scholarly journals Is There a Difference between the Preoperative and Postoperative Serum Levels of Interleukin-6 and Tumor Necrosis Factor-α in Children Submitted to Adenotonsillectomy?

2021 ◽  
Author(s):  
Jose Neto Ribeiro de Souza ◽  
Fernanda de Oliveira Feitosa de Castro ◽  
Camila Lemes de Souza ◽  
Mikhael Romanholo El Cheikh ◽  
Hugo Valter Lisboa Ramos ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Recurrent Tonsillitis ◽  
Tnf Α ◽  
Factor Α ◽  
Prospective Longitudinal ◽  
Necrosis Factor

Abstract Introduction Palatine and pharyngeal tonsils are the first line of defense against pathogens. Clinically, two alterations may require surgical removal of the tonsils: hypertrophy and recurrent tonsillitis. The two conditions probably result from a dysfunction of the immune system. Objective To evaluate possible differences in the plasma levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) in patients submitted to adenotonsillectomy. Methods Prospective, longitudinal study with 25 children undergoing adenotonsillectomy separated into 3 different groups: recurrent tonsillitis (RT), composed of 7 patients; recurrent hypertrophy tonsillitis (RTTH), with 8 patients; and the tonsillar hypertrophy (TH) group, with 10 patients. Ten healthy control children (SD) were also included in the study. Peripheral blood was collected, and plasma was separated to measure the levels of TNF-α, IL-6, and IL-10. The Mann-Whitney test was used for statistical analysis. Results The plasma level of IL-6 was higher in the RT (p = 0.0394) and TH (p = 0.0009) groups, compared with the control group. The TH group also had higher levels of IL-6 than the RT group (p = 0.039). The IL-6/IL-10 ratio was higher in the RT (p = 0.029) and TH (p = 0.0005) groups compared with the control group. Between the RT and RTTH groups, the IL-6/IL-10 ratio was higher in the RT group, with a statistically significant difference (p = 0.0091). Conclusion Patients with a history of chronic tonsillitis had higher levels of IL-6, compared with the control group.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

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 The Effect of Slow Stroke Back Massage on Primary Dysmenorrhea: Levels of Beta-Endorphin, Interleukin-6, Tumor Necrosis Factor-α, and Pain Intensity

2020 ◽  
Vol 8 (4) ◽  
pp. 376-382
Author(s):  
Mukhoirotin Mukhoirotin??? ◽  
Kurniawati Kurniawati??? ◽  
Herin Mawarti
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Primary Dysmenorrhea ◽  
Menstrual Pain ◽  
Factor Α ◽  
And Control ◽  
Necrosis Factor

Objectives: Dysmenorrhea is one of several gynecological issues that occur among women of reproductive age. In addition, it appears as pain that forms in the pelvis or lower abdomen and spreads to the back and thighs. The peripheral blood among women with dysmenorrhea increases the synthesis and the concentration of oxytocin, F2α prostaglandin hormone, vasopressin, interleukin-6 (IL-6), and tumor necrosis factor-α (TNFα). In this regard, this study aimed to determine the effect of slow-stroke back massage (SSBM) on the levels of β-endorphins, IL-6, TNF-α, and menstrual pain intensity (MPI). Materials and Methods: Based on the aim of the study, the posttest only quasi-experimental method with the control group design approach, pretest-posttest control group approach, and purposive sampling techniques were applied for sample selection. The samples were divided into SSBM and control groups each containing 20 subjects. The numeric rating scale (NRS), β-endorphin, IL-6, and TNFα levels were measured using the indirect enzyme-linked immunosorbent assay. Then, data were analyzed by paired sample t test and independent-samples t test with α ≤ 0.05. Results: The results revealed that SSBM had an effect on the intensity of menstrual pain (P<0.05), and differences were found between β-endorphin levels, IL-6, TNFα, and MPI among SSBM and control (P<0.05) groups. Accordingly, SSBM can stimulate releasing β-endorphin levels and reducing pro-inflammatory cytokines (IL-6 and TNFα). Conclusions: In general, SSBM is a nonpharmacological action that is effective in primary dysmenorrhea.

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 Incidence of Toxoplasmosis in Psoriasis Patients and Possible Correlation with Tumor Necrosis Factor-α

2020 ◽  
Vol 17 (1(Suppl.)) ◽  
pp. 0214
Author(s):  
Entsar J. Saheb ◽  
Yasser A.H Al-Issa ◽  
Israa Salim Mussa ◽  
Khawla H. Zghair
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
City Hospital ◽  
Tnf Α ◽  
Medical City ◽  
Positive Rate ◽  
Factor Α ◽  
Necrosis Factor

            Toxoplasma gondii is an opportunistic parasite in immune-compromised persons. The prevalence of toxoplasmosis in psoriasis patients is investigated. In addition, the treatment effect on psoriasis patients infected with toxoplasmosis through evaluating Tumor Necrosis Factor-α (TNF-α) cytokine levels is studied. Blood samples were collected from 130 individuals who involved 60 control samples and 70 samples with psoriasis. They attended Medical City Hospital in Baghdad province from October 2017 - February 2018. Then, the anti- T. gondii antibodies (IgM and IgG) and TNF- α in the sera were determined via the enzyme linked immune-sorbent assay. The highest rate of anti-Toxoplasma IgG was in psoriasis patients before treatment, it was 45 (64.29%) compared with the control which was 33 (55.00%), while the highest sero-positive rate of T. gondii IgM in the control group was 14 (23.33%) compared with patients with psoriasis 10 (14.29%). The highest rate of toxoplasmosis was in the age group (21-30) years in psoriasis patients which was 14 (31.82%). In addition, the TNF- α levels in psoriatic patients before treatment were 180.2±2.2 µg/ml, and after treatment were 223.3±41.1 µg/ml compared with the healthy control group 90.5±1.9 µg/ml. These findings suggest that incidental rate of toxoplasmosis is higher in psoriasis patients. Thus, the incidental rate of toxoplasmosis could be considered as an indication to the high risk of psoriasis.

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