scholarly journals Role of soluble gp130 in the tumour necrosis factor-α expression and its production by peripheral blood mononuclear cells

2003 ◽  
Vol 12 (6) ◽  
pp. 355-359
Author(s):  
E. Jablonskaca ◽  
W. Puzewska ◽  
M. Marcinczyk ◽  
J. Jablonski
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Peripheral Blood ◽  
Tumour Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Soluble Gp130

Background:In our previous study we found that rhsIL-6R, along with recombinant human interleukin-6, plays a regulatory role in the immune response by modulating the tumour necrosis factor-α (TNF-α) expression and its production by peripheral blood mononuclearcells (PBMC). We also suggested that sIL-6R with IL-6 secreted by human PMN (neutrophils) influenced the TNF-α expression and its production by autologous PBMC.Aims:Since soluble gp130 (sgp130) is a natural inhibitor for sIL-6R/interleukin-6 responses, in the present study we estimated an effect of exogenous recombinant human sgp130 and sgp130 secreted by PMN on the TNF-α expression and its production by PBMC.Methods:Cells were isolated from whole blood of healthy persons. The PMN were cultured in 96-well plates for 1 h at 37°C in a humidified incubator with 5% CO2. After the incubation, the culture supernatant of PMN was removed and added to the PBMC. PBMC were incubated for 1 h at 37°C in the same conditions. Cytoplasmic protein fractions of PMN and, for comparative purpose of PBMC, were analysed for presence of sgp130 by western blotting with the use of monoclonal antibody capable of detecting this protein. In the culture supernatants of PMN we examined the concentrations of sgp130 by human enzyme-linked immunosorbent assay. TNF-α was measured at the protein levels as well as the mRNA levels.Results and conclusions:The present results revealed that exogenous recombinant human sgp130 modulates the TNF-α expression and production by PBMC. In contrast, we did not find any effect of sgp130 secreted by PMN on the TNF-α expression and its production by autologous PBMC.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

Role of salivary tumour necrosis factor α in HIV-positive patients with oral manifestations

2007 ◽  
Vol 18 (8) ◽  
pp. 565-569 ◽  
Author(s):  
Tomoaki Ino ◽  
Akio Tada ◽  
Akira Tominaga ◽  
Yasuo Komori ◽  
Hiroshige Chiba ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Oral Manifestations ◽  
Tumour Necrosis Factor Α ◽  
Cd4 Cells ◽  
Tnf Α ◽  
Factor Α ◽  
Hiv 1 ◽  
Necrosis Factor

In HIV-1-infected patients, oral manifestations such as recurrent apthous ulcers are often seen. A total of 29 HIV-infected patients were examined to determine salivary tumour necrosis factor α (TNF α) concentrations by enzyme-linked immunosorbent assay, the amount of HIV-1 RNA copy by Amplicor HIV-1 Monitor test, number of CD4 cells by flow cytometry and oral manifestations by oral examination. TNF α concentration was significantly correlated with the amount of HIV-1 RNA, however, not with the number of CD4 cells in HIV-1-infected patients. Further, patients with oral manifestations showed significantly higher concentrations of TNF α in saliva and HIV-1 RNA copies in serum than those without oral manifestations. Following recovery from oral ulcers, TNF α concentration was decreased by half to 20 times lower than the level of that during ulcer incidence. Our results suggest that salivary TNF α is a good indicator for oral manifestations and HIV RNA amounts in HIV-1-infected patients.

