scholarly journals Hubungan ekspresi Tumor Necrosis Factor Alpha (TNF-α) dengan destruksi tulang akibat kolesteatoma

2015 ◽  
Vol 45 (1) ◽  
pp. 36 ◽  
Author(s):  
Sara Yosephine Aruan ◽  
Askaroellah Aboet ◽  
Devira Zahara ◽  
Aliandri Aliandri ◽  
Abdul Rachman Saragih
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Bone Destruction ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Tnf Α ◽  
Factor Alpha ◽  
Cross Sectional Design ◽  
Necrosis Factor

Latar belakang: Kolesteatoma merupakan penyakit yang menyebabkan destruksi tulang dan  komplikasi yang berbahaya. Tumor Necrosis Factor Alpha (TNF-a) merupakan sitokin utama yang terlibatdalam proses tersebut. Tujuan: Mengetahui hubungan ekpresi TNF-a dengan destruksi tulang akibatkolesteatoma pada penderita Otitis Media Supuratif Kronis (OMSK)  tipe bahaya. Metode: Penelitian inimerupakan penelitian analitik dengan menggunakan cross sectional design. Pemeriksaan imunohistokimiadilakukan untuk menilai ekspresi TNF-a pada kolesteatoma. Hasil: Ekspresi TNF-a yang positif/overexpressionlebihbanyakpada kelompok destruksi tulang derajat sedang yaitu sebanyak 57,9%. Terdapathubunganyang bermakna antara ekspresi TNF-adengan derajat destruksitulang (p=0,001).Kesimpulan:Terdapathubungan antara ekspresi TNF-adengandestruksi tulang akibat kolesteatoma padapenderitaOMSKtipe bahaya. Kata kunci: TNF-a, Destruksi tulang, Kolesteatoma, OMSKABSTRACT Background: Cholesteatoma is a disease which promotes bone destruction resulting in potentially serious complication.  The Tumor Necrosis Factor Alpha (TNF-a) is one of the main cytokine involvedin this process. Purpose: To find out the relationship between TNF-a expression and bone destruction indangerous type of CSOM. Method: This is a cross sectional analytical research. Thirty cholesteatomasamples were observed by immunohistochemical  examination for  TNF-a expression. Result: We foundover-expression of TNF-a in the group with moderate bone destruction (57.9%). There was a significantdifference between TNF-a expression with the degree of bone destruction (p=0,001). Conclusion: Therewas an association between TNF-a expression with   bone destruction in dangerous type of CSOM. Keywords: TNF-a, Bone destruction, Cholesteatoma, CSOM

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 Assessment of tumor necrosis factor- alpha in gingivitis and periodontitis patients

2017 ◽  
Vol 5 (2) ◽  
pp. 108 ◽  
Author(s):  
Sajeev Shrestha ◽  
Manisha Neupane ◽  
Shivalal Sharma ◽  
Madhab Lamsal
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pocket Depth ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Tumor necrosis factor-α, one of the cytokines, is released in various chronic inflammatory diseases including periodontitis.Aims: To estimate the level of Tumor necrosis factor- alpha (TNF-α) in gingivitis and periodontitis patientsSettings and Design: A cross-sectional study was conducted. A total of 75 patients were recruited by purposive sampling technique among the patients visiting the Department of Periodontology and Oral Implantology during the period one year from August 2014 to July 2015.Material and methods: The recruited samples were divided into gingivitis and periodontitis groups based on clinical attachment level (CAL). A periodontitis subject was defined as having at least 4 sites with pocket depth (PD) >3mm and at least 4 sites with CAL>3 mm, while gingivitis group included the subjects having no CAL measurements greater than 3 mm with signs of inflammation. The TNF-α level was measured using the RayBio Human TNF-alpha ELISA (Enzyme-linked Immunosorbent Assay) kit.Results: The Median TNF-α interquartile range (IQR) (minimum-maximum) in gingivitis and periodontitis was 58.37 (32.63 – 198.77) and 111.89 (39.27 – 215.0) pg/ml, respectively.Conclusion: The level of TNF-α was found to be higher in periodontitis group compared to gingivitis group, although the result was not statistically significant.

