bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increase of chemokine levels in sputum precedes exacerbation of acute asthma attacks
Authors: Kurashima Kazuyoshi , Mukaida Naofumi , Fujimura Masaki , Schröder Jens-M , Matsuda Tamotsu , Matsushima Kouji 
Published: January 2018

Abstract
Basophils and eosinophils can be activated in vitro by several chemokines such as RANTES, monocyte chemotactic and activating factor (MCAF/MCP-1), macrophage inflammatory peptide-1α (MIP-1α), and interleukin-8 (IL-8). To explore the clinical relevance of the in vitro observations, we measured here the concentrations of these chemokines in sputa from asthmatic patients during acute attacks. Before the onset of a late-phase exacerbation, sputum MCAF/MCP-1, MIP-1α, and IL-8 levels transiently but markedly increased from the basal levels in all of the patients with exacerbation, whereas the sputum levels of these chemokines remained unchanged during the course in the patients without a late-phase exacerbation. These results suggest the involvement of these chemokines in the late-phase exacerbation of asthma.
Regulated expression of a 16-kd galectin-like protein in activated rat macrophages
Authors: Rabinovich Gabriel , Castagna Leonardo , Landa Carlos , Riera Clelia M , Sotomayor Claudia 
Published: January 2018

Abstract
We investigated the presence of a galectin-like protein in rat mononuclear cells using a polyclonal antibody raised against a soluble lactose-binding lectin purified from adult chicken liver that immunoreacted strongly with a broad protein band of about 16 kd in Western blot assays. Immunochemical studies revealed a constitutive expression of this protein in mononuclear cells mainly in the macrophage (Mφ) population. Subcellular localization was assessed by Western blot assays of the cytosolic and membrane fractions of different cell populations studied: (1) spleen mononuclear cells, (2) T cell-enriched, (3) B cell- and Mφ-enriched populations, and (4) peritoneal cells, processed in the presence of lactose. In broad agreement with immunocytochemical studies of nonpermeabilized and permeabilized cells, Western blot assays suggest that this protein is localized mainly in the cytoplasmic compartment but also associated with the cell surface. By flow cytometric analyses we detected about a 14% of ED1 double-positive cells corresponding to Mφs that constitutively express this galectin-like protein associated with their cell surface. The cytosolic fraction obtained from the Mφ-enriched cell population showed hemagglutinating activity specifically inhibited by β-galactoside–related sugars. Moreover, this galectin-like protein was retained in a lactosyl-Sepharose matrix and specifically eluted with lactose. In this work, evidence is also provided to show that different stimuli are able to modulate the expression of the galectin-like protein. Expression was upregulated in inflammatory and activated Mφs, revealing a significant increase in phorbol ester– and formylmethionine oligopeptide–treated cells. Both stimuli involving protein kinase C activation pathway have been able not only to up-regulate the total expression of this protein but also to modulate its subcellular localization.
Ceramide selectively inhibits early events in the response of human neutrophils to tumor necrosis factor
Authors: Fuortes Michele , Jin Wen-wen , Nathan Carl 
Published: January 2018

Abstract
Cell spreading and the respiratory burst of neutrophils responding to soluble, physiological agents and adherent to model biological surfaces are typically delayed in onset by 15 min or more. The lag period may be a physiologically important feature of the action of such agents on neutrophils in that it may allow for migration before secretion. However, the mechanism that interposes such a long delay between stimulus and response is unknown. Tumor necrosis factor α (TNF-α) mediates some of its actions by triggering sphingomyelinase to generate ceramide. In adherent human neutrophils, however, exogenous ceramide did not mimic TNF-α’s ability to stimulate cell spreading, paxillin tyrosine phosphorylation, or the respiratory burst. On the contrary, ceramide suppressed each such response. Ceramide did so by extending the lag period in the cells’ response to TNF-α. Ceramide extended the lag period whether it was added exogenously or generated endogenously by sphingomyelinase, and the effect was reversible. Remarkably, however, ceramide inhibited cell spreading or the respiratory burst only if added together with TNF-α or within the next few minutes. Neutrophils ignored ceramide if it was added later, even if the TNF-α-triggered respiratory burst had not yet commenced. These features suggest that an early, brief elevation of ceramide in response to TNF-α could mediate the lag period. By temporarily inhibiting tyrosine phosphorylation, cell spreading, and the respiratory burst, ceramide or a functionally similar mediator could serve as a phase coordinator of the neutrophil’s response to soluble agonists.
Dendritic cells from different tissues induce production of different T cell cytokine profiles
Authors: Everson Michael P , McDuffie Deborrah S , Lemak David G , Koopman William J , McGhee Jerry R , Beagley Kenneth W 
Published: January 2018

