scholarly journals Moderate Dose of Lipopolysaccharide Induces Tumor Necrosis Factor-alpha and Interleukin-6 Production by Human Monocyte-derived Macrophages

2021 ◽  
Vol 9 (A) ◽  
pp. 468-472
Author(s):  
Nuraiza Meutia ◽  
Lokot Donna Lubis ◽  
Eka Roina Megawati
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Human Monocyte ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

BACKGROUND: Macrophages have been widely used for in vitro studies. Despite different types and doses of stimulatory agents that have been tested, there is no consensus for the method. AIM: This study was aimed to determine a sufficient dose of lipopolysaccharide (LPS) to stimulate inflammatory response in macrophages. METHODS: Whole blood was collected from four donors after written informed consent. The monocytes were isolated from peripheral blood mononuclear cells and stimulated with macrophage colony-stimulating factor, LPS, and Interferon-gamma for 6 days until differentiated into macrophages. The production of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6) were quantified after 24-h further stimulation with 100 ng/mL and 2 μg/mL of LPS. RESULTS: Both doses increased TNF-α _production compare to their controls, but not statistically different (p > 0.05). There were also no differences in IL-6 production between treatments, 56.55 ± 32.30 pg/mL and 70.96 ± 65.08 pg/mL, respectively. CONCLUSION: A dose of 100 ng/mL of LPS was sufficient to stimulate inflammatory response in human monocyte-derived macrophages. A 24-h duration of macrophage stimulation was sufficient to observed the production TNF-α.

scholarly journals Shiga Toxin 1-Induced Inflammatory Response in Lipopolysaccharide-Sensitized Astrocytes Is Mediated by Endogenous Tumor Necrosis Factor Alpha

2009 ◽  
Vol 78 (3) ◽  
pp. 1193-1201 ◽  
Author(s):  
Verónica I. Landoni ◽  
Marcelo de Campos-Nebel ◽  
Pablo Schierloh ◽  
Cecilia Calatayud ◽  
Gabriela C. Fernandez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Brain Inflammation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Hemolytic-uremic syndrome (HUS) is generally caused by Shiga toxin (Stx)-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in HUS development. However, inflammatory mediators such as bacterial lipopolysaccharide (LPS) and polymorphonuclear neutrophils (PMN) contribute to HUS pathophysiology by potentiating Stx effects. Acute renal failure is the main feature of HUS, but in severe cases, patients can develop neurological complications, which are usually associated with death. Although the mechanisms of neurological damage remain uncertain, alterations of the blood-brain barrier associated with brain endothelial injury is clear. Astrocytes (ASTs) are the most abundant inflammatory cells of the brain that modulate the normal function of brain endothelium and neurons. The aim of this study was to evaluate the effects of Stx type 1 (Stx1) alone or in combination with LPS in ASTs. Although Stx1 induced a weak inflammatory response, pretreatment with LPS sensitized ASTs to Stx1-mediated effects. Moreover, LPS increased the level of expression of the Stx receptor and its internalization. An early inflammatory response, characterized by the release of tumor necrosis factor alpha (TNF-α) and nitric oxide and PMN-chemoattractant activity, was induced by Stx1 in LPS-sensitized ASTs, whereas activation, evidenced by higher levels of glial fibrillary acid protein and cell death, was induced later. Furthermore, increased adhesion and PMN-mediated cytotoxicity were observed after Stx1 treatment in LPS-sensitized ASTs. These effects were dependent on NF-κB activation or AST-derived TNF-α. Our results suggest that TNF-α is a pivotal effector molecule that amplifies Stx1 effects on LPS-sensitized ASTs, contributing to brain inflammation and leading to endothelial and neuronal injury.

scholarly journals Endogenous Interleukin-6 Plays a Crucial Protective Role in Streptococcal Toxic Shock Syndrome via Suppression of Tumor Necrosis Factor Alpha Production

