scholarly journals Tumour necrosis factor-related apoptosis-inducing ligand expression in patients with diabetic nephropathy

2018 ◽  
Vol 19 (3) ◽  
pp. 147032031878574 ◽  
Author(s):  
Wei-wei Chang ◽  
Wei Liang ◽  
Xin-ming Yao ◽  
Liu Zhang ◽  
Li-jun Zhu ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Mononuclear Cells ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Mrna Levels ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor

Objective: The objective of this study was to evaluate the expression profile of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in patients with diabetic nephropathy (DN). Methods: A total of 126 Chinese subjects were enrolled in this study, including 42 patients with diabetes mellitus (DM), 42 patients with DN and 42 healthy controls. Real-time polymerase chain reaction was performed to analyze levels of TRAIL mRNA in peripheral blood mononuclear cells (PBMCs). Serum levels of soluble TRAIL (sTRAIL) and various cytokines were detected with a commercially available enzyme-linked immunosorbent assay kit. Results: Compared with the control group, the levels of TRAIL mRNA in PBMCs and sTRAIL in sera were both significantly decreased in the DM and DN patients ( P < 0.05). Conversely, levels of interleukin (IL)-1, IL-6, tumour necrosis factor-α and monocyte chemotactic protein-1 were higher in the DN group than in the control group. Serum levels of TRAIL positively correlated with TRAIL mRNA levels in all of the subjects examined ( P < 0.05). Conclusions: These results provide support and a theoretical basis for further research of TRAIL in regard to the pathogenesis of DN.

Production of tumour necrosis factor by cells exposed to sulphonamide reactive metabolites

1992 ◽  
Vol 70 (5) ◽  
pp. 719-722 ◽  
Author(s):  
Michael J. Rieder ◽  
Monica Mask ◽  
Ingrid A. Bird
Keyword(s):  
Inflammatory Response ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Mononuclear Cells ◽  
Reactive Metabolites ◽  
Peripheral Blood Mononuclear ◽  
Tnf Α ◽  
Presence And Absence ◽  
Necrosis Factor

Hypersensitivity reactions are the most common adverse events associated with therapy with the sulphonamide antibiotics. These reactions have been shown to occur among individuals with pharmacogenetically determined differences in the capacity of their cells to detoxify reactive products of oxidative metabolism of the sulphonamides. These reactions appear to be propagated by an inflammatory response by the immune system. To investigate the role of the cytokine tumour necrosis factor (TNF-α) in these reactions, we studied the production of TNF-α by peripheral blood mononuclear cells (PBMCs) that had been incubated with sulfamethoxazole and murine microsomes in the presence and absence of a microsomal-activating system and TNF-α production by PBMCs in the presence and absence of the hydroxylamine derivative of sulfamethoxazole. The PBMCs showed a time-related increase in the production of TNF-α. There was no increase in TNF-α production seen during incubation with sulphonamide reactive metabolites; rather, there was a decrease in TNF-α elaboration that was most marked when PBMCs were incubated with the hydroxylamine of sulfamethoxazole. There is no evidence from these in vitro studies that TNF-α is involved as a mediator of the inflammatory response in sulphonamide hypersensitivity adverse drug reactions.Key words: sulphonamide, tumour necrosis factor, adverse drug reaction, hydroxylamine.

Investigation of the Influenza-Like Symptoms Associated with Recombinant Human Erythropoietin Therapy

1997 ◽  
Vol 25 (3) ◽  
pp. 127-134 ◽  
Author(s):  
A Takemasa ◽  
N Yorioka ◽  
M Yamakido
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Recombinant Human Erythropoietin ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Tumour Necrosis Factor Α ◽  
Peripheral Blood Mononuclear ◽  
Human Erythropoietin ◽  
Factor Α ◽  
Necrosis Factor

The mechanism by which fever and influenza-like symptoms occur, after the administration of recombinant human erythropoietin (rHuEPO) to patients on continuous ambulatory peritoneal dialysis, was investigated. Peripheral blood mononuclear cells, obtained from two patients with fever and/or influenza-like symptoms related to the administration of rHuEPO for the treatment of anaemia were cultured with or without rHuEPO (100, 200, and 300 U/ml). Production of interleukin-1 β and tumour necrosis factor-α was higher in cultures with rHuEPO than in cultures without rHuEPO, although the dose relationships were not clear. These findings suggest that increased production of interleukin-1 β and tumour necrosis factor-α, induced by administration of rHuEPO, may cause fever and influenza-like smptoms.

scholarly journals Chlamydia pneumoniae-induced tumour necrosis factor alpha responses are lower in children with asthma compared with non-asthma

2018 ◽  
Vol 5 (1) ◽  
pp. e000239 ◽  
Author(s):  
Tamar Anne Smith-Norowitz ◽  
Kobkul Chotikanatis ◽  
Diana Weaver ◽  
Jared Ditkowsky ◽  
Yitzchok Meir Norowitz ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Chlamydia Pneumoniae ◽  
Mononuclear Cells ◽  
Tumour Necrosis Factor Alpha ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

IntroductionChlamydia pneumoniae respiratory tract infection has been implicated in the pathogenesis of reactive airway disease and asthma. Innate cytokine responses that are protective of infection with intracellular pathogens may be impaired in patients with asthma. Tumour necrosis factor alpha (TNF-α) is a cytokine related to functions of monocytes and may inhibit C. pneumoniae infection. We investigated TNF-α responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMCs) in patients with asthma and non-asthma, and whether ciprofloxacin, azithromycin or doxycycline affects TNF-α responses.MethodsPBMC (1.5×106) from paediatric patients with asthma (n=19) and non-asthmatic controls (n=6) were infected or mock infected for 1 hour with or without C. pneumoniae AR-39 at a multiplicity of infection=0.1, and cultured+ciprofloxacin, azithromycin or doxycycline (0.1 ug/mL) for 48 hours. TNF-α levels were measured in supernatants by ELISA.ResultsWhen PBMC from patients with asthma were infected with C. pneumoniae, levels of TNF-α were significantly lower than in subjects without asthma (48 hours) (5.5±5.6, 38.4±53.7; p=0.0113). However, baseline responses (no infection with C. pneumoniae) were similar in asthma and non-asthma (1.0±1.7, 1.1±1.2; p=0.89). When PBMC frompatiens with asthma were infected with C. pneumoniae+ciprofloxacin, azithromycin or doxycycline, TNF-α levels increased (25%–45%); this affect was not observed in PBMC from patients without asthma.ConclusionsWe identified differences in the quantity of TNF-α produced by C. pneumoniae-infected PBMC in asthma compared with non-asthma.

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