Abstract
The precise role of antigen-presenting cells (APC) in regulating the balance of T-helper type 1 (Th1) and T-helper type 2 (Th2) cytokine production is unclear. Dendritic cells (DC), the most potent APC for activation of naive T cells, were found to regulate Th1 and Th2 cytokine profiles in a fashion dependent upon their tissue of origin. Spleen (systemic) DC induce mainly Th1 cytokines and Peyer’s patch (mucosal) DC induce predominantly Th2 cytokines. These findings support the current concept that different tissues, each with its distinct microenvironment of cytokines, hormones, and cellular elements, are involved in the selection, promotion, and/or maintenance of different immune responses. With regard to DC, it is apparent that the tissue of DC origin determines the cytokine profiles produced by T cells and that DC from different tissues favor either cellular versus humoral immune responses by influencing T cell cytokine production.
Identification of factors from rat neutrophils responsible for cytotoxicity to isolated hepatocytes
Authors: Ho John S , Buchweitz John P , Roth Robert A , Ganey Patricia E 
Published: January 2018

Abstract
Activated polymorphonuclear neutrophils (PMNs) have been shown to be cytotoxic to rat hepatic parenchymal cells in vitro. This cytotoxicity could be observed without direct cell-cell contact, since the conditioned medium from PMNs activated with formyl-Met-Leu-Phe (fMLP) was effective in hepatocyte killing. To identify the toxic factor(s) released by PMNs, degranulation was induced by fMLP in PMNs pretreated with cytochalasin B. The contents released from the phagocytes were subjected to gel filtration on a Sephadex G-100 column. Resulting fractions were tested for cytotoxicity to isolated hepatocytes by using release of alanine aminotransferase as a marker for hepatocyte injury. Cytotoxicity was associated with fractions containing cathepsin G and elastase and not with other fractions, including those containing myeloperoxidase. The former two enzymes were purified to homogeneity with a carboxymethyl cellulose column. Each of these enzymes demonstrated concentration-dependent cytotoxicity to hepatocytes at concentrations &gt;2 μg/mL. Moreover, they exhibited an additive cytotoxic effect. Effective concentrations for the combined cathepsin C and elastase in the incubation mixture were similar to the concentrations of these enzymes in PMN-conditioned medium that produced cytotoxicity to hepatocytes. Cytotoxicity of either purified enzyme or of conditioned medium could be prevented by plasma α-1-antitrypsin or soybean trypsin-chymotrypsin inhibitor, which were also potent inhibitors of enzymic activity of both cathepsin G and elastase. By contrast, the serine protease inhibitors, aprotinin and 4-(2-aminoethyl)-benzenesulfonyl fluoride, were less effective in inhibiting cathepsin G and elastase activities as well as cytotoxicity caused by the purified proteases or PMN-conditioned medium. These results support the hypothesis that cathepsin G and elastase are important mediators of hepatic parenchymal cell killing produced by activated PMNs in vitro.
Cytokines induced by Sendai virus in human peripheral blood leukocytes
Authors: Hua Ji , Liao Mei-June , Rashidbaigi Abbas 
Published: January 2018

Abstract
Human peripheral blood leukocytes (hPBL) are a rich source of natural leukocyte interferon (IFN-α) when treated with Sendai virus. Sendai virus treatment of hPBL will also result in significant production of several chemokines and cytokines such as macrophage inflammatory protein-1α (MIP-1α), MIP-1β, RANTES, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-8, in a time-dependent way. A significant amount of MCP-1 is constitutively produced in overnight culture of leukocytes. The most abundant cytokine is IFN-α, which is induced to its maximum level approximately 11–15 h after addition of Sendai virus. The amount of IFN-α induced at 15 h after Sendai virus treatment is more than 16-fold higher than those of MIP-1α, MIP-1β, and RANTES. IFN-α is also induced more than 60-fold higher than TNF-α and IL-8. The amount of IL-6 induced is approximately 400-fold less than IFN-α. Limited amounts of other cytokines such as IL-1α, IL-1β, macrophage colony-stimulating factor, TNF-β, and IFN-γ are also induced in Sendai virus-treated hPBL. No measurable amount of granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor, leukemia inhibitory factor, IL-2, IL-3, IL-4, IL-5, IL-7, IL-10, IL-11, or IL-12 was induced in the supernatant of Sendai virus-treated hPBL.
Effects of released products from platelets on neutrophilic adhesion to endothelial cells and nylon fibers
Authors: Oryu Makoto , Sakamoto Haruhiko , Ogawa Yoshitada , Tanaka Sumiko , Sakamoto Noriko 
Published: January 2018

