scholarly journals Induction of cystine transport activity in mouse peritoneal macrophages by bacterial lipopolysaccharide

1995 ◽  
Vol 310 (2) ◽  
pp. 547-551 ◽  
Author(s):  
H Sato ◽  
K Fujiwara ◽  
J Sagara ◽  
S Bannai
Keyword(s):  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Bacterial Lipopolysaccharide ◽  
Tnf Alpha ◽  
Transport Activity ◽  
Necrosis Factor Alpha ◽  
Ifn Gamma ◽  
Factor Alpha ◽  
Mouse Peritoneal Macrophages

The transport of cystine has been investigated in mouse peritoneal macrophages cultured in vitro. The transport activity for cystine was very low in freshly isolated macrophages but was potently induced during culture in the presence of bacterial lipopolysaccharide (LPS) at concentrations as low as 0.1 ng/ml. The transport activity for cystine was enhanced when the cells were incubated with tumour necrosis factor-alpha (TNF-alpha), but not with interferon-gamma (IFN-gamma) or interleukin-1. IFN-gamma was rather repressive in the induction of the activity by LPS or TNF-alpha. The transport activity for cystine induced by LPS has been characterized. Cystine was transported mainly by Na(+)-independent system and the uptake of cystine was inhibited by extracellular glutamate and homocysteate, but not by aspartate, indicating that the transport of cystine in macrophages treated with LPS is mediated by System xc-. Glutathione content of the macrophages increased when they were exposed to LPS, and this increase was, at least in part, attributable to the induced activity of the cystine transport.

scholarly journals Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.

1993 ◽  
Vol 177 (2) ◽  
pp. 511-516 ◽  
Author(s):  
X Zhang ◽  
D C Morrison
Keyword(s):  
Tumor Necrosis ◽  
Peritoneal Macrophages ◽  
Tnf Alpha ◽  
No Production ◽  
Necrosis Factor Alpha ◽  
Priming Effects ◽  
Alpha Production ◽  
Factor Alpha ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Preculture of thioglycollate-elicited C3HeB/FeJ mouse peritoneal macrophages in vitro with subthreshold stimulatory concentrations of lipopolysaccharide (LPS) can induce hyporesponsiveness (desensitization) to both tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production when these cells are subsequently stimulated with 100 ng/ml of LPS. We have established, however, that the primary dose of LPS required for inducing downregulation of NO production is significantly lower than that required for inducing downregulation of TNF-alpha production. Further, when LPS-pretreated macrophages become refractory to subsequent LPS stimulation for NO production, the secondary LPS-stimulated TNF-alpha production is markedly enhanced, and vice versa. These results indicate that LPS-induced TNF-alpha and NO production by macrophages are differentially regulated, and that the observed desensitization process may not reflect a state in which macrophages are totally refractory to subsequent LPS stimulation. Rather, our data suggest that LPS-pretreated macrophages become selectively primed for differential responses to LPS. The LPS-induced selective priming effects are not restricted to LPS stimulation, but extend as well to stimuli such as zymosan, Staphylococcus aureus, and heat-killed Listeria monocytogenes.

scholarly journals Cytokine serum levels in patients infected by human immunodeficiency virus with and without Trypanosoma cruzi coinfection

2005 ◽  
Vol 38 (6) ◽  
pp. 483-487 ◽  
Author(s):  
Denise Bertulucci Rocha Rodrigues ◽  
Dalmo Correia ◽  
Mônica Dias Marra ◽  
Luis Eduardo Ramirez Giraldo ◽  
Eliane Lages-Silva ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Chagas Disease ◽  
Interleukin 1 ◽  
Serum Levels ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Ifn Gamma ◽  
Immunodeficiency Virus ◽  
Factor Alpha

This study assessed the number of CD4 T lymphocytes, the parasitemia and serum levels of interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), IL-4 and IL-10 of patients infected by human immunodeficiency virus (HIV) and human immunodeficiency virus/Chagas' disease coinfection. CD4 T lymphocytes were low in the two groups of patients, although significantly lower in patients without Chagas' disease. Serum levels of IFN-gamma, IL-4 and TNF-alpha were significantly higher in patients with HIV/Chagas' disease. IL-4/IFN-gamma ratios were higher in patients with HIV/Chagas' disease, which showed a clear balance in favor of Th2-like cytokines in this group of patients. This Th2 balance was higher in patients with detectable parasitemia. We conclude that, although immunosuppression was observed, with CD4 T lymphocytes bellow 200/µm³, these patients did not display reactivation of T. cruzi infection and that a balance favorable to Th2 was associated with the presence of parasitemia.

