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 Modulation of Anti-Tumor Necrosis Factor Alpha (TNF-α) Antibody Secretion in Mice Immunized with TNF-α Kinoid

2012 ◽  
Vol 19 (5) ◽  
pp. 699-703 ◽  
Author(s):  
Eric Assier ◽  
Luca Semerano ◽  
Emilie Duvallet ◽  
Laure Delavallée ◽  
Emilie Bernier ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Neutralizing Capacity ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACTTumor necrosis factor alpha (TNF-α) blockade is an effective treatment for patients with TNF-α-dependent chronic inflammatory diseases, such as rheumatoid arthritis, Crohn's disease, and psoriasis. TNF-α kinoid, a heterocomplex of human TNF-α and keyhole limpet hemocyanin (KLH) (TNF-K), is an active immunotherapy targeting TNF-α. Since the TNF-K approach is an active immunization, and patients receiving this therapy also receive immunosuppressant treatment, we evaluated the effect of some immunosuppressive drugs on the generation of anti-TNF-α antibodies produced during TNF-K treatment. BALB/c mice were injected intramuscularly with TNF-K in ISA 51 adjuvant. Mice were also injected intraperitoneally with one of the following: phosphate-buffered saline, cyclophosphamide, methylprednisolone, or methotrexate. Anti-TNF-α and anti-KLH antibody levels were assessed by enzyme-linked immunosorbent assay and the anti-TNF-α neutralizing capacity of sera by L929 bioassay. Our results showed that current treatments used in rheumatoid arthritis, such as methylprednisolone and methotrexate, do not significantly alter anti-TNF-α antibody production after TNF-K immunization. In contrast, the administration of cyclophosphamide (200 mg/kg) after immunization significantly reduced anti-TNF-α antibody titers and their neutralizing capacity.

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 Korelasi Tingkat Depresi dengan Kadar Tumor Necrosis Factor-Alpha (TNF-α) pada Penderita Asma Bronkial Tidak Terkontrol

2017 ◽  
Vol 3 (2) ◽  
pp. 74
Author(s):  
Muhammad Ali Apriansyah ◽  
Rudi Putranto ◽  
Eddy Mart Salim ◽  
Hamzah Shatri
Keyword(s):  
Tumor Necrosis Factor ◽  
Bronchial Asthma ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level ◽  
Necrosis Factor

Pendahuluan. Prevalensi depresi hamper mencapai 50% pada pasien yang berobat di pelayanan tertier klinik asma. Tumor Necrosis Factor-Alpha (TNF-α) telah diketahui sebagai sitokin pro-inflamasi yang berperan penting dalam mekanisme patogenesis sejumlah penyakit inflamasi kronik, termasuk asma bronkial dan depresi. Belum ada data penelitian mengenai hal tersebut di Indonesia.Metode. Penelitian ini merupakan studi cross sectional yang dilakukan pada 40 pasien asma bronkial tidak terkontrol di alergi imunologi klinik unit rawat jalan Rumah Sakit Umum Pusat (RSUP) Moh Hoesin Palembang selama kurun waktu mulai bulan Juni 2014 sampai dengan Agustus 2014. Asma bronkial tidak terkontrol dinilai dengan menggunakan kuesioner Asthma Control Test (ACT), sedangkan gejala depresi dinilai dengan kuisioner Beck Depression Inventory (BDI). Konfirmasi diagnosis depresi dilakukan dengan kriteria dari Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSMIV TR)/ International Code Diagnose 10 (ICD-10). Sementara itu, kadar TNF-α serum diukur dengan metode quantitative enzyme-linked immunosorbent assay (ELISA).Hasil. Nilai median tingkat depresi dan TNF-α serum pada penelitian ini adalah 16 (10 – 45) dan 4,09 (1,29 – 19,57) pg/mL.Tidak didapatkan korelasi yang bermakna secara statistik antara tingkat depresi dan kadar TNF-α (r = -0,265, p = 0,098).Simpulan. Tidak didapatkan korelasi yang bermakna antara tingkat depresi dengan kadar TNF-α pada penderita asma bronkial tidak terkontrol.Kata Kunci: asma bronkial tidak terkontrol, kadar TNF-α, Tingkat depresi The Correlation of Depression Level with Tumor Necrosis Factor-Alpha (TNF-α) Concentration in Uncontrolled Bronchial Asthma PatientsIntroduction. Depression occurs at high rates in people with chronic diseases, including bronchial asthma, with the prevalence of depression approaches 50% in tertiary care asthma clinic. Tumor necrosis factor alpha (TNF-α) is known to play a critical role in the pathogenic mechanism of a number of chronic inflammatory disease, including bronchial asthma and depression. There has not been any research data on the subject in Indonesia. The objective of this study was to investigate the correlation between depressive level and TNF-α level in uncontrolled bronchial asthma. Methods. This was a cross sectional study conducted in 40 patients with uncontrolled bronchial asthma at the allergy immunology clinic outpatient of Dr Moh Hoesin Hospital Palembang, during June 2014 until August 2014. Uncontrolled bronchial asthma was assessed using the Asthma Control Test (ACT) questionnaire, whereas depressive symptoms were assessed by Beck Depression Inventory (BDI) questionnaire, and diagnosis was confirmed by the criteria of the Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSM-IV TR) / International Code Diagnose 10 (ICD-10). Serum levels of TNF-α was measured by the method of quantitative enzyme-linked immunosorbent assay (ELISA). Results. The median value of the level of depression and serum TNF- α in this study were 16 (10 - 45) and 4.09 (1.29 - 19.57) pg/mL. There was no significant correlation between depressive level and TNF-α level ( r = -0.265 , p = 0.098 ). Conclusions. There was no significant correlation between depressive level and TNF-α level in uncontrolled bronchial asthma Keywords: depressive level, TNF-α level, uncontrolled asthma bronchial