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

scholarly journals Analysis of Subcellular RNA Fractions Revealed a Transcription-Independent Effect of Tumor Necrosis Factor Alpha on Splicing, Mediated by Spt5

2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Independent Effect ◽  
Necrosis Factor Alpha ◽  
Pol Ii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Genes ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) modulates the expression of many genes, primarily through activation of NF-κB. Here, we examined the global effects of the elongation factor Spt5 on nascent and mature mRNAs of TNF-α-induced cells using chromatin and cytosolic subcellular fractions. We identified several classes of TNF-α-induced genes controlled at the level of transcription, splicing, and chromatin retention. Spt5 was found to facilitate splicing and chromatin release in genes displaying high induction rates. Further analysis revealed striking effects of TNF-α on the splicing of 25% of expressed genes; the vast majority were not transcriptionally induced. Splicing enhancement of noninduced genes by TNF-α was transient and independent of NF-κB. Investigating the underlying basis, we found that Spt5 is required for the splicing facilitation of the noninduced genes. In line with this, Spt5 interacts with Sm core protein splicing factors. Furthermore, following TNF-α treatment, levels of RNA polymerase II (Pol II) but not Spt5 are reduced from the splicing-induced genes, suggesting that these genes become enriched with a Pol II-Spt5 form. Our findings revealed the Pol II-Spt5 complex as a highly competent coordinator of cotranscriptional splicing.

scholarly journals HSP70 Induction by ING Proteins Sensitizes Cells to Tumor Necrosis Factor Alpha Receptor-Mediated Apoptosis

2006 ◽  
Vol 26 (24) ◽  
pp. 9244-9255 ◽  
Author(s):  
Xiaolan Feng ◽  
Shirin Bonni ◽  
Karl Riabowol
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Kinase Inhibitor ◽  
Heat Shock Gene ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Primary Fibroblasts ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT ING proteins affect apoptosis, growth, and DNA repair by transducing stress signals such as DNA damage, binding histones, and subsequently regulating chromatin structure and p53 activity. p53 target genes, including the p21 cyclin-dependent kinase inhibitor and Bax, an inducer of apoptosis, are regulated by ING proteins. To identify additional targets downstream of p33ING1 and p32ING2, cDNA microarrays were performed on phenotypically normal human primary fibroblasts. The 0.36% of genes affected by ING proteins in primary fibroblasts were distinct from targets seen in established cells and included the HSP70 heat shock gene, whose promoter was specifically induced >10-fold. ING1-induced expression of HSP70 shifted cells from survival to a death pathway in response to tumor necrosis factor alpha (TNF-α), and p33ING1b protein showed synergy with TNF-α in inducing apoptosis, which correlated with reduced NF-κB-dependent transcription. These findings are consistent with previous reports that HSP70 promotes TNF-α-mediated apoptosis by binding I-κΒ kinase gamma and impairing NF-κB survival signaling. Induction of HSP70 required the amino terminus of ING1b but not the plant homeodomain region that was recently identified as a histone binding domain. Regulation of HSP70 gene expression by the ING tumor suppressors provides a novel link between the INGs and the stress-regulated NF-κB survival pathway important in hypoxia and angiogenesis.

scholarly journals Comparative Analysis of Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Activity in Serum and Lethality in Mice and Rabbits Pretreated with the Staphylococcal Superantigen Toxic Shock Syndrome Toxin 1

2001 ◽  
Vol 69 (11) ◽  
pp. 7169-7172 ◽  
Author(s):  
Martin M. Dinges ◽  
Patrick M. Schlievert
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Host Susceptibility ◽  
Necrosis Factor Alpha ◽  
Lethal Effects ◽  
Tnf Α ◽  
Factor Alpha ◽  
Toxic Shock Syndrome Toxin ◽  
Necrosis Factor

ABSTRACT Host susceptibility to lipopolysaccharide (LPS) is correlated with the levels of circulating tumor necrosis factor alpha (TNF-α) that develop in response to circulating LPS. Mice are resistant, relative to rabbits, to the lethal effects of LPS. This study indicates that mice and rabbits are equally sensitive to the lethal effects of circulating TNF-α but that mice are more resistant than rabbits to the induction of circulating TNF-α by LPS.

scholarly journals Major Outer Membrane Protein Omp25 of Brucella suis Is Involved in Inhibition of Tumor Necrosis Factor Alpha Production during Infection of Human Macrophages

