bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antineutrophil monoclonal antibody (1F12) alters superoxide anion release by neutrophils and Kupffer cells
Authors: Bautista Abraham P , Spolarics Zoltan , Jaeschke Hartmut , Smith C Wayne , Spitzer John J 
Published: January 2018

Abstract
The formation of oxygen-derived radicals by phagocytes is regulated by chemotactic agents, cytokines, and adhesion molecules, such as CD11b/CD18 (Mac-1). In the rat system, we investigated the effect of monoclonal antibody 1F12 against rat neutrophils on hepatic sequestration of neutrophils and superoxide release by hepatic phagocytes. Within 15 min after 1F12 injection, there was profound neutropenia, which persisted for 24 h. The majority of the “lost” neutrophils were sequestered in the liver 4 h after treatment. Zymosan-induced superoxide release in vitro by isolated hepatic neutrophils from 1F12-treated rats was significantly attenuated at 4 and 24 h. The phorbol myristate acetate mediated superoxide release was inhibited 24 h after treatment. Superoxide anion release by normal adherent neutrophils in the presence of agonists was also inhibited by 1F12 in vitro. The in vivo administration of 1F12 primed the Kupffer cells to release superoxide. In vitro treatment of Kupffer cells with 1F12 also stimulated superoxide release. Monoclonal antibody WT.3 (also directed against rat neutrophils), which does not cause neutropenia, did not alter superoxide generation by neutrophils and Kupffer cells. These results indicate that 1F12 may be useful in attenuating inflammation and tissue injury associated with neutrophil activation. However, the activation of Kupffer cells to release toxic oxygen-derived metabolites may predispose the liver to injury in certain pathological conditions. J. Leukoc. Biol. 55: 328–335; 1994.
Targeting HIV-1 to FcγR on human phagocytes via bispecific antibodies reduces infectivity of HIV-1 to T cells
Authors: Howell Alexandra L , Guyre Paul M , You Kwan-sa , Fanger Michael W 
Published: January 2018

Abstract
In addition to CD4, the primary receptor to which the human immunodeficiency virus type 1 (HIV-1) binds, mononuclear phagocytes (monocytes) express three classes of Fc receptors for immunoglobulin G (FcγR). We have previously shown that infection of monocytes by HIV-1 is inhibited when bispecific antibodies (BsAbs) are used to target the virus to either the type I, type II, or type III FcγR on these cells. Infection of monocytes was not inhibited when HIV-1 was targeted to either human leukocyte antigen class I or CD33. We have extended these studies to examine the ability of BsAbs plus polymorphonuclear leukocytes (neutrophils, PMNs) and monocytes to reduce infectivity of HIV-1 to cells from the human T cell lymphoma line, H9. The production of HIV-1 following interaction of virus with BsAb and phagocytes was determined in an indicator cell assay by mixing BsAb, HIV-1, and phagocytes with uninfected H9 cells. Productive infection of H9 cells was quantitated on subsequent days by measuring p24 gag antigen levels in supernatants by enzyme-linked immunosorbent assay. Our findings show that the addition of interferon-γ-activated PMNs or monocytes to cultures of HIV-1 plus H9 cells in the absence of BsAb results in a marked reduction in p24 levels equivalent to 85 to 90% of control levels. With the combination of BsAb (anti-FcγRI anti-gpl20) plus IFN-γ-activated phagocytes, levels of p24 in H9 cultures were below those at culture initiation. These findings demonstrate that IFN-γ-activated phagocytes can affect the natural course of HIV-1 infection of T cells, a finding of potential clinical importance. J. Leukoc. Biol. 55: 385–391; 1994.
Rapid modification of ribosomal S6 kinase II (S6KII) in rabbit peritoneal neutrophils stimulated with chemotactic factor fMet-Leu-Phe
Authors: Huang Chi-Kuang , Coleman Herman , Stevens Tim , Liang Li 
Published: January 2018

