bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of psychoneuroendocrine factors on spaceflight-induced immunological alterations
Authors: Meehan R , Whitson R , Sams C 
Published: January 2018

Abstract
This paper summarizes previous in-flight infections and novel conditions of spaceflight that may suppress immune function. Granulocytosis, monocytosis, and lymphopenia are routinely observed following short duration orbital flights. Subtle changes within the monocyte and T cell populations can also be noted by flow cytometric analysis. The similarity between the immunological changes observed after spaceflight and other diverse environmental stressors suggest that most of these alterations may be neuroendocrine-mediated. Available data support the hypothesis that spaceflight and other environmental stressors modulate normal immune regulation via stress hormones, other than exclusively glucocorticoids. It will be essential to simultaneously collect in-flight endocrine, immunologic, and infectious illness data to determine the clinical significance of these results. Additional research that delineates the neuroendocrine mechanisms of stress-induced changes in normal immune regulation will allow clinicians in the future to initiate prophylactic immunomodulator therapy to restore immune competence altered by the stress of long-duration spaceflight and therefore reduce morbidity from infectious illness, autoimmune disease, or malignancy.
Cell contact between T cells and synovial fibroblasts causes induction of adhesion molecules and cytokines
Authors: Bombara Michael R , Webb Deborah L , Conrad Patricia , Marior Christopher W , Sarr Timothy , Ranges Gerald E , Aune Thomas M , Grave Jeffrey M , Blue Marie-Luise 
Published: January 2018

Abstract
Human activated T cells adhere to synovial fibroblast-like cells in vitro. The present study was conducted to investigate the consequences of T cell-synovial fibroblast interactions with regard to induction of adhesion molecules and proinflammatory cytokines. A sensitive Western blot technique, polymerase chain reaction (PCR) amplification, and fluorescence-activated cell sorter (FACS) analysis were used to analyze the induction of VCAM-1 and ICAM-1 expression in T cell-synovial fibroblast cocultures. VCAM-1 and ICAM-1 expression could be induced in synovial fibroblast-like cells by 2 h. PCR amplification showed that both forms of VCAM-1 mRNA are found after the interaction of synovial fibroblasts with T cells. Up- regulation of VCAM-1 and ICAM-1 was confined to synovial fibroblasts; T cells did not express VCAM-1 or increased ICAM-1. In contrast to the T cell-synoviocyte interaction, the interaction between T cells and dermal fibroblasts resulted in the up-regulation of ICAM-1 but not VCAM-1, suggesting tissue-specific regulation of VCAM-1. The T cell-synovial fibroblast interaction also resulted in increased levels of tumor necrosis factor (TNF), interferon- 7, and interleukin-6 in coculture supernatant. Of the neutralizing antibodies used against these cytokines, only anti- TNF could significantly inhibit VCAM-1 and ICAM-1 expression. When T cells were separated from synoviocytes by a chamber that allowed medium exchange but no cell contact, VCAM-1 and ICAM-1 failed to be up-regulated and cytokine accumulation in cocultures was drastically reduced. Our results demonstrate mutual cell activation of T cells and synoviocytes upon cell contact as shown by the release of T cell- and synoviocyte-specific cytokines and suggest a cell contact-mediated and T cell-initiated mechanism for the chronic accumulation and retention of mononuclear cells via VCAM-l/ICAM-1 by synovial fibroblasts in the rheumatoid synovium.
Preincubation with anti-CD4 influences activation of human T cells by subsequent co-cross-linking of CD4 with CD3
Authors: Tsygankov Alexander Y , Brӧker Barbara M , Guse Andreas H , Meinke Uta , Roth Edith , Rossmann Cornelia , Emmrich Frank 
Published: January 2018

Abstract
Under physiological conditions, T cell activation by major histocompatibility complex (MHC)-anti- gen complexes requires engagement of both the T cell receptor (TcR) and the CD4 (or GD8) accessory molecules. It has been shown, however, that ligation of CD4 and GD8 can also inhibit T cell activation in an MHG-independent way. Therefore, the role of CD4 in T cell activation and the mechanism of the suppression of T cell functions by anti-CD4 are as yet unclear. We activated T cells by CD4/CD3 co-cross-linking and studied the effect of preincubation with anti-CD4 on this activation. We show here that anti-GD4 affects T cell activation in a complex, time-dependent manner. Whereas short preincubations with anti-GD4 usually enhanced T cell proliferation in response to subsequent co-cross-linking of CDS with GD4, longer preincubations led to its decrease. The observed suppression of proliferation after a long preincubation with anti-CD4 was apparently due to impairment of TcR signaling, as assessed by measurement of Ca2+ mobilization and tyrosine phosphorylation in T cells. These results add a temporal element to the previously observed synergism between the TcR and CD4 in T cell activation.
Granulocyte-macrophage colony-stimulating factor plays a role in the functional activity of mast cells
Authors: Meade Robin , Neddermann Kim M , Greenfield Robert S , Braslawsky Gary , Bursuker Isia 
Published: January 2018

