scholarly journals TNF-αPromotes IFN-γ-Induced CD40 Expression and Antigen Process in Myb-Transformed Hematological Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Wenyi Gu ◽  
Jiezhong Chen ◽  
Lei Yang ◽  
Kong-Nan Zhao
Keyword(s):  
Dendritic Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Mixed Lymphocyte Reaction ◽  
Interleukin 4 ◽  
Dependent Manner ◽  
Ifn Γ ◽  
Cd40 Expression ◽  
Dose Dependent ◽  
Necrosis Factor

Tumour necrosis factor-α, interferon-γand interleukin-4 are critical cytokines in regulating the immune responses against infections and tumours. In this study, we investigated the effects of three cytokines on CD40 expression in Myb-transformed hematological cells and their regulatory roles in promoting these cells into dendritic cells. We observed that both interleukin-4 and interferon-γincreased CD40 expression in these hematological cells in a dose-dependent manner, although the concentration required for interleukin-4 was significantly higher than that for interferon-γ. We found that tumour necrosis factor-αpromoted CD40 expression induced by interferon-γ, but not by interleukin-4. Our data showed that tumour necrosis factor-αplus interferon-γ-treated Myb-transformed hematological cells had the greatest ability to take up and process the model antigen DQ-Ovalbumin. Tumour necrosis factor-αalso increased the ability of interferon-γto produce the mixed lymphocyte reaction to allogenic T cells. Furthermore, only cotreatment with tumour necrosis factor-αand interferon-γinduced Myb-transformed hematological cells to express interleukin-6. These results suggest that tumour necrosis factor-αplays a key regulatory role in the development of dendritic cells from hematological progenitor cells induced by interferon-γ.

scholarly journals Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

1992 ◽  
Vol 1 (6) ◽  
pp. 375-377 ◽  
Author(s):  
Fang Jun ◽  
Zheng Qin Yue ◽  
Wang Hong Bin ◽  
Ju Dian Wen ◽  
Yi Yang Hua
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Mediator ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Inflammatory Effect

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.

Effects of Plasma, Tumour Necrosis Factor, Endotoxin and Dexamethasone on Extracellular Proteolysis by Neutrophils from Healthy Subjects and Patients with Emphysema

1989 ◽  
Vol 77 (1) ◽  
pp. 35-41 ◽  
Author(s):  
David Burnett ◽  
Anita Chamba ◽  
Susan L. Hill ◽  
Robert A. Stockley
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Leukotriene B4 ◽  
Chronic Obstructive ◽  
Polymorphonuclear Leucocytes ◽  
Dependent Manner ◽  
Control Subjects ◽  
Interleukin 1Α ◽  
Dose Dependent ◽  
Necrosis Factor

1. Neutrophils from patients with chronic obstructive bronchitis and emphysema or age-matched control subjects were cultured on a substrate of 125I-fibronectin. The neutrophils from patients with lung disease digested significantly more fibronectin and released more elastase into the culture supernatant than did cells from control subjects. Preincubation of neutrophils from emphysematous patients with plasma from control subjects significantly inhibited fibronectin digestion by the patients' neutrophils by, on average, 10%. Preincubation of control subjects' neutrophils with plasma from emphysematous patients had no effect on fibronectin digestion. 2. Tumour necrosis factor increased fibronectin digestion in a dose-dependent manner when the cytokine was added to the adherent cells but not when preincubated with the polymorphonuclear leucocytes in suspension. Bacterial endotoxin in concentrations above 6 μg/ml significantly increased fibronectin digestion by neutrophils, but leukotriene B4, interferon-μ and interleukin-1α had no significant effects. 3. Dexamethasone inhibited fibronectin digestion by neutrophils in a dose-dependent manner, from 11% at 10−10 mol/l to 68% at 10−3 mol/l.

scholarly journals Tumour necrosis factor-alpha but not lipopolysaccharide enhances preference of murine dendritic cells for Th2 differentiation

Immunology ◽  
2003 ◽  
Vol 108 (1) ◽  
pp. 42-49 ◽  
Author(s):  
Kazuhiro Kikuchi ◽  
Yoshiki Yanagawa ◽  
Toshimasa Aranami ◽  
Chikako Iwabuchi ◽  
Kazuya Iwabuchi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Th2 Differentiation ◽  
Necrosis Factor

scholarly journals S-Adenosylmethionine attenuates the lipopolysaccharide-induced expression of the gene for tumour necrosis factor α

1999 ◽  
Vol 342 (1) ◽  
pp. 21-25 ◽  
Author(s):  
Walter H. WATSON ◽  
Yanming ZHAO ◽  
Rajender K. CHAWLA
Keyword(s):  
Liver Injury ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Elevated Serum ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Tumour Necrosis Factor Α ◽  
Tnf Gene ◽  
Factor Α ◽  
Necrosis Factor