Abstract
The ribosomal S6 kinase II (S6KII) in rabbit neutrophils was studied by immunoblotting with antibodies prepared against recombinant S6KII. A protein with apparent molecular weight of 80,000 Da in SDS-gel was recognized by the antibodies. A shift of the apparent molecular weight to 84,000 Da in SDS-gel was observed in cells stimulated with the chemotactic factor fMet-Leu-Phe. Cytochalasin B and phorbol 12-myristate 13-acetate, but not A23187, stimulated both the tyrosine phosphorylation of p41mapk and the change of the mobility of S6KII. Pretreatment of the cells with quin 2/AM inhibited almost completely the tyrosine phosphorylation of p41mapk induced by fMet-Leu-Phe, but only partially the change in mobility of S6KII. Under various conditions, near maximum conversion of S6KII was observed even if only about 40% of the maximum level of tyrosine phosphorylation of p41mapk was achieved. The results suggest that rapid modification of S6KII occurs in chemotactic factor-stimulated neutrophils. Furthermore, the modification of S6KII induced by fMet-Leu-Phe requires either only partial tyrosine phosphorylation of p41mapk or the activation of kinase(s) other than the p41mapk isoform. J. Lcukoc. Biol. 55: 430–436; 1994.
Interleukin-10 is a potent inhibitor of tumor cytotoxicity by human monocytes and alveolar macrophages
Authors: Nabioullin Roustem , Sone Saburo , Mizuno Kazuto , Yano Seiji , Nishioka Yasuhiko , Haku Takashi , Ogura Takeshi 
Published: January 2018

Abstract
The effects of purified human interleukin-10 (IL-10) on the expression of antitumor activity of human monocytes and alveolar macrophages (AMs) obtained by centrifugal elutriation and bronchoalveolar lavage, respectively, from the same healthy donors were examined. Monocytes and AMs were incubated for 16 h in medium with lipopolysaccharide (LPS) in the presence or absence of IL-10 or IL-4, and then their tumoricidal activity was assayed by measuring 125I-IUdR release from human melanoma (A375) cells. Addition of IL-10 to cultures of monocytes or AMs with LPS resulted in dose-dependent suppression of their cytotoxicity against A375 cells, the suppression of the activity of monocytes being the higher. IL-10 also suppressed the synergistic effects of interferon-γ and desmethyl muramyldipeptide in activation of monocytes. IL-10 inhibited the early induction phase of monocyte activation but not the effector phase (monocyte-mediated cytotoxicity). IL-10 plus IL-4 inhibited the antitumor activities of AMs and monocytes much more than either IL-10 or IL-4 alone. IL-10 and IL-4 at sub-optimal concentrations also showed synergistic inhibitory effects. These findings suggest that IL-10 may be important in vivo in down-regulating the antitumor activities of monocytes and AMs in the lung by inhibiting their productions of antitumor effector molecules. J. Leukoc. Biol. 55: 437–442; 1994.
Chemokine expression in trinitrochlorobenzene-mediated contact hypersensitivity
Authors: Gautam Subhash , Battisto Jack , Major Jennifer A , Armstrong David , Stoler Mark , Hamilton Thomas A 
Published: January 2018

Abstract
The expression of the murine IP-10 and MCP-1 genes has been examined in the skin of mice during contact hypersensitivity reactions to the hapten trinitrochlorobenezene (TNCB). In both naive and passively sensitized animals, challenge with TNCB resulted in elevated expression of both genes as early as 4 h as detected by Northern hybridization analysis. Twenty-four hours after challenge, expression was markedly reduced in naive animals but remained elevated in sensitized animals. This prolonged expression of chemokine gene products correlates with the tissue swelling response generally used as a measure of delayed-type hypersensitivity (DTH) in this model and suggests that the continued expression of these genes results from the stimulation of hapten-specific T helper cells. Examination of cell type expression patterns by in situ hybridization using 3H-radiolabeled riboprobes confirmed the results of Northern hybridization experiments. Both genes were expressed predominantly in cells exhibiting the morphology of connective tissue fibroblasts, although the distribution of cells positive for IP-10 mRNA expression differed from that of cells expressing MCP-1 mRNA. IP-10 expression was localized almost exclusively to a population of connective tissue cells surrounding the fur follicle. MCP-1 expression was rarely found associated with fur follicles but instead was distributed throughout the dermis in cells embedded in the collagenous extracellular matrix. Surprisingly, neither endothelial cells lining the small vessels located deep within the dermis nor epidermal keratinocytes were positive under any of the conditions utilized in the present study. Expression of both IP-10 and MCP-1 has been previously reported in a variety of distinct cell types in vitro. The present results indicate that only a subset of the cell types with such potential are stimulated to express these chemokine genes in vivo during hapten-mediated DTH responses, implying the presence of subtle cell type- and tissue-specific control mechanisms. J. Leukoc. Biol. 55: 452–460; 1994.
Fluoride prevents degranulation of the azurophilic and specific granules in electropermeabilized neutrophils
Authors: Niessen Hans W M , Kessels G C Roger , Verhoeven Arthur J 
Published: January 2018