Abstract
In this study, the effects of platelet release products (PRPr), ATP, and ADP on the adhesion of human neutrophils to human umbilical vein endothelial cells (HUVEC) and nylon fibers (NF) are described and the implications of various adhesion molecules are considered. Adhesion of neutrophils to HUVEC and NF was increased by PRPr, ATP, and ADP, while their adhesion-increasing actions were cancelled or considerably repressed by apyrase treatment. When anti-CD11a or anti-CD11b was added to neutrophils with PRPr, ATP, or ADP, the adhesion-increasing action was cancelled or considerably repressed. On the other hand, anti-ICAM-1 and anti-CD35 had no significant effects on this action. The above results indicated that platelets, through ATP and ADP in PRPr, increased the adhesion of neutrophils to endothelial cells and foreign bodies. Although it was suggested that the adhesion-increasing action was at least partially based on CD11a and CD11b, ICAM-1 and CD35 had no part in the enhancement of the adhesion.
Polymorphonuclear neutrophils pulsed with synthetic peptides efficiently activate memory cytotoxic T lymphocytes
Authors: Reali Eva , Guerrini Remo , Moretti Sabrina , Spisani Susanna , Lanza Francesco , Tomatis Roberto , Traniello Serena , Gavioli Riccardo 
Published: January 2018

Abstract
Polymorphonuclear neutrophils (PMNs), traditionally considered effector cells in the inflammatory response, have recently been regarded as potential regulators of the immune response. In the present study we investigate whether PMNs are efficient antigen-presenting cells for reactivation of memory cytotoxic T lymphocytes (CTLs). PMNs were pulsed with synthetic peptides derived from Epstein-Barr virus (EBV) antigens. We have used the IVTDFSVIK (IVT) peptide derived from the Epstein-Barr virus—encoded nuclear antigen 4 protein, corresponding to the immunodominant epitope of HLA-A11–restricted CTL responses, and the CLGGLLTMV (CLG) peptide derived from the latent membrane protein 2 antigen, representing a subdominant epitope of HLA-A2–restricted CTL responses. The data indicate that peptide-pulsed PMNs selectively activate specific CTL responses to both immunodominant and subdominant epitopes. The efficiency of CTL induction by PMNs was comparable to that observed with the conventional method of EBV-specific CTL reactivation with the autologous lymphoblastoid cell line, as well as with peptide-pulsed monocyte-enriched adherent cells. On the contrary, unactivated peptide-pulsed lymphocytes failed to induce an epitope-specific CTL response. These results demonstrate that PMNs efficiently present antigens to memory virus-specific CTLs and suggest that they may have a role as antigen-presenting cells.
Expansion of the γδ T cell subset in vivo during bloodstage malaria in B cell-deficient mice
Authors: van der Heyde Henri C , Elloso M Merle , Chang Wun-Ling , Pepper Barbara J , Batchelder Joan , Weidanz William P 
Published: January 2018

Abstract
Mice rendered B cell-deficient either by chronic anti-μ treatment initiated at birth or by gene knockout (JHD and μ-MT mice) suppressed acute Plasmodium chabaudi infections with a time course similar to intact control mice. Moreover, both kinds of B cell-deficient mice showed a 50- to 100-fold increase in splenic γδ T cell number after suppression of parasitemia compared with uninfected B cell-deficient controls; the magnitude of this increase resulted in significantly (P &lt; 0.05) greater numbers of splenic γδ T cells in the B cell-deficient mice than in infected B cell-intact controls (about 10-fold). In contrast, the number of splenic CD4+ αβ T cells was only slightly elevated (&lt; 2-fold) in both kinds of B cell-deficient mice compared with their intact controls. The number of splenic γδ T cells following suppression of P. vinckei parasitemia was approximately ninefold greater in JHD mice than in C57BL/6 controls, whereas similar numbers of splenic CD4+ αβ T cells were detected. Maximal numbers of γδ T cells were in cell-cycle in both JHD and C57BL/6 mice during descending P. chabaudi parasitemia, but the number of γδ T cells in cell-cycle was greater in B cell-deficient mice than in intact controls. Interleukin-10 (IL-10), a potent TH1 cell-suppressive molecule, does not appear to down-regulate the γδ T cell response during malaria in B cell-intact mice because the magnitude of the γδ T cell response was not significantly greater in IL-10 knockout mice compared with heterozygote controls. These findings collectively indicate that a markedly enhanced expansion of the γδ T cell population occurs in the absence of B cells, and this expansion occurs predominantly during acute malaria when parasite burdens are similar in B cell-deficient animals and intact controls.
Chemotaxis by human neutrophils and their cytokineplasts treated with inhibitors of nitric oxide synthase: no suppression of orientation or trajectory
Authors: Malawista Stephen E , de Boisfleury Chevance Anne 
Published: January 2018