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 Increased Pulmonary Tumor Necrosis Factor Alpha, Interleukin-6 (IL-6), and IL-17A Responses Compensate for Decreased Gamma Interferon Production in Anti-IL-12 Autovaccine-Treated,Mycobacterium bovisBCG-Vaccinated Mice

2010 ◽  
Vol 18 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Danielle Freches ◽  
Marta Romano ◽  
Hannelie Korf ◽  
Jean-Christophe Renauld ◽  
Jacques Van Snick ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACTInterleukin-12 (IL-12) and IL-23 (which share a p40 subunit) are pivotal cytokines in the generation of protective Th1/Th17-type immune responses upon infection with the intracellular pathogenMycobacterium tuberculosis. The role of IL-12 and IL-23 in protection conferred by the tuberculosis vaccineMycobacterium bovisbacillus Calmette-Guérin (BCG) is, however, less well documented. By using an autovaccine approach, i.e., IL-12p70 cross-linked with ovalbumin and PADRE peptide formulated with the GSK proprietary adjuvant system AS02V, we could specifically neutralize IL-12 while leaving the IL-23 axis intact. Neutralization of IL-12 beforeM. tuberculosischallenge rendered C57BL/6 mice highly susceptible, resulting in 30-fold-higher CFU in spleen and lungs and accelerated mortality. In contrast, neutralization of IL-12 in BCG-vaccinated mice prior toM. tuberculosischallenge only marginally affected vaccine-mediated protection. Analysis of cytokine production in spleen and lungs 3 weeks post-TB challenge by enzyme-linked immunosorbent assay and functional and flow cytometric assays showed significantly reduced mycobacterium-specific gamma interferon (IFN-γ) responses inM. tuberculosis-infected and BCG-vaccinated mice that had been treated with the autovaccine. Purified protein derivative-induced tumor necrosis factor alpha (TNF-α), IL-6, and IL-17A levels, however, were highest in lungs from BCG-vaccinated/IL-12-neutralized animals, and even unstimulated lung cells from these mice produced significant levels of the three cytokines. Mycobacterium-specific IL-4 and IL-5 production levels were overall very low, but IL-12 neutralization resulted in increased concanavalin A-triggered polyclonal secretion of these Th2-type cytokines. These results suggest that TNF-α, IL-6, and IL-17A may be more important pulmonary effector molecules of BCG-mediated protection than IFN-γ in a context of IL-12 deficiency.

scholarly journals Assessment of Unstimulated Whole Salivary Tumor Necrosis Factor Alpha (TNF-α) and Cellular Micronuclei Levels in Snuff (Naswar) Users and Non-Users for Early Diagnosis of Oral Squamous Cell Carcinoma

2021 ◽  
Vol 18 (14) ◽  
pp. 7230
Author(s):  
Waqar Muhammad ◽  
Muhammad M. Khan ◽  
Shafaq Zafar ◽  
Montaser N. Alqutub ◽  
Abdulrahman M. AlMubarak ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Control Subjects ◽  
Tnf Α ◽  
Factor Alpha ◽  
The Mean ◽  
Necrosis Factor

The aim of the study was to investigate the unstimulated whole saliva (UWS) tumor necrosis factor alpha (TNF-α) and cellular micronuclei in snuff dippers (Naswar) compared to healthy control subjects. The case control study was conducted over 9 months at a tertiary care center. Sixty patients were divided into two groups: Snuff dippers (SD) (Naswar) and non-snuff dippers (NSD) (control subjects). The included self-reported SD used Snuff twice daily for more than 12 months. UWS was collected and salivary TNF-α assessment was performed using enzyme-linked immunosorbent assay (ELISA). For cellular micronuclei, buccal mucosa was brushed to obtain cells in Naswar users, fixed with a dibutylphthalate polystyrene xylene (DPX) mounting to view micronuclei. Means and standard deviations were compared using the t-test and outcomes were related using Pearson correlation, considering p ≤ 0.05 as significant. The mean age of participants was 38.85 ± 11.56 years. The mean duration of snuff use was 20.43 ± 12.79 years and the common site for Naswar placement was the lower vestibule (n = 19, 63.3%). TNF-α levels among SD were 9.6 ± 3.3 pg/mL, which were significantly higher than levels in NSD, 5.2 ± 3 pg/mL (p < 0.05). The number of cellular micronuclei in SD was 30.7 ± 7.8, which was comparatively higher than in NSD, which was 9.2 ± 3.3 (p < 0.05). The duration of snuff use was positively correlated to TNF-α levels (p = 0.048) rather than the micronuclei number (p = 0.97). SD showed higher levels of TNF-α and cellular micronuclei compared with NSD (control subjects); a positive correlation was shown with the duration of snuff use. We conclude that TNF-α and micronuclei are potential salivary biomarkers for an oral biological effect in snuff (Naswar) users.

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.

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