2001 ◽  
Vol 69 (8) ◽  
pp. 4823-4830 ◽  
Author(s):  
Véronique Jubier-Maurin ◽  
Rose-Anne Boigegrain ◽  
Axel Cloeckaert ◽  
Antoine Gross ◽  
Maria-Teresa Alvarez-Martinez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Macrophage Infection ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Tnf Α ◽  
Brucella Suis ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Brucella spp. can establish themselves and cause disease in humans and animals. The mechanisms by whichBrucella spp. evade the antibacterial defenses of their host, however, remain largely unknown. We have previously reported that live brucellae failed to induce tumor necrosis factor alpha (TNF-α) production upon human macrophage infection. This inhibition is associated with a nonidentified protein that is released into culture medium. Outer membrane proteins (OMPs) of gram-negative bacteria have been shown to modulate macrophage functions, including cytokine production. Thus, we have analyzed the effects of two major OMPs (Omp25 and Omp31) of Brucella suis 1330 (wild-type [WT] B. suis) on TNF-α production. For this purpose, omp25and omp31 null mutants of B. suis(Δomp25 B. suis and Δomp31 B. suis, respectively) were constructed and analyzed for the ability to activate human macrophages to secrete TNF-α. We showed that, in contrast to WTB. suis or Δomp31 B. suis, Δomp25 B. suis induced TNF-α production when phagocytosed by human macrophages. The complementation of Δomp25 B. suis with WT omp25 (Δomp25-omp25 B. suis mutant) significantly reversed this effect: Δomp25-omp25 B. suis-infected macrophages secreted significantly less TNF-α than did macrophages infected with the Δomp25 B. suismutant. Furthermore, pretreatment of WT B. suis with an anti-Omp25 monoclonal antibody directed against an epitope exposed at the surface of the bacteria resulted in substancial TNF-α production during macrophage infection. These observations demonstrated that Omp25 of B. suis is involved in the negative regulation of TNF-α production upon infection of human macrophages.

scholarly journals Gamma Interferon and Lipopolysaccharide Interact at the Level of Transcription To Induce Tumor Necrosis Factor Alpha Expression

2001 ◽  
Vol 69 (5) ◽  
pp. 2847-2852 ◽  
Author(s):  
Julia Y. Lee ◽  
Kathleen E. Sullivan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Necrosis Factor Alpha ◽  
Rnase Protection ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Lipopolysaccharide (LPS) is a very potent inducer of tumor necrosis factor alpha (TNF-α) expression from monocytes and macrophages. Another inflammatory cytokine, gamma interferon (IFN-γ), can potentiate the effects of LPS, but the mechanism is not thoroughly understood. Previous reports emphasized the ability of IFN-γ to upregulate CD14 expression (the receptor for LPS), and nearly all studies have utilized sequential stimulation with IFN-γ followed by LPS to exploit this phenomenon. This study demonstrates that IFN-γ can upregulate the effect of LPS at the level of transcription. Human monoblastic Mono-Mac-6 cells produced up to threefold-greater levels of TNF-α when simultaneously stimulated with LPS and IFN-γ compared to treatment with LPS alone. RNase protection studies showed a similar increase in RNA beginning as early as within 30 min. The synthesis of TNF-α mRNA in IFN-γ- and LPS-treated Mono-Mac-6 cells was also temporally prolonged even though the message turnover rate was identical to that seen in LPS stimulated cells. The modulatory effect of IFN-γ may be mediated by Jak2.

scholarly journals Correlation between tumor necrosis factor-alpha and septic shock in children

2013 ◽  
Vol 53 (1) ◽  
pp. 1 ◽  
Author(s):  
Khrisanti Dinata ◽  
Ari L. Runtunuwu ◽  
Jose M. Mandei ◽  
Julius H. Lolombulan
Keyword(s):  
Septic Shock ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Strong Positive Correlation ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Positive Correlation ◽  
Factor Alpha ◽  
Necrosis Factor

Background The crucial role cytokines play in the pathophysiologyof sepsis is widely accepted. Infection stimulates the productionof cytokines in various cell types. Tumor necrosis factor-alpha(TNF-a) is one of the most extensively investigated cytokines inexperimental and clinical sepsis. Tumor necrosis factor-alpha hasbeen shown to mediate lethality in experimental sepsis.Objective To evaluate for a possible correlation between TNF-alevel and septic shock in children.Methods This cross-sectional study was conducted in Manadofrom June to September 2011. A total of 40 patients with arecent diagnosis of sepsis or septic shock were included. Plasmaspecimens were collected from subjects for measurement ofTNF-a concentration. Logistic regression analysis was used toassess the correlation between TNF-a level and sepsis, as well asthe probability of shock in children with sepsis, with P<0.05 asstatistically significant.Results There was a strong positive correlation betweenTNF-a level and the probability of shock in children with sepsis(regression coefficient = 0. 78, P = 0.002).Conclusions There is a strong positive correlation betweenTNF-a level with the probability of shock in children with sepsis.Higher plasma level ofTNF-a is associated with higher probabilityof septic shock.

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