Abstract
Inhibitors of nitric oxide (NO) synthase are reported to inhibit both the adherence of polymorphonuclear leukocytes (PMN) to substrate and chemotaxis (directed locomotion) of PMN as determined in Boyden chamber assays. In the current study, we examined both human blood PMN and granule-poor motile cytoplasts derived from them (cytokineplasts, CKP), under direct microscopic observation with concomitant time-lapse video recording, for their ability to respond chemotactically to an erythrocyte destroyed by laser microirradiation. In this system we can observe directly and continuously the orientation and trajectory of PMN before, during, and after establishment of a chemotactic gradient. For both PMN and CKP we employed three different inhibitors of NO synthase (Nω-methyl-l-arginine, N-iminoethyl-l-ornithine, and diphenyleneiodonium) in at least twice the concentrations employed to inhibit chemotaxis of PMN in Boyden chambers or killing of bacteria in CKP. Although small differences in adhesion might not have been appreciated, treated PMN and CKP were each indistinguishable from untreated controls in their ability to orient in a newly created chemotactic gradient and in their trajectories toward the chemotactic target.
Unique CD8+ T cell-rich lymphoid aggregates in human uterine endometrium
Authors: Yeaman Grant R , Guyre Paul M , Fanger Michael W , Collins Jane E , White Hillary D , Rathbun Wayne , Orndorff Kenneth A , Gonzalez Jorge , Stern Judy E , Wira Charles R 
Published: January 2018

Abstract
Using confocal scanning laser microscopy of viable tissue sections, we have demonstrated organized lymphoid aggregates (LA), that have a unique structure, in the stratum basalis of uterine endometrium. These LA consist of a core of B cells surrounded by more numerous T cells and an outer halo of monocytes/macrophages. The T cells in the LA were almost exclusively CD8+CD4-. These CD8+ LA, in terms of both their T cell and B cell components, were either small or absent during the early proliferative stage of the menstrual cycle, significantly larger in size at mid-cycle and during the secretory phase, and absent in post-menopausal women, suggesting that their development is hormonally influenced. This new finding of a menstrual cycle-dependent, phenotypically unique, organized immune cell structure may lead to new insights into the mechanisms by which the endometrium accepts a semiallogeneic graft while providing resistance to infectious organisms.
Macrophage differentiation and expression of macrophage colony-stimulating factor in murine milky spots and omentum after macrophage elimination
Authors: Zhu Hong , Naito Makoto , Umezu Hajime , Moriyama Hiroshi , Takatsuka Hisakazu , Takahashi Kiyoshi , Shultz Leonard D 
Published: January 2018

Abstract
To elucidate the differentiation mechanisms of macrophages in the murine omentum, we studied the repopulation of these cells and the expression of macrophage colony-stimulating factor (M-CSF) in the milky spots and omental tissues in mice depleted of macrophages following administration of liposome-encapsulated dichloromethylene diphosphonate (clodronate). The macrophages in the omentum were spindle or dendritic in shape, expressed several macrophage-specific antigens and Ia antigen, and phagocytized intraperitoneally injected carbon particles. In the milky spots, macrophages and macrophage precursors were detected, and the number of precursors increased alter elimination of macrophages by intraperitoneal injection of liposome-encapsulated clodronate. Macrophage precursors in the milky spots proliferated, moved to the omentum, and transformed into dendritic-shaped macrophages. Expression of M-CSF mRNA extracted from the milky spots was markedly enhanced at 2 and 3 days after macrophage depletion. Localization of M-CSF protein and mRNA was observed in the stromal cells of the milky spots. In osteopetrosis (op/op) mutant mice that are defective in the production of functional M-CSF omental macrophages were absent. These results indicate that M-CSF locally produced in the milky spots plays an important role in providing a microenvironment for development and differentiation of omental macrophages.
Expression of TNF-α by human plasma cells in chronic inflammation
Authors: Di Girolamo Nick , Visvanathan Kumar , Lloyd Andrew , Wakefield Denis 
Published: January 2018