Intracellular deficiency of S-adenosylmethionine (AdoMet) and elevated serum concentrations of tumour necrosis factor α (TNF) are hallmarks of toxin-induced liver injury. In these models, the administration of either exogenous AdoMet or antibody/soluble receptor for TNF attenuates the injury. We have demonstrated previously that the administration of exogenous AdoMet to AdoMet-deficient rats attenuated lipopolysaccharide (LPS)-induced liver injury and serum TNF concentrations. Here we report that AdoMet lowered the amount of TNF secreted by LPS-stimulated murine macrophage cells (RAW 264.7) in a dose-dependent manner. The inhibition of TNF release was correlated with changes in the steady-state TNF mRNA concentrations. Changes in TNF mRNA were not due to its altered stability and might have been due to an attenuation of the transcription rate of the TNF gene. The inhibition of TNF release in RAW cells was not mediated by GSH because treatment with AdoMet did not increase intracellular GSH. In addition, N-acetylcysteine, whereas it did increase GSH concentration, had no effect on LPS-stimulated TNF release in these cells. Exogenous AdoMet also attenuated LPS-induced serum TNF levels in normal rats sensitized with lead. Thus AdoMet administration might exert its hepatoprotective effects at least in part by its inhibitory effect on expression of the gene for TNF.

scholarly journals Maternal Expressions (Serum Levels) of Alpha Tumour Necrosis Factor, Interleukin 10, Interleukin 6 and Interleukin 4 in Malaria Infected Pregnant Women Based on Parity in a Tertiary Hospital in Southeast, Nigeria

2020 ◽  
pp. 35-41
Author(s):  
Obeagu, Emmanuel Ifeanyi ◽  
Obeagu, Getrude Uzoma ◽  
Amaeze, Augustine Amaeze ◽  
Asogwa, Eucharia Ijego ◽  
Chukwurah, Ejike Felix ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Public Health Problem ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Tnf Α ◽  
Necrosis Factor

Malaria has been reported as a condition caused by infestation with Plasmodium parasite specie, which is a great public health problem globally, particularly in developing countries like Nigeria. This study was carried out in Federal Medical Centre Umuahia in Abia State, Nigeria. The study was done to determine the maternal serum levels of alpha tumour necrosis factor, interleukin 10, interleukin 6, and interleukin 4 in malaria-infected pregnant women based on parities in Southeast, Nigeria.  A total of 150 subjects between the ages of 18-45 years were recruited for the study comprising 50 subjects each of 3 parities (groups A-C). A commercial ELISA Kit was used to measure all the cytokines. Neither statistically significant differences were found for TNF-α (p=0.636), IL-10 (p=0.892), IL-6 (p=0.306) and IL-4 (p=0.222) between prime parity and second parity nor for TNF-α (p=0.356), IL-10 (p=0.896), IL-6 (p=0.304) and IL-4 (p=0.298) between prime parity and multi-parity of malaria-infected pregnant women. TNF-α (p=0.255), IL-10 (p=0.524), IL-6 (p=0.616), and IL-4 (p=0.672) between second parity and on multi-parity respectively. The study showed no changes in the cytokines studied among the malaria-infected pregnant women based on parities. It shows that the number of pregnancies in women infected with malaria has no changes in the levels of the cytokines studied.

The importance of resolution of inflammation in the pathogenesis of ANCA-associated vasculitis

2004 ◽  
Vol 32 (3) ◽  
pp. 502-506 ◽  
Author(s):  
L. Harper ◽  
J.M. Williams ◽  
C.O. Savage
Keyword(s):  
Endothelial Cells ◽  
Dendritic Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Vessel Wall ◽  
Autoimmune Response ◽  
Multiple Organs ◽  
Anca Associated Vasculitis ◽  
Persistent Inflammation ◽  
Necrosis Factor

The primary small-vessel systemic vasculitides are disorders that target small blood vessels, inducing vessel wall inflammation, and are associated with the development of anti-neutrophil cytoplasmic antibodies. Multiple organs are attacked, including the lungs and kidneys. Increasing knowledge of pathogenesis suggests that the antibodies activate neutrophils inappropriately, leading to endothelial and vascular damage. Cytokines, such as tumour necrosis factor, can facilitate damage by priming the neutrophils and activating endothelial cells. Apoptosis of infiltrating neutrophils is also disrupted by anti-neutrophil cytoplasmic antibody activation, and removal of these effete cells occurs in a pro-inflammatory manner, promoting persistent inflammation. The autoimmune response may be promoted by aberrant phagocytosis of apoptotic neutrophils by dendritic cells. Understanding the pathogenesis can help to rationalize existing therapies and indicate new approaches to therapy.

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