scholarly journals Gender-Related Cytokine Patterns in Sera of Schistosomiasis Patients with Symmers' Fibrosis

2004 ◽  
Vol 11 (3) ◽  
pp. 627-630 ◽  
Author(s):  
David Nascimento Silva-Teixeira ◽  
Cristiane Contigli ◽  
José Roberto Lambertucci ◽  
José Carlos Serufo ◽  
Virmondes Rodrigues

ABSTRACT Cytokine levels were compared between schistosomiasis patients affected by intense fibrosis defined by ultrasound examination and graded from F-0 to F-3. The concentrations of interleukin-1β (IL-1β), IL-4, IL-5, IL-10, IL-13, gamma interferon, and tumor necrosis factor alpha (TNF-α) were determined by enzyme-linked immunosorbent assay of serum samples. Levels of IL-4, IL-5, and TNF-α in the sera of F-3 patients were significantly higher than those found in F-0 individuals, while levels of IL-13 were lower. Levels of IL-4, IL-5, and TNF-α in serum were significantly higher in F-3 males than in F-0 males or F-3 females. Conversely, levels of IL-13 were significantly lower in F-3 females than in F-0 females and males.

2012 ◽  
Vol 19 (5) ◽  
pp. 699-703 ◽  
Author(s):  
Eric Assier ◽  
Luca Semerano ◽  
Emilie Duvallet ◽  
Laure Delavallée ◽  
Emilie Bernier ◽  
...  

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.


2017 ◽  
Vol 3 (2) ◽  
pp. 74
Author(s):  
Muhammad Ali Apriansyah ◽  
Rudi Putranto ◽  
Eddy Mart Salim ◽  
Hamzah Shatri

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


2017 ◽  
Vol 5 (2) ◽  
pp. 108 ◽  
Author(s):  
Sajeev Shrestha ◽  
Manisha Neupane ◽  
Shivalal Sharma ◽  
Madhab Lamsal

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.


2010 ◽  
Vol 18 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Danielle Freches ◽  
Marta Romano ◽  
Hannelie Korf ◽  
Jean-Christophe Renauld ◽  
Jacques Van Snick ◽  
...  

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.


Author(s):  
Waqar Muhammad ◽  
Muhammad M. Khan ◽  
Shafaq Zafar ◽  
Montaser N. Alqutub ◽  
Abdulrahman M. AlMubarak ◽  
...  

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.


2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang

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.


2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active


2013 ◽  
Vol 87 (23) ◽  
pp. 12935-12948 ◽  
Author(s):  
Jie Zhang ◽  
Kezhen Wang ◽  
Shuai Wang ◽  
Chunfu Zheng

NF-κB plays central roles in regulation of diverse biological processes, including innate and adaptive immunity and inflammation. HSV-1 is the archetypal member of the alphaherpesviruses, with a large genome encoding over 80 viral proteins, many of which are involved in virus-host interactions and show immune modulatory capabilities. In this study, we demonstrated that the HSV-1 ICP0 protein, a viral E3 ubiquitin ligase, was shown to significantly suppress tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation. ICP0 was demonstrated to bind to the NF-κB subunits p65 and p50 by coimmunoprecipitation analysis. ICP0 bound to the Rel homology domain (RHD) of p65. Fluorescence microscopy demonstrated that ICP0 abolished nuclear translocation of p65 upon TNF-α stimulation. Also, ICP0 degraded p50 via its E3 ubiquitin ligase activity. The RING finger (RF) domain mutant ICP0 (ICP0-RF) lost its ability to inhibit TNF-α-mediated NF-κB activation and p65 nuclear translocation and degrade p50. Notably, the RF domain of ICP0 was sufficient to interact with p50 and abolish NF-κB reporter gene activity. Here, it is for the first time shown that HSV-1 ICP0 interacts with p65 and p50, degrades p50 through the ubiquitin-proteasome pathway, and prevents NF-κB-dependent gene expression, which may contribute to immune evasion and pathogenesis of HSV-1.


2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein

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.


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