitous presence in normal and especially inflamed tissues, (2) their potential to become activated in response to appropriate stimuli, and (3) their repertoire of secretory products. By release of proteases, growth factors (bFGF, GM-CSF, TGF-α, IGF-I, PDGF, VEGF/VPF, TGF-β), and other monokines (IL-1, IL-6, IL-8, TNF-α, substance P, prostaglandins, interferons, thrombospondin 1), activated macrophages have the capability to influence each phase of the angiogenic process, such as alterations of the local extracellular matrix, induction of endothelial cells to migrate or proliferate, and inhibition of vascular growth with formation of differentiated capillaries. This review describes macrophage physiology and the influence of macrophage secretory products on the different phases of angiogenesis in vitro and in vivo. J. Lcukoc. Biol. 55: 410–422; 1994.
Differential expression of CD43 (leukosialin, sialophorin) by mononuclear phagocyte populations
Authors: Howell David N , Ahuja Vinita , Jones Lisa , Blow Osbert , Sanfilippo Fred P 
Published: January 2018

Abstract
CD43 is a hematopoietic cell antigen whose distribution includes T lymphocytes, plasma cells, neutrophils, and platelets. Although it has been detected on peripheral blood monocytes, its expression by other mononuclear phagocytes has not been well documented. Possible changes in monocyte/macrophage CD43 expression in response to inflammation are also poorly defined. To examine these questions, the expression of CD43 by rat peripheral blood monocytes and both resident and elicited peritoneal macrophages was examined. By flow cytometry with two anti-CD43 monoclonal antibodies, blood monocytes were found to express large amounts of surface CD43, whereas surface CD43 expression by resident peritoneal macrophages was negligible. Peritoneal macrophage populations elicited by intraperitoneal injection of thioglycollate were uniformly positive for surface CD43, although the level of expression was lower than that found on monocytes. By labeling resident macrophages with a fluorescent tracer dye, this phenotypic shift was found to reflect an influx of CD43-positive elicited macrophages coupled with a disappearance of CD43-negative resident cells. Evidence from both flow cytometry and Western blotting studies suggests that the CD43 expressed by elicited peritoneal macrophages is less heavily sialylated than that expressed by blood monocytes. These findings, coupled with recent evidence that CD43 influences cellular adhesion, indicate that differential expression of CD43 may play a role in monocyte/macrophage trafficking. J. Leukoc. Biol. 55: 536–544; 1994.
Heterogeneous spontaneous and interleukin-4–induced nitric oxide production by human monocytes
Authors: Mautino Gisèle , Paul-Eugène Nathalie , Chanez Pascal , Vignola Antonio M , Kolb Jean Pierre , Bousquet Jean , Dugas Bernard 
Published: January 2018

Abstract
The generation of nitric oxide by human monocytes has long been a subject of controversy because of the difficulty of rationalizing this production. In this work we evaluated the capacity of human monocytes to produce nitric oxide (NO) as measured by nitrite (NO2-) release. Resting unstimulated monocytes (2 106 cells/ml) were found to produce significant amounts of NO2- after 8 to 12 days in culture. This production appeared to be highly heterogeneous. Indeed, approximatively, 75% of monocytes from the different donors produced up to 10 μM NO2- and were considered low producers; the last 25% produced higher amounts of NO2- (from 10 to 110 μM) and were considered high producers. In any case the spontaneous production of NO2- by monocytes was overcome in the presence of 1 mM Nω-monomethyl-l-arginine (LNMMA). This inhibitory effect was reversed in the presence of an excess of l-arginine (5 mM), indicating that this process is effectively dependent on l-arginine metabolism. Because interleukin-4 (IL-4) is considered an important NO-regulatory cytokine, its regulatory effect on this spontaneous production of NO was also evaluated. In the presence of a defined dose of IL-4 (1 to 100 ng/ml) the spontaneous production of the high-producing population of monocytes was abrogated, whereas IL-4 stimulated the production by the low-producing population of monocytes, which was suppressed in the presence of LNMMA. The present data indicate that NO production by human monocytes is heterogeneous and that IL-4 can be a potent inducer or inhibitor of this production, suggesting a variability in the activation state of these cells. J. Leukoc. Biol. 56: 15–20; 1994.
Cellular and viral determinants that regulate HIV-1 infection in macrophages
Authors: Stevenson Mario , Gendelman Howard E 
Published: January 2018