Abstract
A peptide homologous to a region of murine granulocyte-macrophage colony-stimulating factor (mGM-CSF), P27-38, which was shown to be a GM-CSF antagonist, inhibited the function of serotonin release from murine mast cells. Peptide P27-38 inhibited immunoglobulin £ (IgE)-mediated serotonin release in a dose-dependent manner when induced by either specific antigen or anti-IgE antibody. In contrast, non-receptor- mediated release of serotonin by agents such as compound 48/80 or the calcium ionophore A23187 were not affected by the GM-CSF antagonist. Similar effects were observed with GM-CSF-neutralizing antibodies. The inhibitory effect of P27-38 and the neutralizing antibodies on serotonin release could be reversed by the addition of exogenous GM-CSF to the stimulated mast cells, indicating that the inhibitory activity was probably due to an effect on endogenously produced GM-CSF. These findings suggest that GM-CSF produced by stimulated mast cells is involved in the regulation of their activity in an autocrine manner.
Graded changes in the response of individual human basophils to stimulation: distributional behavior of early activation events
Authors: MacGlashan Donald W , Bochner Bruce S , Warner Jane A 
Published: January 2018

Abstract
These studies examine the distribution of single-cell responses in basophil preparations in the context of four events that may be associated with early activation by anti-immunoglobulin E (IgE) antibody and the bacterial peptide fMet-Leu-Phe (fMLP). In general, we measured the single-cell response distributions after challenge with a concentration of stimulus that resulted in an optimal response and compared this with the distribution that occurred after challenge with suboptimal concentrations of the same stimulus. The elevation in cytosolic calcium, as detected in Fura-2-labeled basophils, after challenge with anti-IgE or fMLP showed graded characteristics in that the distributions were unimodal under conditions of optimal or suboptimal challenge with little skewing from a normal distribution. Similarly, the up-regulation of the cell surface adhesion molecule CD11b, as determined by flow cytometry, showed graded unimodal increases after challenge with anti-IgE antibody at optimal and suboptimal concentrations. In addition, stimulation of basophils led to increased F-actin polymerization. After challenge with an optimal concentration of anti-IgE antibody, the F-actin content of basophils increased to a maximum between 10 and 15 min and returned to near prechallenge levels by 60 min. There was a close correlation between the maximum increase in F-actin content and histamine release regardless of the stimulus; anti-IgE antibody, fMLP, and phorbol ester (PMA) responses lay on the same regression line. The single-cell F-actin polymerization distributions were also unimodal and graded according to the magnitude of the histamine release response. During measurements of the calcium response under the microscope we noted that basophils underwent significant changes in morphology after challenge with any stimulus. These changes were related to both degranulation and nondegranulation events and could be quantitated by a series of imageprocessing algorithms, which are presented. The kinetics of the morphological change, measured as a change in cell perimeter, paralleled degranulation. Single-cell distributions of the morphologic changes were also unimodal under conditions of both optimal and suboptimal stimulation. Therefore, no evidence of all-or-nothing responses could be observed in the context of these four early activation events. In general, the response distributions resembled normal distributions at both optimal and suboptimal levels of stimulation, which indicated that single basophils responded in a graded manner. J. Leukoc. Biol. 55: 13–23; 1994.
Distinct patterns of differentiation induced in the monocytic cell line Mono Mac 6
Authors: Ziegler-Heitbrock H W Löms , Schraut Winfried , Wendelgaß Petra , Ströbel Marion , Sternsdorf Thomas , Weber Christian , Aepfelbacher Martin , Ehlers Monika , Schütt Christine , Haas Jürgen G 
Published: January 2018