2005 ◽  
Vol 73 (6) ◽  
pp. 3745-3748 ◽  
Author(s):  
Hongyan Diao ◽  
Masashi Kohanawa
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Protective Role ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT During a Streptococcus pyogenes infection in interleukin-6 (IL-6)-deficient mice, there is elevation of serum tumor necrosis factor alpha (TNF-α) levels, muscular necrosis, and death compared with infection of C57BL/6 mice. Anti-TNF-α monoclonal antibody treatment decreased mortality and muscular necrosis in the infected IL-6-deficient mice. These results suggest that IL-6 plays a crucial protective role via suppression of TNF-α production in S. pyogenes infection.

scholarly journals RESPON ADAPTASI MOLEKULER IMUNITAS TUBUH PENDUDUK YANG BERADA DI LINGKUNGAN TERPAPAR POLUSI UDARA

2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Mohammad Zulkarnain ◽  
Rostika Flora
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Latar Belakang: Perindustrian di berbagai wilayah dunia telah berpengaruh terhadap polusi ataupencemaran udara. Paparan polusi udara secara terus-menerus dapat mengakibatkan penurunan sistem imun.Tujuan penelitian ini adalah untuk mengetahui respon molekuler imunitas tubuh penduduk yang berada dilingkungan terpapar polusi udara.Metode: Jenis penelitian ini adalah observasional analitik dengan rancangan cross sectional. Populasipenelitian ini adalah seluruh masyarakat yang tinggal di sekitar Pabrik Karet Gandus dan TPA sampahSukawinatan Palembang yang berjumlah 60 orang yang memenuhi kriteria inklusi. Pemeriksaan kadar TNF-α dan IL-6 menggunakan teknik ELISA Human kit, pengukuran kadar H2S dilakukan pada jarak 250 meter,dengan metode biru metilen.Hasil Penelitian: Kadar H2S di sekitar TPA Sampah Sukawinatan (0,428 ppm) lebih tinggi dibandingkankadar H2S disekitar Pabrik Karet Gandus (0,332 ppm). Tidak terdapat perbedaan yang bermakna rerata kadarTNF-α (p=0,701) dan rerata kadar IL-6(p=0,618) antara kedua lokasi. Nilai korelasi karakteristik respondendengan kadar TNF-α dan kadar IL-6 di dua lokasi penelitian sangat lemah dan tidak bermakna secarastatistik. Nilai korelasi antara dengan IL-6 sangat lemah dan tidak bermakna secara statistik di sekitar PabrikKaret Gandus (r= 0,284; p=0,128) dan di sekitar TPA sampah Sukawinatan (r=-0,258;p=0,169).Kesimpulan: Meskipun kadar H2S di sekitar TPA Sampah Sukawinatan lebih tinggi, diharapkan pendudukyang berada disekitar Pabrik karet dan TPA sampah menggunakan alat pelindung diri seperti masker saatberada diluar rumah dan menjaga asupan nutrisi dengan baik agar kekebalan tubuh terjaga.Kata kunci: Hidrogen Sulfida, tumor necrosis factor-alpha, interleukin-6.

scholarly journals Changes in the Levels of Pro-Inflammatory Cytokines in Patients with Generalized Periodontitis and Hypertension, Depending on the Method of Treatment

2017 ◽  
Vol 24 (4) ◽  
Author(s):  
T. Vicharenko ◽  
M. Rozhko
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines

Inflammatory mediators have an important role in the pathogenesis of periodontal disease. One of the leading mediators of the initiation of the pathological process is interleukin-1 (IL-1) – an endogenous pyrogen, a lymphocyte-activating factor. Numerous pro-inflammatory effects of interleukin-1β (IL-1β) occur in synergy with tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), effects on hematopoiesis, participates in nonspecific anti-infective defense.The objective of the study is to determine levels of interleukin-6 and tumor necrosis factor alpha (TNF-α) in patients with hypertension II stage and generalized periodontitis of the II degree depending on the treatment method.There were examined 30 patients with hypertension of the II stage and with generalized periodontitis of the II degree. Patients’ age ranged from 35 to 54 years. These patients were divided into two groups. The control group included 10 patients without general somatic pathology and with healthy periodontitis of the same age. The result of the analysis of tumor necrosis factor alpha (TNF-α) in patients in the first group before the treatment was 10.69±2.33 pg/ml. After the treatment this indicator was 6.97±1.57 pg/ml (p>0.1) in patients of the first group.In patients of the second group the tumor necrosis factor alpha (TNF-α) was 9.49±2.2 pg/ml; after the treatment according to the offered scheme this figure decreased up to 2.77±0.9 pg/ml (p<0.01). The level of tumor necrosis factor alpha (TNF-α) in the control group was 1.5±0.77 pg/ml.Interleukin-6 was 9.91±2.04 pg/ml before the treatment in the first group. After the treatment according to the standard scheme, the level of interleukin-6 was 6.33±0.97 pg/ml (p>0.1). In the second group, before the treatment the level of  interleukin-6 was 9.65±2.41 pg/ml; after the treatment according to the offered scheme it was 2.62±0.5 pg/ml (p<0.01). In the control group the interleukin-6 level was 2.24±0.51 pg/ml.Analyzing the obtained results after the treatment in both groups we can conclude: after the treatment of generalized periodontitis of the II degree in patients with hypertension of the II stage, indices of pro-inflammatory cytokines decreased and ranged in normal limits; in patients from the second group (who received the offered scheme of treatment -including medicines) indexes of pro-inflammatory cytokines were significantly lower than in patients with the standard treatment scheme; the proposed scheme of treatment is more effective for treatment patients with generalized periodontitis of the II degree and hypertension of the II stage.

scholarly journals Local Role for Tumor Necrosis Factor Alpha in the Pulmonary Inflammatory Response to Mycobacterium tuberculosis Infection

2002 ◽  
Vol 70 (4) ◽  
pp. 2082-2089 ◽  
Author(s):  
Sherilyn Smith ◽  
Denny Liggitt ◽  
Elizabeth Jeromsky ◽  
Xiaoxia Tan ◽  
Shawn J. Skerrett ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The local intrapulmonary role of tumor necrosis factor alpha (TNF-α) in a protective host response during acute and chronic infection with Mycobacterium tuberculosis is incompletely understood. To directly assess its role in the intrapulmonary immune response, we compared the responses of transgenic mice with a local pulmonary blockade of TNF-α (SPCTNFRIIFc mice) to mice with globally inhibited TNF-α (TNFRKO mice) and mice with normal immune systems (control mice). Consistent with previous reports, 100% of TNFRKO mice died by 28 days after aerosol infection, and these mice had markedly increased numbers of bacteria and widespread tissue necrosis in their lungs compared to controls. The median survival time of the SPCTNFRIIFc mice was 142 days, and 75% died by 180 days. Even though the numbers of bacteria in the lungs of the SPCTNFRIIFc mice were marginally increased compared to controls, these mice had a persistent neutrophilic inflammatory response and increased expression of proinflammatory cytokines (interleukin-1α/β [IL-1α/β], IL-18, gamma interferon, IL-6, and macrophage migration inhibitory factor) and chemokines (eotaxin, macrophage inflammatory protein 1α/β, gamma interferon-inducible protein 10, macrophage chemotaxic protein 1, and TCA-3) in their lungs. These studies with the SPCTNFRIIFc mice provide direct evidence for the local importance of TNF-α in the proper regulation of host defense to M. tuberculosis. The studies also suggest that when the local actions of TNF-α are selectively impaired in the lungs, tissue destruction and death ensue, at least in part, due to persistent expression of proinflammatory mediators that would normally be downregulated.