scholarly journals The role of macrophages in the regulation of erythroid colony growth in vitro

Blood ◽  
1992 ◽  
Vol 80 (7) ◽  
pp. 1702-1709
Author(s):  
CQ Wang ◽  
KB Udupa ◽  
DA Lipschitz
Keyword(s):  
Interleukin 1 ◽  
Colony Growth ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Colony Number ◽  
Factor Alpha ◽  
Macrophage Colony ◽  
Dose Dependent

Depletion of macrophages from murine marrow by the use of a monoclonal anti-macrophage antibody resulted in a significant increase in the number of erythroid burst forming units (BFU-E). This increase could be neutralized by the addition back to culture of macrophages or macrophage conditioned medium indicating that the suppression was mediated by soluble factors. To further characterize this effect, the addition to culture, either alone or in combination, of interleukin-1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and granulocyte-macrophage colony-stimulating factor (GM-CSF) on the growth of BFU-E and the colony-forming unit granulocyte-macrophage (CFU-GM) was examined in macrophage-containing and macrophage-depleted cultures. The addition of IL-1 alpha to culture stimulated the release of both TNF alpha and GM-CSF and acted synergistically with both cytokines, resulting in a dose-dependent suppression of BFU-E and stimulation of CFU-GM growth. The increase in CFU-GM caused by the addition of IL-1 alpha was mediated by GM-CSF but not by TNF alpha as the increase was prevented by the addition of a monoclonal anti-GM-CSF antibody but not by anti-TNF alpha. When either TNF alpha or GM-CSF was neutralized by monoclonal antibodies the addition of IL-1 alpha resulted in a significant increase in BFU-E growth. The addition of GM-CSF to culture caused a dose-dependent suppression of BFU-E that was mediated by TNF alpha, as colony number was not reduced when GM-CSF and a monoclonal anti-TNF alpha antibody were simultaneously added to culture. TNF alpha- induced suppression of BFU-E only occurred in the presence of macrophages. In macrophage-depleted cultures, a dose-dependent suppression of BFU-E could be induced if subinhibitory concentrations of IL-1 alpha or GM-CSF were simultaneously added with increasing concentrations of TNF alpha. The effects of IL-1 alpha or GM-CSF and TNF alpha were markedly synergistic so that the doses required to induce suppression when added simultaneously was only 10% of that required when either were added to culture alone. Suppression of BFU-E by GM-CSF or the combined addition of GM-CSF and TNF alpha did not require IL-1 alpha because inhibition was not neutralized by the addition of anti-IL-1 alpha antibody.

scholarly journals Cytokine formation within rat glomeruli during experimental endotoxemia.

1993 ◽  
Vol 3 (11) ◽  
pp. 1783-1791
Author(s):  
B Fouqueray ◽  
C Philippe ◽  
A Herbelin ◽  
J Perez ◽  
R Ardaillou ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Lag Period ◽  
Bone Marrow Derived Cells ◽  
Factor Alpha ◽  
And Function ◽  
Lipopolysaccharide Challenge

Increasing evidence supports a role of cytokines, tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), and IL-6 in the development of endotoxin-induced acute renal failure. Several activities of these cytokines require a local rather than a systemic production and function. Thus, this study investigates the chronology of cytokine expression in glomeruli isolated from normal rats or rats given iv lipopolysaccharide injections. Detectable levels of TNF alpha could be found in glomeruli isolated from normal rats as assessed by L-929 fibroblast lytic assay and ELISA. Glomeruli isolated from rats given lipopolysaccharide transiently released increased amounts of TNF alpha in relation to the dose of lipopolysaccharide (10 to 500 micrograms/kg body wt) and the lag period between lipopolysaccharide injection and glomerular isolation (20 to 120 min). TNF alpha was released in similar amounts by glomeruli from normal rats that were exposed in vitro to lipopolysaccharide challenge (0.01 to 10 micrograms/mL), indicating that lipopolysaccharide had direct effects on the release of TNF alpha from glomerular cells. These cells consisted mainly of resident cells because reduction of glomerular infiltration by bone marrow-derived cells after the irradiation of normal rats did not affect TNF alpha release. Glomerular IL-1 and IL-6 production was evaluated by specific bioassays under identical conditions. No IL-1 activity could be detected in the medium or within the glomerular cells at any time within 120 min after lipopolysaccharide injection. By contrast, glomerular IL-6 production was induced after lipopolysaccharide challenge both in vivo and in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Human neutrophils produce high levels of the interleukin 1 receptor antagonist in response to granulocyte/macrophage colony-stimulating factor and tumor necrosis factor alpha.