Abstract
The human Mono Mac 6 cell line exhibits many characteristics of mature blood monocytes including expression of the CD14 molecule and production of cytokines, such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor. To determine whether these cells can be further differentiated, we treated the cells for up to 3 days with either prostaglandin E2 (PGE2; 10-5 or 10-6 M), lipopolysaccharide (LPS; 10–20 ng/ml), or tetradecanoylbhorbol-13-acetate (TPA; 10–50 ng/ml). All three re-agents reduced proliferation and expression of the early myelomonocytic antigen CD33, and all increased phagocytosis of staphylococci and constitutive expression of mRNA for the macrophage colony-stimulating factor (M-CSF) receptor. By contrast, with respect to CD23 FcRII) expression, GD14 expression, and production of O2-, the three reagents induced distinct responses. Expression of CD23 (FcRII) on Mono Mac 6 cells (36%) was not increased by LPS and TPA but was increased by PGE2 treatment to 48%, with a 50% increase of fluorescence intensity. The CD14 antibody My4 stained more than 75% of untreated Mono Mac 6 cells with a specific mean fluorescence intensity of 87.5 channels. This staining was increased more than twofold by both PGE2 and LPS. Staining with the GD14 antibody UGHM1 (6%) was increased to 43% by PGE2 and to 43% by LPS. This increase in CD14 cell surface expression was accompanied by a rise in soluble CD14 and enhancement of CD14 mRNA. By contrast, TPA treatment resulted in a twofold decrease of CD14 cell surface staining with no significant change in sGD14, while CD14 mRNA was transiently down-regulated. Secretion of O2- (stimulated by TPA) was already detectable in untreated Mono Mac 6 cells 6.1 mmol/106 cells/30 min), and this response was enhanced 10-fold by pretreatment with LPS but not with PGE2 or TPA. The kinetics of M-GSF receptor mRNA, CD14 expression, and O2- production revealed that these monocytic features started to increase at 6–24 h and were maximal at 2 days. These data suggest that the three re-agents induce maturation of the Mono Mac 6 cells to different levels or into different branches of the monocyte system with the notable differences that PGE2 enhances CD23 expression, LPS enhances O2- secretion, and TPA down-regulates CD14. J. Leukoc. Biol. 55: 73–80; 1994.
Regulation of interferon-α-inducible cellular genes in human immunodeficiency virus-infected monocytes
Authors: Baca Lisa M , Genis Peter , Kalvakolanu Dhananjaya , Sen Ganes , Meltzer Monte S , Zhou Aimin , Silverman Robert , Gendelman Howard E 
Published: January 2018

Abstract
Cellular mechanisms that control susceptibility to opportunistic infection in human immunodeficiency virus (HIV)-infected individuals remain poorly understood. HIV may induce certain cellular genes that restrict HIV replication and protect cells against other superinfecting viral pathogens. Indeed, HIV-infected monocytes resist infection by vesicular stomatitis virus (VSV). HIV-induced VSV interference in monocytes increases with time after HIV infection. Such interference was evident 6 h after HIV infection and reached maximal levels at 14 days. Monocytotropic but not T cell-tropic HIV strains elicited these effects, signaling a requirement for viral entry and/or replication. Viral interference was independent of interferon (IFN) and was unaffected by addition of neutralizing IFN-α and -β antibodies. The well-described IFN-α-inducible antiviral pathways were examined to determine their relationship to the cellular mechanism(s) underlying VSV interference. HIV and IFN-α both induced the expression of 2–5A synthetase and Mx gene. In contrast, the guanylate-binding protein (GBP), 6–16, and 9–27 cellular genes were up-regulated by IFN-α but not HIV. MxA was detected in HIV-infected monocytes but not in uninfected monocytes. The association between Mx expression and resistance to VSV, coupled with previously described anti-VSV activities by human MxA, suggested that Mx may be an effector molecule for the HIV-induced anti-VSV activities. These results, taken together, suggest that HIV can induce antiviral cellular gene expression, independent of IFN. J. Lcukoc. Biol. 55: 299–309; 1994.
Legionella pneumophila inhibits superoxide generation in human monocytes via the down-modulation of α and β protein kinase C isotypes
Authors: Jacob T , Escallier J C , Sanguedolce M V , Chicheportiche C , Bongrand P , Capo C , Mege J L 
Published: January 2018