Abstract
Tumor necrosis factor-α (TNF-α) is a potent proinflammatory cytokine and mediator of the inflammatory response. It has been implicated in the pathogenesis of many inflammatory disorders, including rheumatoid arthritis (RA), septic shock, and Crohn's disease. Using a specific anti-human TNF-α antibody we detected immunoreactivity for this cytokine in the cytoplasm of inflammatory cells in several chronic inflammatory disorders, including RA, scleritis, and polyarteritis nodosa. These cells were identified predominantly as IgG-expressing plasma cells. Lymph nodes from patients with Hodgkin's lymphoma and breast cancer, but not from control subjects, were also found to contain TNF-α-positive plasma cells. Cultured EBV-B lymphocytes and a human plasma cell line (ARH-77) when stimulated with phorbol myristate acetate demonstrated cytoplasmic TNF-α immunoreactivity. Western blot analysis of cell membranes and conditioned media from both cell types revealed the presence of the 26-kDa membrane-bound form and the 17-kDa soluble form of TNF-α, respectively. TNF-α was quantitated by enzymelinked immunosorbent assay and found to be biologically active as determined by the L929 cytotoxicity assay. This is the first demonstration that plasma cells may be capable of modulating immune and inflammatory responses, not only by antibody production, but also by their secretion of a key inflammatory mediator, TNF-α. J.
HIV infection of macrophages and pathogenesis of AIDS dementia complex: interaction of the host cell and viral genotype
Authors: Cunningham A L , Naif H , Saksena N , Lynch G , Chang J , Li S , Jozwiak R , Alali M , Wang B , Fear W , Sloane A , Pemberton L , Brew B 
Published: January 2018

Abstract
AIDS dementia complex (ADC) develops in only a third of HIV-infected patients who progress to AIDS. Macrophages and microglial cells are the major cellular sites of productive HIV replication in brain. Using 11 blood isolates of HIV from asymptomatic patients there was marked variation in tropism and the level of productive infection in recently adherent monocytes and monocyte-derived macrophages cultured in vitro. However, less variation was seen with 19 blood isolates from advanced HIV infection and 11 postmortem tissue isolates from brain, cerebrospinal fluid, spleen, and lung. Newly adherent monocytes expressed CCR5 in all seven patients tested, consistent with their susceptibility to infection but not explaining the above variability. There is also marked regional variability in neuropathology in the brain of patients with ADC. We have demonstrated that there was marked variation in the V3 sequences of HIV clones from different regions of the cortex of a patient with ADC, suggesting independent evolution of HIV replication in brain. Furthermore, production of the neurotoxin quinolinic acid from HIV-infected macrophages varied, depending on the host and source of HIV isolate. Hence variations in viral genotype, production by infected macrophages, and subsequent toxin production may contribute to the variability in neuropathology between individuals and between different regions of the brain in the same individual.
Role of proinflammatory cytokines and β-chemokines in controlling HIV replication
Authors: Vicenzi Elisa , Biswas Priscilla , Mengozzi Manuela , Poli Guido 
Published: January 2018

Abstract
Several members of the cytokine network play an important role in controlling the replication of the human immunodeficiency virus (HIV) in several experimental systems. Their effects can be categorized in the following three functional groups: (1) HIV-inductive cytokines; (2) HIV-suppressive cytokines; (3) cytokines with both activating and inhibiting capacities. Studies on the mechanism of action of these molecules have highlighted the fact that several steps of the retrovirus life cycle, from binding to budding of progeny virions from the infected cell, are affected by cytokines. This general concept has been recently substantiated by the discovery that certain β-chemokines can act as blockers of viral entry by interfering with HIV coreceptors. Finally, it is important to recognize that cytokines have gone beyond their role as potential pathogenetic or protective endogenous cofactors in HIV replication and disease progression, and are becoming experimental therapeutic agents for HIV disease, best illustrated thus far by the case of interleukin-2.