SERUM LEVELS OF TUMOR NECROSIS FACTOR-α (TNF-α), INTERLEUKIN-6 (IL-6), AND INTERLEUKIN-1β (IL-1β) IN DENGUE-INFECTED PATIENTS Hober D, Poli L, Roblin B, Gestas P, Chungue E, Granic G, Imbert P, Pecarere JL, Vergez-Pascal R, Wattre P. Am J Trop Med Hyg. 1993;48

Çelik I, Akalin S, Erbaş T. Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment. Eur J Endocrinol 1995;132:668–72. ISSN 0804–4643 Contrary to the usual inhibitory role of tumor necrosis factor-α (TNF-α) thyroid metabolism, it also has specific stimulatory effects in autoimmune thyroid disorders, including induction of HLA class II antigen-presenting cell—T cell interaction. Despite high intrathyroidal concentrations, various studies were not able to demonstrate high serum levels of TNF-α in patients with Graves' disease. To investigate this discrepancy we determined TNF-α and interleukin 6 (IL-6) levels in 25 hyperthyroid patients who responded to propylthiouracil treatment (16 with Graves' disease and nine with toxic multinodular goiter) and compared them with the levels found in euthyroid patients with simple diffuse goiter (n = 15) and normal healthy controls (n = 15). Median IL-6 levels were high in both Graves' disease and toxic multinodular goiter patients before propylthiouracil treatment (23 and 26.5 pg/ml, respectively). After restoring euthyroidism there was a statistically significant decline to near-normal levels (3 and 10 pg/ml, respectively). On the other hand, median serum TNF-α levels were high only in Graves' disease patients (20 pg/ml) and could not be normalized with antithyroid medication (20 pg/ml) compared to that of controls (5 pg/ml). Tumor necrosis factor-α, but not IL-6, was found to be high in the sera of Graves' disease patients when euthyroid, which may be due to an ongoing antigen–antibody interaction, a feature of autoimmune attack. It remains to be determined whether the degree of TNF-α and/or IL-6 elevation will be a predictor of disease recurrence. Ismail Çelik, Section of Oncology, Dept. of Medicine, Hacettepe University Institute of Oncology, Ankara 06100, Turkey

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Changes in serum level of ghrelin, tumor necrosis factor-alpha and interleukin-6 in children with congenital heart disease

Asian Journal of Medical Sciences ◽

10.3126/ajms.v6i5.12129 ◽

2015 ◽

Vol 6 (5) ◽

pp. 12-16

Author(s):

Shiv Kumar Yadav ◽

Qi Jian YI

Keyword(s):

Congenital Heart Disease ◽

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Congenital Heart ◽

Tumor Necrosis Factor Α ◽

Serum Levels ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Objective: To investigate the changes in serum levels of ghrelin, tumor necrosis factor-α and interleukin-6 in Children with Congenital Heart Disease (CHD) at pre and post percutaneous management of the lesions. Material & Methods: We measured the serum levels of ghrelin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) by enzyme linked immunosorbent assays (ELISA) in 67 patients with CHD and in 20 control subjects; and compared these markers of inflammatory reaction between groups of pre-closure (37 patients) and at the end of 5 minutes (37 patients), 1 month (22 patients) and 3 month (8 patients) post percutaneous management of the lesions. Results: Our results showed that the patients with CHD had significantly higher serum level of Ghrelin, TNF-α and IL-6 in comparison of the controls but gradually return towards the baseline levels at the end of 3 months post percutaneous management of the lesions. Conclusion: The inflammatory reaction is activated in pre-closure and self-limited post-closure in children with CHD. Percutaneous management could improve the inflammatory process, which is safe and effective in children with CHD.DOI: http://dx.doi.org/10.3126/ajms.v6i5.12129 Asian Journal of Medical Sciences Vol.6(5) 2015 12-16

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Tumor Necrosis Factor α and Interleukin-1β Acutely Inhibit AgRP Neurons in the Arcuate Nucleus of the Hypothalamus

International Journal of Molecular Sciences ◽

10.3390/ijms21238928 ◽

2020 ◽

Vol 21 (23) ◽

pp. 8928

Author(s):

Fernanda M. Chaves ◽

Naira S. Mansano ◽

Renata Frazão ◽

Jose Donato

Keyword(s):