Abstract
Legionella pneumophila may subvert monocyte defenses by several mechanisms including the inhibition of phagosome-lysosome fusion or the impairment of oxidative metabolism. We have investigated the effect of L. pneumophila Knoxville 1, a virulent strain that does not inhibit phagosome-lysosome fusion, on the oxidative responsiveness of human monocytes. Infection of monocytes with L. pneumophila for 48 h resulted in marked inhibition of superoxide generation stimulated by phorbol myristate acetate (PMA) but not by zymosan, a particulate agonist. Evidence is provided that L. pneumophila interfered with the transductional pathway (i.e., protein kinase C, PKC) leading to activation of the NADPH oxidase in monocytes. The phosphorylation of 34-, 48-, 62-, 68-, and 80-kDa proteins stimulated by PMA was markedly inhibited in infected monocytes. In addition, the expression of both α and β PKC isotypes was partially inhibited in infected monocytes. Taken together, our data suggest that the down-modulation of PKC isotypes plays a role in the inhibition of PMA-stimulated superoxide generation. J. Leukoc. Biol. 55: 310–312; 1994.
Priming of human monocyte superoxide production and arachidonic acid metabolism by adherence to collagen- and basement membrane–coated surfaces
Authors: Gudewicz Paul W , Frewin Mary Beth , Heinel Lynn A , Minnear Fred L 
Published: January 2018

Abstract
Monocytes (mφs) come into intimate contact with basement membranes and extracellular matrix proteins as they extravasate from the blood to the interstitium or to sites of tissue injury. We examined the in vitro effects of mφ adherence to an endothelial cell-derived basement membrane or to purified extracellular matrix proteins on phorbol myristate acetate (PMA)-stimulated superoxide production and prostanoid secretion. Elutriation-purified human peripheral blood mφs were adhered to tissue culture wells that were precoated with the following purified proteins: bovine serum albumin (BSA), collagen type I (COL I), collagen type IV (COL IV), fibronectin (FN), or laminin (LM). To model the provisional matrix at sites of tissue injury, mφs were also adhered to wells coated with either denatured collagen type I or gelatin (GEL) or coated with basement membrane (BM) derived from endothelial cell monolayers. The mφs were adhered to the protein-coated surfaces for 1 h at 37° in serum-free medium and washed to remove nonadherent cells, and the number of adherent mφs was measured. Monolayers of mφs were also incubated for an additional 18 h, at which time both adherence and cell spreading were measured. PMA-stimulated superoxide production by adherent mφs was determined after 1 and 18 h of adherence to the protein-coated surfaces. PMA-stimulated release of two prostanoids, prostaglandin E2 (PGE2) and thromboxane B2 (TxB2), was measured after 18 h of mφ adherence to the surfaces. Following 18 h of adherence, PMA-stimulated superoxide anion secretion and secretion of PGE2 and TxB2 were augmented or primed by mφs adherent to COL I, GEL, or BM. In contrast, no such priming effects were observed by mφs adherent to COL IV, FN, or LM. The results suggest that adherence to basement membranes, collagen type I-containing surfaces in the interstitium, or denatured collagen at sites of tissue injury primes mφ respiratory burst and arachidonate metabolism to inflammatory agonists. Induction of priming events by substrate-specific adherence may be an important factor regulating host defense functions of mφs in the extracellular matrix. J. Leukoc. Biol. 55: 423–429; 1994.
Slow calcium waves imaged in myeloid cells derived from neonatal cord blood
Authors: Roberts G M , Davies E V , Hallett M B 
Published: January 2018

Abstract
Myeloid cells were derived from neonatal cord blood by culture with granulocyte-macrophage colony-stimulating factor for approximately 8 days. The resultant cell population contained large adherent cells (diameter ≥90 μm), expressing formylated peptide receptors that were functionally coupled to cytosolic free Ca2+ signaling. Imaging of the cytosolic free Ca2+ changes in these cells revealed initial focal release of Ca2+ from a site from within the cell, with elevated Ca2+ also near the cell edge. Increased cytosolic free Ca2+ moved as a slow oscillating wave across the cell (velocity 1 μm/s). As similar events may occur in mature neutrophils and monocytes but be difficult to resolve because of the small size of these cells, it was concluded that neonatal myeloid cells may provide a useful model system for the investigation of Ca2+ signaling in myeloid cells. J. Lcukoc. Biol. 55: 461–466; 1994.
HIV-1 envelope protein gp120 affects phenotype and function of monocytes in vitro
Authors: Dürrbaum-Landmann Iris , Kaltenhäuser Erika , Flad Hans-Dieter , Ernst Martin 
Published: January 2018

