scholarly journals Induction of matrix metalloproteinase-1 by tumor necrosis factor-α is mediated by interleukin-6 in cultured fibroblasts of keratoconus

2016 ◽  
Vol 241 (18) ◽  
pp. 2033-2041 ◽  
Author(s):  
Genlai Du ◽  
Chengxing Liu ◽  
Xiaona Li ◽  
Weiyi Chen ◽  
Rui He ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Molecules ◽  
Necrosis Factor

Inflammatory molecules and matrix metalloproteinase (MMPs) have been found over-expressed in the tear film of patients with keratoconus. However, the mechanistic link between inflammatory molecules and MMPs in the pathogenesis of keratoconus remains still elusive. Therefore, we investigated the effect of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) on MMP-1 expression and used IL-6 antibody (IL-6 Ab) to examine the role of IL-6 on TNF-α mediated regulation of MMP-1 in fibroblasts of normal cornea and keratoconus. Real-time polymerase chain reaction, Enzyme-linked immunosorbent assay, and Western blot data demonstrated that MMP-1 and IL-6 were expressed in fibroblasts of normal cornea and keratoconus. Levels of MMP-1 and IL-6 were significantly higher in keratoconus than normal cornea. TNF-α treatment led to a significant increase in IL-6 levels. IL-6 treatment induced MMP-1 synthesis in normal cornea and keratoconus. TNF-α increased MMP-1 expression in a dose- and time-dependent manner and this response was completely inhibited by the IL-6 Ab. In conclusion, these results indicate that fibroblasts of keratoconus shows increased levels of IL-6 and MMP-1 gene and protein expression and IL-6 mediates the TNF-α-induced MMP-1 expression.

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 PROFIL TNF-α SESUDAH SENAM LANSIA PADA LANSIA DI PANTI WREDHA BETHANIA LEMBEAN KOTA MANADO

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Michael Tulong ◽  
Siantan Supit ◽  
Joice N. A. Engka
Keyword(s):  
Informed Consent ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Enzyme Linked Immunosorbent Assay ◽  
Test Design ◽  
Tnf Α ◽  
Post Test ◽  
Factor Α ◽  
Necrosis Factor

Abstract: Tumor Necrosis Factor- α (TNF-α) is a systemic pro-inflammatory cytokine which is responsible to a trauma, injury, or inflammation in human body. Physical activity can physiologically affect the human body, inter alia the immune system. This was an experimental study with a post test design. This study aimed to determine the profile of TNF-α after doing gymnastics among the elderly at nursing home Bethania Lembean. Samples included 30 peoples who met the inclusion criteria, i.e. over 64 years old, followed the gymnastics for 5 weeks regularly, approbated as respondents, healthy, and signed the informed consent. The TNF-α concentration measurements were done by using enzyme-linked immunosorbent assay (ELISA) Quantikine ®Human TNF-α. The results showed that the average conventration of TNF-α after elderly gymnastics was 70.54 pg/ml, with the highest value of 88.90 pg/mL and the lowest value of 12.54 pg/mL. For all respondents, TNF-α was within normal limit and ranged between 10-100 pg / mL. Conclusion: In this study, TNF-α concentrations after elderly gymnastics for 5 weeks were within normal limitsKeywords: TNF-α, elderly gymnasticsAbstrak: Tumor Necrosis Factor-α (TNF-α) merupakan suatu sitokin sistemik pro-inflamasi, yang berespons terhadap suatu cedera trauma atau peradangan yang terjadi dalam tubuh manusia. Kegiatan fisik dapat berdampak cukup besar pada tubuh manusia, dimana dapat merubah sistem imun tubuh secara fisiologis. Penelitian ini bersifat eksperimental dengan rancangan post test design dan bertujuan untuk mengetahui profil TNF-α sesudah senam lansia di Panti Wredha Bethania Lembean. Sampel penelitian berjumlah 30 orang yang memenuhi kriteria inklusi yaitu berumur di atas 64 tahun, teratur mengikuti senam lansia selama 5 minggu, bersedia menjadi responden, sehat saat di periksa, dan menandatangani informed consent. Pengukuran konsentrasi TNF-α di lakukan dengan menggunakan enzyme-linked immunosorbent assay (ELISA) Quantikine ®Human TNF-α. Hasil penelitian memperlihatkan bahwa rerata kadar TNF-α sesudah senam lansia 70,54 pg/ml, dengan nilai tertinggi 88,90 pg/mL dan nilai terendah 12,54 pg/mL. Berdasarkan hasil yang di dapat, semua kadar TNF-α masih dalam batas normal dengan nilai 10-100 pg/mL. Simpulan: TNF-α sesudah senam lansia selama 5 minggu masih dalam batas normal.Kata kunci:TNF-α, senam lansia

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