Cloning and phylogenetic analysis of Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) from Indian dromedaries (Camelus dromedarius)

2011 ◽  
Vol 34 (3) ◽  
pp. 291-298
Author(s):  
G. Nagarajan ◽  
Shelesh Kumar Swami ◽  
S.K. Ghorui ◽  
K.M.L. Pathak ◽  
R.K. Singh ◽  
...  
Keyword(s):  
Phylogenetic Analysis ◽  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Camelus Dromedarius ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment

1995 ◽  
Vol 132 (6) ◽  
pp. 668-672 ◽  
Author(s):  
Ismail Çelik ◽  
Sema Akalin ◽  
Tomris Erbaş
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Serum Levels ◽  
Graves Disease ◽  
Tnf Α ◽  
Factor Α ◽  
Hyperthyroid Patients ◽  
Necrosis Factor

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

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

2012 ◽  
Vol 39 (5) ◽  
pp. 979-985 ◽  
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.

scholarly journals Free Cholesterol-loaded Macrophages Are an Abundant Source of Tumor Necrosis Factor-α and Interleukin-6

2005 ◽  
Vol 280 (23) ◽  
pp. 21763-21772 ◽  
Author(s):  
Yankun Li ◽  
Robert F. Schwabe ◽  
Tracie DeVries-Seimon ◽  
Pin Mei Yao ◽  
Marie-Christine Gerbod-Giannone ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Free Cholesterol ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Vulnerable Plaques ◽  
Iκb Kinase ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Two key features of atherosclerotic plaques that precipitate acute atherothrombotic vascular occlusion (“vulnerable plaques”) are abundant inflammatory mediators and macrophages with excess unesterified, or “free,” cholesterol (FC). Herein we show that FC accumulation in macrophages leads to the induction and secretion of two inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). The increases in TNF-α and IL-6 mRNA and protein were mediated by FC-induced activation of the IκB kinase/NF-κB pathway as well as activation of MKK3/p38, Erk1/2, and JNK1/2 mitogen-activated protein kinases (MAPK). Activation of IκB kinase and JNK1/2 was needed for the induction of both cytokines. However, MKK3/p38 signaling was specifically involved in TNF-α induction, and Erk1/2 signaling was required for IL-6. Most interestingly, activation of all of the signaling pathways and induction of both cytokines required cholesterol trafficking to the endoplasmic reticulum (ER). The CHOP branch of the unfolded protein response, an ER stress pathway, was required for Erk1/2 activation and IL-6 induction. In contrast, one or more other ER-related pathways were responsible for activation of p38, JNK1/2, and IκB kinase/NF-κB and for the induction of TNF-α. These data suggest a novel scenario in which cytokines are induced in macrophages by endogenous cellular events triggered by excess ER cholesterol rather than by exogenous immune cell mediators. Moreover, this model may help explain the relationship between FC accumulation and inflammation in vulnerable plaques.

scholarly journals Perbedaan Kadar Leptin pada Anak yang Menderita Infeksi Dengue

Sari Pediatri ◽  
2016 ◽  
Vol 15 (1) ◽  
pp. 1
Author(s):  
Anggia Farrah Rizqiamuti ◽  
Sri Endah Rahayuningsih ◽  
Dedi Rachmadi ◽  
Rachmat Budi
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Latar belakang. Infeksi dengue merupakan infeksi akut yang dapat mempengaruhi kadar leptin. Perbedaan spectrum klinis infeksi dengue menyebabkan perbedaan kadar interleukin-6 (IL-6) dan tumor necrosis factor-α(TNF-α). Tujuan. Mengetahui perbedaan kadar leptin pada anak yang menderita infeksi dengue.Metode.Penelitian analitik dengan rancangan potong lintang. Subjek penelitian adalah pasien DB, DBD, dan SSD (pascasyok) yang memenuhi kriteria klinis dan telah dibuktikan melalui pemeriksaan serologis. Analisis data menggunakan uji Kruskal Wallis dan Mann-Whitney untuk menentukan perbedaan kadar leptin pada DB dengan DBD dan SSD.Hasil. Pasien infeksi dengue 48 anak terdiri dari 27 DB, 11 DBD, dan 10 SSD. Terdapat perbedaan bermakna kadar leptin antara DB dengan DBD, dan SSD p=0,002. Rerata kadar leptin pada DD 703,4 (374,1–3616,7), DBD 2.172 (554,3–16631,1), dan SSD 1.321 (250,5–4.714,6). ng/mL Kadar leptin DBD lebih tinggi dibandingkan dengan DD (p<0,001), namun kadar leptin antara DBD dan SSD tidak berbeda bermakna (p=0,132) dan kadar leptin antara SSD (postsyok) dan DD tidak berbeda bermakna (p=0,158).Kesimpulan. Kadar leptin pada DBD lebih tinggi dibandingkan dengan DD, sedangkan kadar leptin antara DBD dan SSD (postsyok) tidak berbeda.

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

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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