Abstract
We investigated the effect of human immunodeficiency virus type 1 (HIV-1) recombinant gp120 (rec.gp120) on phenotype and function of cultured monocytes. Rec.gp120 significantly reduced the accessory function of monocytes to stimulate autologous lymphocytes with anti-CD3, the Fc receptor–mediated chemiluminescence of monocytes, and the expression of CD4 and Fc receptor I/II, while the expression of the monocyte marker GD14 and major histocompatibility complex class I and II was not influenced. According to these phenotypic results, preincubation of monocytes with rec.gp120 depressed anti-CD3 antibody-induced T cell stimulation and Fc receptor-mediated phagocytosis as determined by chemiluminescence. Interferon-γ release of lymphocytes induced by purified protein derivative of tuberculin was enhanced by gp120. These effects of isolated gp120 on monocyte immune functions in vitro might contribute to the understanding of the pathophysiology of HIV-1 infection in viva J. Leukoc. Biol. 55: 545–551; 1994.
Serotonin-stimulated aortic endothelial cells secrete a novel T lymphocyte chemotactic and growth factor
Authors: Katz Marcia F , Farber Harrison W , Dodds-Stitt Zoe , Cruikshank William W , Bear Dennis J 
Published: January 2018

Abstract
Atherosclerotic lesions contain multiple cell types including smooth muscle cells, macrophages, and T lymphocytes. The development of an extralymphatic T lymphocyte focus of inflammation in this condition requires chemoattractant-induced cell migration and growth factor-induced cell activation. In a previous study, we described a novel 13–15-kDa T lymphocyte-specific chemotactic cytokine, endothelial cell–derived lymphocyte chemoattractant activity (ED-LCA), secreted by serotonin-stimulated bovine aortic endothelial cells that is distinct from previously identified endothelial cell–derived interleukins (IL) 1, 6, and 8. Because of the association between T lymphocyte chemotactic and growth factor activity, in the current study we investigated the effect of ED-LCA on T cell growth. We assessed its capacity to induce markers of the passage of T cells from the resting (G0) state into the G1 phase of the cell cycle, such as receptors for IL-2 (IL-2R) and transferrin (TFR) and class II major histocompatibility complex antigens (HLA-DR). Incubation of G0 freshly isolated human T lymphocytes for 48 h with chromatographically resolved, partially purified ED-LCA resulted in a threefold increase in expression of the p55 subunit of IL-2R, a threefold increase in TFR, and a twofold increase in HLA-DR. Passage into the G1 phase of the cell cycle was confirmed by cell cycle analysis employing acridine orange. Evaluation of CD4+ and CD8+ T cell subsets by double-antibody labeling demonstrated that the p55 subunit of IL-2R was induced in both T cell subsets. Although incubation of human T cells with ED-LCA alone did not induce proliferation, addition of exogenous IL-2 to T cells pulsed with ED-LCA for 24 h caused a proliferative response with a stimulation index of 3. By up-regulating functional cell surface receptors for IL-2, ED-LCA is a competence growth factor for T lymphocytes and primes them to respond to IL-2. By virtue of its effect on T cells, as a chemotactic and competence factor, this endothelial cell-derived mitoattractant could participate with other T cell growth factors like IL-2 in the recruitment and amplification of the extralymphatic T cell component of atherosclerosis. J. Leukoc, Biol. 55: 567–573; 1994.
Erythrocytes increase leukotriene C4 release from human eosinophils: characterization and examination of possible mechanisms
Authors: Raible Donald G 
Published: January 2018

Abstract
There has been considerable interest in the role of eosinophils in the pathogenesis of asthma and allergic diseases. While examining the conditions necessary for the release of leukotriene C4 (LTC4) from human eosinophils activated by immunoglobulin G-Sepharose (IgG-Seph), we observed that red blood cells (RBCs) potentiated eosinophil LTC4 release. The time course of IgG-Seph-stimulated LTC4 release was prolonged in the presence of RBCs. After 45 min of incubation, eosinophils without RBCs released 0.95 ± 0.11 ng/106 cells, and those with RBCs released 3.69 ± 0.67 ng/106 cells. Control experiments indicated that the effect was not due to platelet contamination of the RBCs and could not be reproduced with RBC supernatants or RBC membrane ghosts. An interesting characteristic of this interaction was that the eosinophils and RBCs had to be in close contact for the enhancement to occur. We also observed that at low calcium concentrations (0.6 mM), the eosinophils had to be primed with fMLP for the RBC effect to occur, but priming was not required at higher calcium concentrations. Several possible mechanisms that would explain the RBC effect on eosinophil LTC4 release were examined: (1) RBCs block the metabolism of LTC4; (2) RBCs protect the eosinophils from oxidative damage; (3) RBCs provide a substrate (or enzyme) that allows increased eosinophil LTC4 production. These mechanisms failed to explain our observation that erythrocytes enhance eosinophil LTC4 release, however, suggesting that alternative mechanisms are responsible for this effect J. Leukoc. Biol. 56: 65–73; 1994.