Activated tumour necrosis factor-α shedding process is associated with in-hospital complication in patients with acute myocardial infarction

2005 ◽  
Vol 108 (4) ◽  
pp. 339-347 ◽  
Author(s):  
Yudai SHIMODA ◽  
Mamoru SATOH ◽  
Motoyuki NAKAMURA ◽  
Tomonari AKATSU ◽  
Katsuhiko HIRAMORI
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Tumour Necrosis Factor ◽  
Peripheral Blood ◽  
Tumour Necrosis ◽  
Mrna Levels ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

TACE [TNF-α (tumour necrosis factor-α)-converting enzyme] plays an essential role in the shedding of TNF-α, which could affect the outcome of AMI (acute myocardial infarction). To investigate the clinical significance of the TACE–TNF-α system in AMI, we examined TACE-mediated TNF-α synthesis in PBMCs (peripheral blood mononuclear cells), which are a possible source of TNF-α in AMI. Forty-one patients with AMI and 15 healthy subjects (HS) were enrolled in the present study. PBMCs were isolated from peripheral blood on day 1 and 14 after the onset of AMI. TACE and TNF-α mRNA levels and intracellular median fluorescence intensity were measured by real-time RT (reverse transcriptase)–PCR and flow cytometry respectively. TACE-mediated TNF-α production was evaluated in cultured PBMCs with PMA, which is known to activate TACE. Spontaneous TACE and TNF-α levels were higher in AMI patients than in HS (P<0.001). TACE and TNF-α levels in PMA-stimulated PMBCs were markedly increased in AMI patients compared with HS (P<0.001). There was a positive correlation between TACE and TNF-α levels in AMI. Although spontaneous and stimulated levels of TACE and TNF-α decreased 14 days after the onset of AMI, levels in AMI patients were higher than in HS. In AMI patients with in-hospital complications (n=15; pump failure in ten, recurrent myocardial infarction in one, malignant ventricular arrhythmia in three and cardiac death in one), spontaneous and stimulated levels of TACE and TNF-α were higher than in patients without complications (P<0.01). These levels were higher in AMI patients with in-hospital complications 14 days after onset. These results demonstrate that TACE-mediated TNF-α maturation in PBMCs may play an important role in poor outcomes from AMI, suggesting that TACE may be a potential target for the inhibition of cellular TNF-α production in AMI.

scholarly journals Cytokine profile after rubella vaccine inoculation: evidence of the immunosuppressive effect of vaccination

2003 ◽  
Vol 12 (4) ◽  
pp. 203-207 ◽  
Author(s):  
Alexander L. Pukhalsky ◽  
Galina V. Shmarina ◽  
Maria S. Bliacher ◽  
Irina M. Fedorova ◽  
Anna P. Toptygina ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Cytokine Production ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tumour Necrosis Factor Α ◽  
Lymphocyte Response ◽  
Rubella Vaccine ◽  
Live Virus ◽  
Factor Α ◽  
Necrosis Factor

Background:Immunization with live virus vaccines may cause an immunosuppression with lymphopaenia, impaired cytokine production and defective lymphocyte response to mitogenes. These abnormalities were described in subjects vaccinated against measles. This study was performed to analyse the host immune response related to immunosuppression in subjects vaccinated with live attenuated rubella vaccine.Methods:Eighteen schoolgirls, aged 11-13 years, were vaccinated with live attenuated rubella vaccine Rudivax®. Before immunization, and 7 and 30 days after, peripheral blood was collected. Cellular fractions were subjected to flow cytometric analysis, and the lymphocyte response to phytohaemagglutinin was investigated. Plasma samples were analysed for cytokines (interleukin (IL)-4, IL-10, tumour necrosis factor-α, and interferon-γ) by enzyme-linked immunosorbent assay techniques.Results:On day 7 after vaccination, the number of each lymphocyte subset was decreased; however, only for CD3 and CD4 lymphocytes has a significant reduction been shown. On the contrary, tumour necrosis factor-α and IL-10 levels markedly increased and amounted to its maximum on day 30. Simultaneously, a significant reduction in plasma interferon-γand a profound decrease of the lymphocyte response to phytohaemagglutinin were shown. The changes were accompanied with marked elevation of plasma IL-4.Conclusions:Our data indicate that the vaccination with live attenuated rubella vaccine results in moderate but sustained immune disturbance. The signs of immunosuppression, including defective lymphocyte response to mitogene and impaired cytokine production, may persist for at least 1 month after vaccination.

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

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