Abstract
The effect of A1F4- on the degranulation process in human neutrophils was investigated. In intact neutrophils, A1F4- induced degranulation, whereas in electropermeabilized neutrophils A1F4- did not stimulate degranulation. In electropermeabilized neutrophils, fluoride ions proved to be inhibitory for the degranulation induced by addition of Ca2+ and/or GTP-γ-S. Another phosphatase inhibitor, okadaic acid, inhibited degranulation induced by Ca2+ or by GTP-γ-S but not degranulation induced by the combination of Ca2+ plus GTP-γ-S. It is concluded that under suboptimal conditions of stimulation with Ca2+ or GTP-γ-S, protein dephosphorylation plays an important role in the degranulation response in human neutrophils. J. Leukoc. Biol. 55: 489–495; 1994.
HIV-1 associated down-modulation of CD4 gene expression is differentially restricted in lymphocytic and monocytic cell lines
Authors: Geleziunas R , Bour S , Wainberg M A 
Published: January 2018

Abstract
We previously demonstrated that chronic infection of a monocytic cell line (U-937) with human immunodeficiency virus type 1 (HIV-1) was not accompanied by down-modulation of CD4 transcription, unlike the situation with CD4+ T lymphocyte lines. To better understand the refractoriness of monocytes to alterations in levels of CD4 mRNA, we treated HIV-IIIB chronically infected U-937 cells with phorbol myristate acetate (PMA), a known stimulus of HIV gene expression. Although PMA caused a significant increase in HIV mRNA levels that was sustained over 7 days, no effect on CD4 transcript levels was noted. Clonal derivatives of HIV-IIIB infected U-937 cells, which produced a variety of infectious and defective particles, were likewise not affected in ability to produce CD4 mRNA. To rule out the possibility that U-937 cells select out HIV-1 variants unable to modulate CD4 mRNA levels, we passaged infectious virus from a U-937 clonal derivative (UHC1) onto different monocytic and T lymphocytic cell lines. In monocytic cell lines (U-937, PLB-985, THP-1), we observed an avirulent infection that did not affect CD4 mRNA levels, whereas UHC1 infection of each of two T lymphocytic cell lines (CEM-T4, Jurkat) caused both cytopathic replication and reductions in GD4 mRNA levels. In one case (Jurkat), variants expressing low CD4 mRNA may have emerged, because the outgrowth no longer expressed viral products. In the other case (CEM-T4), high expression of viral genes was accompanied by CD4 mRNA down-modulation, suggesting either that low-CD4-expressing variants were selected that maintained viral gene expression or that CD4 gene expression was repressed by viral products. J. Leukoc. Biol. 55: 589–595; 1994.
Class I and class II major histocompatibility molecules play a role in bone marrow–derived macrophage development
Authors: Armstrong Jason W , Simske Steven J , Beharka Alison A , Balch Signe , Luttges Marvin W , Chapes Stephen K 
Published: January 2018

Abstract
Class I and class II major histocompatibility complex (MHC) molecules play significant roles in T cell development and immune function. We show that MHCI- and MHCII-deficient mice have low numbers of macrophage precursors and circulating monocytes, as well as abnormal bone marrow cell colony-stimulating factor type 1 secretion and bone composition. We suggest that MHCI and MHCII molecules play a significant role in macrophage development J. Leukoc. Biol. 55: 658–661; 1994.
Human monocytes/macrophages: NO or no NO?
Authors: Denis Michel 
Published: January 2018

Abstract
The production of nitric oxide (NO) and other reactive nitrogen intermediates by cytokine-activated rodent cells is an important component of antimicrobial and/or antineoplasic activity of these cells. This pathway involves the oxidation of arginine to citrulline, with the concomitant release of NO by an inducible form of NO synthase (iNOS). Numerous cell types express iNOS after stimulation with bacterial products and/or cytokines. The role of NO and its derivatives in host resistance is a subject of intense investigation in mouse models of infections or neoplasia. Although human cells such as hepatocytes and endothelial cells have been shown to express an inducible NO synthase, the presence of such a pathway in human monocytes/macrophages has been questioned by many investigators and is a subject of great controversy. In this short review, we discuss some salient points of this debate. J. Leukoc. Biol. 55: 682–684; 1994.
The cooperative effects of TNF-α and IFN-γ are determining factors in the ability of IL-10 to protect mice from lethal endotoxemia
Authors: Smith Sidney R , Terminelli Carol , Kenworthy-Bott Lynne , Calzetta Angela , Donkin Jennifer 
Published: January 2018