1992 ◽  
Vol 176 (2) ◽  
pp. 593-598 ◽  
Author(s):  
S R McColl ◽  
R Paquin ◽  
C Ménard ◽  
A D Beaulieu
Keyword(s):  
De Novo ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Human Neutrophils ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Factor Alpha ◽  
Macrophage Colony

Neutrophils, an abundant cell type at sites of inflammation, have the ability to produce a number of cytokines, including interleukin 1 (IL-1), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor alpha (TNF-alpha). In this study, we have examined the ability of human neutrophils to produce the IL-1 receptor antagonist (IL-1Ra), a 17-23-kD protein recently isolated and cloned from macrophages. Since IL-1Ra has been shown to inhibit both the in vitro and in vivo effects of IL-1, its production by large numbers of tissue-invading neutrophils might provide a mechanism by which the effects of IL-1 are regulated in inflammation. Using antibodies that are specific for IL-1Ra and a cDNA probe encoding for this protein, we were able to show that neutrophils constitutively produce IL-1Ra. However, after activation by GM-CSF and TNF-alpha, IL-1Ra was secreted into the extracellular milieu where it constituted the major de novo synthesized product of activated neutrophils. None of a large array of other potent neutrophil agonists were found to affect the production of IL-1Ra by neutrophils. Quantitative measurements by enzyme-linked immunosorbent assay revealed that intracellular IL-1Ra is in eightfold excess of the amount secreted in supernatants when studying nonactivated neutrophils. However, in GM-CSF- and TNF-alpha-activated cells, this difference was reduced to values between four- and fivefold, as virtually all of the de novo synthesized IL-1Ra was secreted. In activated cells, the intracellular content of IL-1Ra was found to be in the 2-2.5-ng/ml range per 10(6) neutrophils, whereas levels reached the 0.5-ng/ml range in supernatants. This would imply that IL-1Ra is produced in excess of IL-1 by a factor of at least 100, an observation that is in agreement with the reported amounts of IL-1Ra needed to inhibit the proinflammatory effects of IL-1. Neutrophils isolated from an inflammatory milieu, the synovial fluid of patients with rheumatoid arthritis, were found to respond to GM-CSF and TNF-alpha in terms of IL-1Ra synthesis, indicating that the in vitro observations made in this study are likely to occur in an inflammatory setting in vivo.

AdultBrugia malayimitochondrial and nuclear fractions impart Th1-associated sizeable protection against infective larval challenges inMastomys coucha

2009 ◽  
Vol 83 (1) ◽  
pp. 83-95 ◽  
Author(s):  
S. Shakya ◽  
A.K. Srivastava ◽  
S. Misra-Bhattacharya
Keyword(s):  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Control Group ◽  
Rodent Host ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Antibody Isotypes ◽  
Factor Alpha ◽  
Mastomys Coucha

AbstractProtective immunity to the subperiodic human filariid,Brugia malayi, was explored in the rodent host,Mastomys couchaafter vaccination with subcellular fractions derived from the adult stage of the parasite. The highest level of protection was conferred in animals vaccinated with the ‘mitochondria rich’ (MT) fraction, in which microfilaraemia and worm burden were markedly reduced by 67.2 and 65.9%, respectively, followed by the ‘nucleus rich’ (NR) fraction, showing reductions of 62 and 52.3%, respectively, over the non-immunized control group. Mastomys vaccinated with MT and NR, displayed a significant increase in the level of antigen-specific serum immunoglobulin G (IgG). The levels of IgG2a, IgG2b and IgM antibody isotypes were remarkably elevated in both the MT and NR immunized groups, while IgG1 and IgG3 levels were low. Apart from antibodies, both these fractions also led to marked antigen-specific lymphoproliferationin vitro, along with enhanced release of nitric oxide by peritoneal macrophages. There was an increased population of CD4+ and CD8a+T-cells in MT immunized animals, as measured by flow cytometry, accompanied by elevated levels of proinflammatory cytokines; interferon gamma (IFN-γ), tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in the culture supernatants of the activated splenocytes. The results suggest that both NR and MT contain proinflammatory molecules which evoke a protective Th1 type of immune response.

scholarly journals The role of macrophages in the regulation of erythroid colony growth in vitro