scholarly journals EVALUATION OF SERUM INTERLEUKIN-6 AND TUMOR NECROSIS FACTOR-ALPHA LEVELS IN PATIENTS WITH DENGUE FEVER – A TERTIARY CARE HOSPITAL BASED STUDY

2020 ◽  
pp. 185-187
Author(s):  
ROHIN DUBBAL ◽  
SRIRAM BS
Keyword(s):  
Tumor Necrosis Factor ◽  
Dengue Fever ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Dengue Infection ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Objective: The objective of the study was to evaluate the levels of serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) during the course of 3rd and 5th days of dengue infection. Methods: The prospective cohort study was taken up involving 50 adults diagnosed with dengue fever and admitted to Mysore Medical College and Research Institute from December 2015 to November 2016. Detailed history has been taken and clinical examination was carried out. Venous blood sample was collected and serum separated out for estimation of IL-6 and TNF-α levels using ELISA. Results: It has been observed that the levels of IL-6 and TNF-α raised during 3rd day of infection and there is decrease in levels of IL-6 and no changes have been observed in TNF-α levels during 5th day. Conclusion: The study concludes that the IL-6 and TNF-α plays a key role in understanding pathogenesis of severity of dengue infection, TNF-α being more sensitive in reaction to pathogen

scholarly journals Estimation the levels of interleukin 6 and tumor necrosis factor-alpha patients with diabetic type 2 in Tikrit city

2019 ◽  
Vol 24 (4) ◽  
pp. 8
Author(s):  
Muhannad E. Majeed1 ◽  
Mousa M. Marbut2
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Diabetic Patients ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Type 2 is the most common metabolic disorder characterized by the increased  concentration of glucose in blood  due to insulin resistance or relative insulin deficiency. Changes in human behavior and lifestyle over the last century have resulted in a dramatic increase in the incidence of diabetes worldwide. Interleukin 6 is pro inflammatory cytokines  secreted by immune cells, adipose tissue , Muscles  is able to accelerate or inhibit the inflammatory processes .High circulating IL-6 levels have been associated with insulin resistance and greater risk of T2DM . 80 patients with type 2 diabetes mellitus (40 male and 40 female )are diagnosed  by specialized in medicine  in general Salah- Aldin  Hospital in Tikrit city and 40 apparently healthy  Controls (20 male and 20 female ) were included in this study  This study carried out in Tikrit city from 1st October 2017 to 1st of April 2018  Anthropometric measures include, Age ,  BMI , were done for all participants  Fasting serum samples were obtained and used for the measurement of serum glucose Interleukin- 6 (IL-6) and Tumor necrosis factor alpha (TNF-α) . The results of current study showed that Fasting serum glucose (FBS), Interleukin-6 (IL-6), Tumor necrosis factor alpha (TNF-α) are High significant increase (p<0.01) in diabetic patients when compared to control group. In Conclusion, serum interleukin -6 (IL-6) and Tumor necrosis factor – alpha (TNF-α) has high significant increases level in diabetic patients compared to control.   http://dx.doi.org/10.25130/tjps.24.2019.063

scholarly journals Tumor Necrosis Factor Alpha Signaling and Organogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Kai You ◽  
Hui Gu ◽  
Zhengwei Yuan ◽  
Xuewen Xu
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Embryonic Stem ◽  
Inflammatory Factor ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-α) plays important roles in processes such as immunomodulation, fever, inflammatory response, inhibition of tumor formation, and inhibition of viral replication. TNF-α and its receptors are ubiquitously expressed in developing organs and they regulate the survival, proliferation, and apoptosis of embryonic stem cells (ESCs) and progenitor cells. TNF-α is an important inflammatory factor that also regulates the inflammatory response during organogenesis, and its cytotoxic effects can interfere with normal developmental processes, even leading to the onset of diseases. This review summarizes the various roles of TNF-α in organogenesis in terms of its secreting pattern, concentration-dependent activities, and interactions with other signaling pathways. We also explored new potential functions of TNF-α.

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