Abstract
Recent studies have demonstrated that interleukin-10 (IL-10) has the capacity to protect mice from the lethal effects of endotoxin. In this investigation, we have examined the ability of IL-10 to protect both normal mice and Corynebacterium parvum-primed mice against endotoxin lethality. In the overwhelming majority of experiments, recombinant murine IL-10 (rMuIL-10) and recombinant human IL-10 (rHuIL-10) did not protect normal BALB/cJ mice from lipopolysaccharide (LPS)-induced lethality at doses up to 10 μg/mouse. Despite their inability to protect, both IL-10 preparations were highly effective in preventing the increase in serum tumor necrosis factor α (TNF-α) that occurred in response to the lethal dose of LPS. Moreover, a neutralizing antibody against TNF-α gave only partial protection when administered alone to BALB/cJ mice. Treatment with a combination of neutralizing antibodies against TNF-α and interferon-7 (IFN-γ) resulted in complete protection. In contrast to BALB/cJ mice, normal BDF1 mice were protected from lethal endotoxemia by treatment with both rMuIL-10 and rHuIL-10. However, IL-10 did not protect C. parvum-primed BDF1 against LPS lethality even though it caused a reduction in the LPS-induced serum TNF-α response in C. parvum-primed mice as well as in normal BDF1 mice. Neutralizing antibodies against TNF-α and IFN-γ were protective when administered alone to normal BDF1 mice, as previously demonstrated in C. parvum-primed mice. These findings suggest that lethal endotoxemia is a result of the cooperative activities of TNF-α and IFN-γ in normal mice of the BALB/cJ and BDF1 strains as well as in C. parvum-primed BDF1 mice. IL-10 appears to be less effective in protecting mice from lethal endotoxemia when cooperation between IFN-γ and TNF-α is facilitated by high-level production of the cytokines as in C. parvum–primed mice or when there is evidence of strong synergy between them as in normal BALB/cJ mice. J. Leukoc. Biol. 55: 711–718; 1994.
In vivo administration of a monoclonal antibody against the type I IL-1 receptor inhibits the ability of mice to eliminate Mycobacterium paratuberculosis
Authors: Kenefick K B , Adams J L , Steinberg H , Czuprynski C J 
Published: January 2018

Abstract
The purpose of this study was to determine the influence of endogenous interleukin-1 (IL-1) on resistance to paratuberculosis infection in experimentally infected gnotobiotic mice. Following a 6-month treatment with prednisolone to facilitate bacillary multiplication, control mice substantially reduced the numbers of M. paratuberculosis in the liver and ileum. In contrast, mice injected with a monoclonal antibody against the type I IL-1 receptor failed to reduce the numbers of M. paratuberculosis in the liver and ileum and exhibited more liver granulomas, which contained numerous acid-fast bacilli. These results indicate a significant role for endogenous IL-1 in host defense against experimental M. paratuberculosis infection in mice. J. Leukoc. Biol. 55: 719–722; 1994.
Relationship between phagosome acidification, phagosome-lysosome fusion, and mechanism of particle ingestion
Authors: Bouvier Gaelle , Benoliel Anne-Marie , Foa Colette , Bongrand Pierre 
Published: January 2018

Abstract
The fate of pathogens ingested by macrophages is dependent on phagosome acidification and fusion with different intracellular vesicles. Whereas the mode of particle recognition by the phagocyte seems the main determinant of phagosome-lysosome fusion, the influence of membrane reorganization, fusion events, and cell activation in phagosome acidification is not well known. We looked for a relationship between the nature of receptors involved in phagocytosis, phagosome acidification, and phagosome-lysosome fusion. Murine macrophage-like P388D1 cells were made to ingest sheep erythrocytes coated with immunoglobulin G (EIgG) or IgM and complement (ElgMC) or treated with glutaraldehyde and periodate (EGP). The following results were obtained: (1) As expected, the adhesion of the three particle types was differentially inhibited by monoclonal antibodies specific for FcγRII and GDllb/GD18. (2) The phagosomes containing all three particle types displayed similar acidification kinetics with a PH decrease to 6 within the first 10 min after ingestion. (3) Only phagosomes containing EIgG or ElgMG were fused with peroxidase-loaded secondary lysosomes. (4) Coating EGP with IgG only partially restored fusion, even when the surface density of IgG was markedly higher than found on EIgG. It is concluded that phagosome acidification and fusion are regulated by different mechanisms. Also, the lack of fusion observed with EGP is not entirely accounted for by the absence of stimulation of suitable receptors on the phagocyte membrane, because it cannot be restored by providing such a stimulus. J. Leukoc. Biol. 55: 729–734; 1994.
Role of the mevalonate pathway of isoprenoid synthesis in IL-8 generation by activated monocytic cells
Authors: Terkeltaub Robert , Solan Joell , Barry Michael , Santoro Denise , Bokoch Gary M 
Published: January 2018