Blood ◽  
1992 ◽  
Vol 80 (7) ◽  
pp. 1702-1709 ◽  
Author(s):  
CQ Wang ◽  
KB Udupa ◽  
DA Lipschitz
Keyword(s):  
Interleukin 1 ◽  
Colony Growth ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Colony Number ◽  
Factor Alpha ◽  
Macrophage Colony ◽  
Dose Dependent

Abstract Depletion of macrophages from murine marrow by the use of a monoclonal anti-macrophage antibody resulted in a significant increase in the number of erythroid burst forming units (BFU-E). This increase could be neutralized by the addition back to culture of macrophages or macrophage conditioned medium indicating that the suppression was mediated by soluble factors. To further characterize this effect, the addition to culture, either alone or in combination, of interleukin-1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and granulocyte-macrophage colony-stimulating factor (GM-CSF) on the growth of BFU-E and the colony-forming unit granulocyte-macrophage (CFU-GM) was examined in macrophage-containing and macrophage-depleted cultures. The addition of IL-1 alpha to culture stimulated the release of both TNF alpha and GM-CSF and acted synergistically with both cytokines, resulting in a dose-dependent suppression of BFU-E and stimulation of CFU-GM growth. The increase in CFU-GM caused by the addition of IL-1 alpha was mediated by GM-CSF but not by TNF alpha as the increase was prevented by the addition of a monoclonal anti-GM-CSF antibody but not by anti-TNF alpha. When either TNF alpha or GM-CSF was neutralized by monoclonal antibodies the addition of IL-1 alpha resulted in a significant increase in BFU-E growth. The addition of GM-CSF to culture caused a dose-dependent suppression of BFU-E that was mediated by TNF alpha, as colony number was not reduced when GM-CSF and a monoclonal anti-TNF alpha antibody were simultaneously added to culture. TNF alpha- induced suppression of BFU-E only occurred in the presence of macrophages. In macrophage-depleted cultures, a dose-dependent suppression of BFU-E could be induced if subinhibitory concentrations of IL-1 alpha or GM-CSF were simultaneously added with increasing concentrations of TNF alpha. The effects of IL-1 alpha or GM-CSF and TNF alpha were markedly synergistic so that the doses required to induce suppression when added simultaneously was only 10% of that required when either were added to culture alone. Suppression of BFU-E by GM-CSF or the combined addition of GM-CSF and TNF alpha did not require IL-1 alpha because inhibition was not neutralized by the addition of anti-IL-1 alpha antibody.

scholarly journals Fas antigen expression on CD34+ human marrow cells is induced by interferon gamma and tumor necrosis factor alpha and potentiates cytokine-mediated hematopoietic suppression in vitro

Blood ◽  
1995 ◽  
Vol 85 (11) ◽  
pp. 3183-3190 ◽  
Author(s):  
J Maciejewski ◽  
C Selleri ◽  
S Anderson ◽  
NS Young
Keyword(s):  
Tumor Necrosis ◽  
Antigen Expression ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Ifn Gamma ◽  
Fas Antigen ◽  
Cd34 Cells ◽  
Factor Alpha ◽  
Necrosis Factor

Activation of Fas antigen, a cell surface receptor molecule, by its ligand results in transduction of a signal for cell death. The Fas system has been implicated in target cell recognition, clonal development of immune effector cells, and termination of the cellular immune response. Fas antigen expression on lymphocytes is regulated by interferon gamma (IFN gamma) and tumor necrosis factor alpha (TNF alpha), cytokines that also have inhibitory effects on hematopoiesis. We investigated Fas antigen expression on human marrow cells and the effects of Fas activation on hematopoiesis in vitro. Freshly isolated immature hematopoietic cells, as defined by the CD34 marker, did not express Fas antigen at levels detectable by fluorescent staining. CD34+ cells, which include progenitors and stem cells, showed low levels of Fas expression in culture, even in the presence of growth factors. Stimulation by TNF alpha and IFN gamma markedly increased Fas antigen expression on CD34+ cells. Anti-Fas antibody, which mimics the action of the putative ligand, enhanced IFN gamma- and TNF alpha-mediated suppression of colony formation by bone marrow (BM) in a dose-dependent manner. This effect did not require the presence of accessory cells. Colony formation from mature (CD34+ CD38+) and immature (CD34+ CD38-) progenitor cells and long-term culture initiating cells were susceptible to the inhibitory action of anti-Fas antibody in the presence of IFN gamma and TNF alpha. Apoptosis assays performed on total BM cells and CD34+ cells showed that anti-Fas antibody induced programmed cell death of CD34+ BM cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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