Abstract
Macrophages in brain, lung, and lymphatics constitute a major HIV reservoir during subclinical infection and disease. During HIV transmission macrophages are seemingly one of the first cells infected, being as efficient as T cells in supporting productive viral replication. Macrophages control a myriad of cell-mediated immune responses that regulate the levels of infection and lead to viral persistence. HIV determinants control viral entry and productive replication and, taken together with cellular differentiation factors, decide the outcome of virus-macrophage interactions. Most important, many clinical manifestations of HIV infection such as encephalitis, myelopathy, pneumonitis, and lymphadenopathy are closely linked to viral replication. Indeed, tissue pathology often correlates with viral gene expression in tissue macrophages. Taken together, these observations provide strong support for a central role of macrophages in progressive HIV infection and its clinical manifestations. J. Leukoc. Biol. 56: 278–288; 1994.
Brain macrophages: neurotoxic or neurotrophic effector cells?
Authors: Mallat M , Chamak B 
Published: January 2018

Abstract
The development of the central nervous system and various pathological contexts imply remodeling or alteration of neuronal networks associated with tissue recruitment of mononuclear phagocytes. Purification and culture of brain macrophages have provided a tool for investigating the functions of these cells. We discuss different mechanisms whereby macrophages could directly influence the survival of neurons and the growth of their processes. J. Leukoc. Biol. 56: 416–422; 1994.
The IL-1 receptor signaling pathway
Authors: Kuno Kouji , Matsushima Kouji 
Published: January 2018

Abstract
Interleukin-1 (IL-1) exerts pleiotropic effects on a variety of tissues through binding to its receptor. Two distinct types of receptors for IL-1 have been characterized in mouse and human. Most of the IL-1 signal has been shown to be transmitted through type I IL-1R (80 kDa) in T lymphocytes as well as B lymphocytes and monocytes. Type II receptor may act as a suppressor of IL-1 biological activities by competing in binding with type I receptors on the cell surface. Functional studies of the type I IL-1R demonstrated that the cytoplasmic segments, possessing a sequence similarity with the Drosophila Toll gene product or IL-6R β chain, gpl30, are important for transmitting activity that induces cytokine genes. In the past three years, several groups reported that IL-1 and tumor necrosis factor (TNF) rapidly induce sphingomyelin turnover in various types of cells, producing ceramide, which may act as a second messenger molecule in an intracellular signaling cascade. Activation of both acid and neutral sphingomyelinases (SMases) has been suggested, and Schutz et al. proposed that the phosphatidylcholine–phospholipase C/acid SMase pathway is involved in TNF-induced NF-xB activation. However, our recent study showed that the NF-xB activation is induced by IL-1/TNF in fibroblasts from patients with type A Niemann-Pick disease, with acid SMase deficiency. This finding implies that acid SMase activity is not essential for the activation of NF-xB by IL-1/TNF at least in fibroblasts. Other signaling pathways including neutral SMase and unidentified protein kinases may be important for NF-xB–mediated cytokine gene activation. J. Leukoc. Biol. 56: 542–547; 1994.
Macrophages derived from C3H/HeJ (Lpsd) mice respond to bacterial lipopolysaccharide by activating NF-χB
Authors: Ding Aihao , Hwang Sonya , Lander Harry M , Xie Qiao-wen 
Published: January 2018