Abstract
The highly regulated enzyme HMG-CoA reductase generates mevalonate, the precursor of a complex series of isoprenoids that posttranslationally modify (isoprenylate) certain proteins (e.g., the low-molecular-weight GTP-binding proteins) or that are incorporated into cholesterol and other end products. We recently reported that isoprenoids are required for NADPH oxidase activity in granulocytes via LMW GTP-binding protein isoprenylation. In this study, we evaluated the effects of isoprenoid depletion on the expression of proinflammatory genes in human monocytic THP-1 cells. We selected conditions under which pretreatment for 24 h with isoprenoid synthesis inhibitors (HMG-CoA reductase inhibitor lovastatin or compactin at 10 μM) did not compromise cell viability but markedly suppressed H2O2 generation. Under these conditions interleukin-8 (IL-8) production was attenuated (by 50–90%) in response to lipopolysaccharide, granulocyte-macrophage colonystimulating factor, and phorbol myristate acetate. Coincubation of reductase inhibitor-treated cells with mevalonate prevented the attenuation of IL-8 production by reductase inhibitors. The effects of isoprenoid depletion on cytokine production were selective: IL-1β generation was not inhibited but the production of IL-6 and IL-8 was concomitantly suppressed. IL-8 induction was suppressed at least in part through attenuation of the increase in mRNA in stimulated cells. We conclude that isoprenoid generation through the mevalonate pathway is a requirement for IL-8 induction by activated monocytic cells in vitro. Isoprenylation inhibitors have the potential to alter monocyte proinflammatory function. J. Leukoc. Biol. 55: 749–755; 1994.
Comparison of biological responses of human monocytes and THP-1 cells to chemokines of the intercrine-β family
Authors: Vaddi Krishna , Newton Robert C 
Published: January 2018

Abstract
The biological responses of human monocytes and cells of the monomyelocytic THP-1 cell line to stimulation with members of the β chemokine family are described in this report. All three chemokines tested, MCP-1, MIP-lα, and RANTES, elicited mobilization of intracellular free calcium in monocytes and THP-1 cells. The magnitude of response was highest with MCP-1 stimulation. MCP-1 desensitized monocyte responses to MIP-lα and RANTES, but no such desensitization was observed in THP-1 cells. MIP-lα or RANTES did not desensitize either monocytes or THP-1 cells to MCP-1 stimulation. All three chemokines elicited a potent chemotactic response in monocytes that was comparable in magnitude to that of f-Met-Leu-Phe. MIP-lα and RANTES required a fivefold higher dose than MCP-1 to elicit a peak response. On the contrary, THP-1 cells showed no significant chemotactic response. Studies of the desensitization of the monocyte chemotactic response indicated that all three chemokines are capable of causing complete homologous desensitization. Heterologous desensitization was observed only when monocytes were treated with MCP-1 followed by MIP-lα or RANTES. Studies of actin polymerization and cell polarization responses of monocytes indicated that these two responses attained peak magnitude after 10 min of stimulation with any of the chemokines. Dose-response kinetics were similar to those of the chemotactic response. THP-1 cells again failed to show either of these two responses. Finally, the activation potential of the chemokines was measured by their ability to induce respiratory burst. A tenfold higher concentration than that causing peak chemotactic response was required to elicit respiratory burst and no heterologous desensitization was noticed. Respiratory burst could be induced in THP-1 cells with a direct protein kinase C activator but not with any of the chemokines. These results indicate that, of the three examples tested, MCP-1 is the most potent member of the β chemokine family in the biological responses examined. Although a calcium response was elicited in THP-1 cells with chemokines, a lack of subsequent responses indicates some missing links in the downstream signal transduction pathways. J. Lcukoc. Biol. 55: 756–762; 1994.