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 Induction of Interleukin-4 (IL-4) by Legionella pneumophila Infection in BALB/c Mice and Regulation of Tumor Necrosis Factor Alpha, IL-6, and IL-1β

2000 ◽  
Vol 68 (9) ◽  
pp. 5234-5240 ◽  
Author(s):  
Catherine Newton ◽  
Shannon McHugh ◽  
Ray Widen ◽  
Noriya Nakachi ◽  
Thomas Klein ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Legionella Pneumophila ◽  
Tumor Necrosis ◽  
Ex Vivo ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT Infection of BALB/c mice with a sublethal concentration ofLegionella pneumophila causes an acute disease that is resolved by innate immune responses. The infection also initiates the development of adaptive Th1 responses that protect the mice from challenge infections. To study the early responses, cytokines induced during the first 24 h after infection were examined. In the serum, interleukin-12 (IL-12) was detectable by 3 h and peaked at 10 h, while gamma interferon was discernible by 5 h and peaked at 8 h. Similar patterns were observed in ex vivo cultures of splenocytes. A transient IL-4 response was also detected by 3 h postinfection in ex vivo cultures. BALB/c IL-4-deficient mice were more susceptible to L. pneumophila infection than were wild-type mice. The infection induced higher serum levels of acute-phase cytokines (tumor necrosis factor alpha [TNF-α], IL-1β, and IL-6), and reducing TNF-α levels with antibodies protected the mice from death. Moreover, the addition of IL-4 to L. pneumophila-infected macrophage cultures suppressed the production of these cytokines. Thus, the lack of IL-4 in the deficient mice resulted in unchecked TNF-α production, which appeared to cause the mortality. Monocyte chemoattractant protein-1 (MCP-1), a chemokine that is induced by IL-4 during Listeria monocytogenesinfection, was detected at between 2 and 30 h after infection. However, MCP-1 did not appear to be induced by IL-4 or to be required for the TNF-α regulation by IL-4. The data suggest that the early increase in IL-4 serves to regulate the mobilization of acute phase cytokines and thus controls the potential harmful effects of these cytokines.

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 Destructive Arthritis in Vaccinated Interferon Gamma-Deficient Mice Challenged with Borrelia burgdorferi: Modulation by Tumor Necrosis Factor Alpha

2003 ◽  
Vol 10 (1) ◽  
pp. 44-52 ◽  
Author(s):  
John A. Christopherson ◽  
Erik L. Munson ◽  
Douglas M. England ◽  
Cindy L. Croke ◽  
Monica C. Remington ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Borrelia Burgdorferi ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT We found that Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-γ0) mice challenged with B. burgdorferi developed prominent chronic destructive osteoarthropathy. When these mice were treated with anti-tumor necrosis factor alpha (TNF-α) antibody, the severity of the destructive osteoarthritis was enhanced and affected the mobility of the animals. In addition, extensive swelling of the hind paws occurred. In contrast, treatment of B. burgdorferi-vaccinated, challenged IFN-γ0 mice with recombinant TNF-α (rTNF-α) inhibited the development of arthritis, including swelling of the hind paws. Moreover, treatment of vaccinated, challenged IFN-γ0 mice with anti-TNF-α inhibited fourfold the production of an antibody that kills B. burgdorferi, while treatment of vaccinated, challenged IFN-γ0 mice with rTNF-α slightly elevated the level of the borreliacidal antibody. These results suggest that the level of TNF-α directly or indirectly regulates the production of borreliacidal antibody and the development of vaccine-induced destructive Lyme osteoarthritis. Studies are in progress to determine the mechanism by which TNF-α-dependent cytokines generate the destructive arthritis.

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 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 Critical Role of the Complement System in Group B Streptococcus-Induced Tumor Necrosis Factor Alpha Release

2003 ◽  
Vol 71 (11) ◽  
pp. 6344-6353 ◽  
Author(s):  
Ofer Levy ◽  
Rochelle M. Jean-Jacques ◽  
Colette Cywes ◽  
Richard B. Sisson ◽  
Kol A. Zarember ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Alternative Pathway ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Group B ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT Group B Streptococcus (GBS) is a major cause of newborn sepsis and meningitis and induces systemic release of tumor necrosis factor alpha (TNF-α), believed to play a role in morbidity and mortality. While previous studies have shown that GBS can induce TNF-α release from monocytes and macrophages, little is known about the potential modulating effect of plasma or serum on GBS-induced TNF-α release, and there are conflicting reports as to the host receptors involved. In a human whole-blood assay system, GBS type III COH-1 potently induced substantial monocyte TNF-α release in adult peripheral blood and, due to a higher concentration of monocytes, 10-fold-greater TNF-α release in newborn cord blood. Remarkably, GBS-induced TNF-α release from human monocytes was enhanced ∼1,000-fold by heat-labile serum components. Experiments employing C2-, C3-, or C7-depleted serum demonstrated that C3 activation via the alternative pathway is crucial for potent GBS-induced TNF-α release. Accordingly, whole blood from C3-deficient mice demonstrated significantly reduced GBS-induced TNF-α release. Preincubation with human serum enhanced the TNF-α-inducing activity of GBS in a C3- and factor B-dependent manner, implying deposition of complement components via the alternative pathway. GBS-induced TNF-α release was inhibited by monoclonal antibodies directed against each of the components of CR3 and CR4: the common integrin β subunit CD18 and the α subunits CD11b (of CR3) and CD11c (of CR4). Blood derived from CR3 (CD11b/CD18)-deficient mice demonstrated a markedly diminished TNF-α response to GBS. We conclude that the ability of plasma and serum to greatly amplify GBS-induced TNF-α release reflects the activity of the alternative complement pathway that deposits fragments on GBS and thereby enhances CR3- and CR4-mediated monocyte activation.

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