Abstract
The effects of bacterial lipopolysaccharide (LPS) on macrophage gene expression are mediated in part by its ability to induce activation of transcription factor NF-χB. We compared the ability of LPS-treated macrophages from Lpsn (LPS-responsive) C3H/HeN and Lpsd (LPS-hyporesponsive) C3H/HeJ mice to mobilize NF-χB by electrophoretic mobility shift assays with oligonucleotide probes containing a unique NF-χB sequence from the promoter of inducible nitric oxide synthase (iNOS). In response to ng/ml concentrations of LPS, this probe bound proteins that appeared rapidly in the nuclei of thioglycollate-elicited macrophages and bone marrow–derived macrophage cell lines from both Lpsn and Lpsd mice. Only in macrophages from Lpsn mice, however, was LPS able to induce iNOS or tumor necrosis factor α. NF-χB-containing DNA-protein complexes from Lpsd macrophages were formed in lesser amounts than from Lpsn macrophages but shared the same composition, insofar as they displayed the same electrophoretic mobilities and content of heterodimers of p50/RelA (p65) and p50/c-rel. Two conclusions emerge from these findings: (1) NF-χB activity alone is not sufficient for induction of certain LPS-responsive genes and (2) An LPS-response pathway involving activation of NF-χB is preserved in Lpsd mice. The inability of cells from Lpsd mice to induce gene expression in response to LPS thus cannot be attributed to inability to activate NF-χB. J. Leukoc. Biol. 57: 174–179; 1995.
Cellular localization and hormonal regulation of inducible nitric oxide synthase in cycling mouse uterus
Authors: Huang Jian , Roby Katherine F , Pace Judith L , Russell Stephen W , Hunt Joan S 
Published: January 2018

Abstract
Nitric oxide (NO), a potent and versatile free radical, is synthesized in macrophages and mast cells as well as in other types of cells by the inducible form of nitric oxide synthase (iNOS). In this study, cells containing iNOS were identified in the uteri of cycling mice by using a rabbit antibody generated to an iNOS-specific peptide. Macrophages were identified in semiserial sections of the same tissues with the monoclonal antibody, F4/80, and mast cells were identified by toluidine blue staining. In tissue sections of uteri obtained from mice in the four stages of the estrous cycle (8 to 11 mice per stage), iNOS immunoreactivity was strongest in diestrus-I uteri and weakest in diestrus-II uteri. Myometrial mast cells and endometrial epithelial cells were prominent locations of iNOS, and specific protein was also present in myometrial smooth muscle and macrophage-like cells in the endometrial stroma. Because cyclic variations suggested regulation of iNOS expression by ovarian steroid hormones, studies were done using ovariectomized mice. Seven days after ovariectomy, immunoreactive iNOS was low but detectable in mast cells and luminal epithelial cells. In the uteri of ovariectomized, estradiol-17β (E2)–treated mice, mast cells were iNOS+ after 24 h whereas epithelial cells were negative; the reverse was observed in progesterone (P4)-treated mice. Both mast cells and epithelial cells were iNOS+ in the uteri of mice that had received a combination of E2 + P4. These results indicate that several types of uterine cells produce iNOS and that expression of this enzyme in specific cell lineages is governed by ovarian steroid hormones. The data are consistent with the postulate that NO derived from uterine leukocytes and other types of cells plays a role in uterine cyclicity and preparation for pregnancy. J. Leukoc. Biol. 57: 27–35; 1995.
Immunocytochemical localization of granulin-1 to mononuclear phagocytic cells of the teleost fish Cyprinus carpio and Carassius auratus
Authors: Belcourt Daniel R , Okawara Yuji , Fryer James N , Bennett Hugh P J 
Published: January 2018

Abstract
A new class of low-molecular-weight cysteine-rich regulatory growth factors, designated granulins, has been isolated from hematopoietic tissues of a teleost fish (Cyprinus carpio) and structurally characterized. Granulin-1, the predominant form found in carp spleen, was used to raise polyclonal antibodies in rabbits and to establish a radioimmunoassay. This permitted preliminary tissue distribution studies of granulin-1 to be undertaken in carp (Cyprinus carpio) and goldfish (Carassius auratus). Granulin-1 immunoreactivity was found in the melanomacrophage centers of the spleen and head kidney. Carp tissues anatomically involved in the first line of defense against infection, including skin, gills, gut, and also heart, showed intense granulin-1 immunoreactive staining within presumptive macrophage cells. Granulin-1 immunoreactive macrophages prepared from goldfish spleen and head kidney adhered to glass slides, actively phagocytosed carbon particles, and contained granulin-1 immunoreactivity as well as abundant endogenous peroxidase activity. This study demonstrates that granulin-1 is synthesized and stored in macrophages/monocytes of spleen, head kidney, and peripheral tissues of teleost fish. J. Lcukoc. Biol. 57: 94–100; 1995.