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interleukin 1Β ◽

Low Grade ◽

Membrane Excitability ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Obesity-associated low-grade inflammation favors weight gain, whereas systemic infection frequently leads to anorexia. Thus, inflammatory signals can either induce positive or negative energy balance. In this study, we used whole-cell patch-clamp to investigate the acute effects of three important proinflammatory cytokines, tumor necrosis factor α (TNF-α), interleukin-6, and interleukin-1β (IL-1β) on the membrane excitability of agouti-related peptide (AgRP)- or proopiomelanocortin (POMC)-producing neurons. We found that both TNF-α and IL-1β acutely inhibited the activity of 35–42% of AgRP-producing neurons, whereas very few POMC neurons were depolarized by TNF-α. Interleukin-6 induced no acute changes in the activity of AgRP or POMC neurons. Our findings indicate that the effect of TNF-α and IL-1β, especially on the activity of AgRP-producing neurons, may contribute to inflammation-induced anorexia observed during acute inflammatory conditions.

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Tumor Necrosis Factor-α, Interleukin-1β, and Interleukin-6 Plasma Levels in Neonatal Sepsis

Pediatric Research ◽

10.1203/00006450-199304000-00013 ◽

1993 ◽

Vol 33 (4) ◽

pp. 380-383 ◽

Cited By ~ 1

Author(s):

E S J M De Bont ◽

A Martens ◽

J Van Raan ◽

G Samson ◽

W P F Fetter ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Neonatal Sepsis ◽

Plasma Levels ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interleukin 1Β ◽

Factor Α ◽

Necrosis Factor

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Systemic Sclerosis Fibroblasts Show Specific Alterations of Interferon-γ and Tumor Necrosis Factor-α-induced Modulation of Interleukin 6 and Chemokine Ligand 2

The Journal of Rheumatology ◽

10.3899/jrheum.111132 ◽

2012 ◽

Vol 39 (5) ◽

pp. 979-985 ◽

Cited By ~ 8

Author(s):

ALESSANDRO ANTONELLI ◽

POUPAK FALLAHI ◽

SILVIA MARTINA FERRARI ◽

DILIA GIUGGIOLI ◽

MICHELE COLACI ◽

...

Keyword(s):

Systemic Sclerosis ◽

Tumor Necrosis Factor ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interferon Γ ◽

Tnf Α ◽

Ifn Γ ◽

Factor Α ◽

Necrosis Factor

Objective.We evaluated the effect of interferon-γ (IFN-γ) and/or tumor necrosis factor-α (TNF-α) on the secretion of prototype proinflammatory cytokine interleukin 6 (IL-6), compared to T-helper 1 [Th1; chemokine (C-X-C motif) ligand 10 (CXCL10)] or Th2 [chemokine (C-C motif) ligand 2 (CCL2)] chemokines, in primary cultured fibroblasts from patients with systemic sclerosis (SSc) at an early stage of the disease.Methods.Fibroblast cultures from 5 SSc patients (disease duration < 2 yrs) and 5 healthy controls were evaluated for the production of IL-6, CXCL10, and CCL2 at the basal level and after stimulation with IFN-γ and/or TNF-α.Results.SSc fibroblasts basally produced higher levels of IL-6 than controls, while no difference was observed about CCL2 and CXCL10. TNF-α was able to dose-dependently induce IL-6 and CCL2 secretion in SSc, but not in control fibroblasts. By stimulation with increasing doses of IFN-γ, SSc fibroblasts were induced to secrete CCL2 and CXCL10, while no effect was observed on IL-6. The combination of IFN-γ and TNF-α induced a strong secretion of IL-6 and CCL2 in SSc fibroblasts but not in controls. In contrast, the synergistic effect of IFN-γ and TNF-α on CXCL10 secretion was similar in SSc fibroblasts and in controls.Conclusion.SSc fibroblasts participate in the self-perpetuation of inflammation by releasing IL-6, CXCL10, and CCL2 under the influence of IFN-γ and/or TNF-α. SSc fibroblasts are more active than controls in the secretion of IL-6 at baseline, and in the production of IL-6 and CCL2 under the combined IFN-γ/TNF-α stimulation.

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