scholarly journals Tumor Necrosis Factor-Alpha and Interleukin 6 in Human Periapical Lesions

2007 ◽  
Vol 2007 ◽  
pp. 1-4 ◽  
Author(s):  
Ivana Brekalo Pršo ◽  
Willy Kocjan ◽  
Hrvoje Šimic ◽  
Gordana Brumini ◽  
Sonja Pezelj-Ribaric ◽  
...  

Aim. The aim of this study was to evaluate the presence of the cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in human periapical lesions.Subjects and methods. Samples were obtained from three groups of teeth: symptomatic teeth, asymptomatic lesions, and uninflamed periradicular tissues as a control.Results. TNF-alpha levels were significantly increased in symptomatic lesions compared to control. Group with asymptomatic lesions had significantly higher concentrations compared to control. There were no significant differences in TNF-alpha levels between symptomatic and asymptomatic lesions. In group with symptomatic lesions, IL-6 levels were significantly higher than in group with asymptomatic lesions. The IL-6 levels in symptomatic group also showed significantly higher concentration in comparison with control group. In asymptomatic group, the IL-6 level had significantly higher concentrations compared to control.Conclusion. These results indicate that symptomatic lesions represent an immunologically active stage of disease, and asymptomatic lesions are the point from which the process advances toward healing.

2017 ◽  
Vol 24 (4) ◽  
Author(s):  
T. Vicharenko ◽  
M. Rozhko

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.


2021 ◽  
Vol 71 (4) ◽  
pp. 477-489
Author(s):  
Meryem Senturk ◽  
Meryem Eren ◽  
Zeynep Soyer Sarica

Abstract The aim of this study was to determine the effects of L-carnitine and magnesium on the levels of tissue malondialdehyde, 8-hydroxy-2’-deoxyguanosine, and cytokines (tumor necrosis factor alpha, interleukin-6) in streptozotocin-induced experimental diabetes in rats. Eighty male Wistar albino rats (200-250 g) were divided into 8 groups with 10 rats in each group. The groups received the following treatments: Control group; 2 ml distilled water (by gavage); Group 2: 50 mg/kg (b.w.) i.p. streptozotocin; Group 3: 125 mg/kg (b.w.) magnesium; Group 4: 300 mg/kg (b.w.) L-carnitine; Group 5: 125 mg/kg (b.w.) magnesium +300 mg/kg (b.w.) L-carnitine; Group 6: 50 mg/kg (b.w.) streptozotocin +125 mg/kg (b.w.) magnesium; Group 7: 50 mg/kg (b.w.) streptozotocin +300 mg/kg (b.w.) L-carnitine and Group 8: 50 mg/kg (b.w.) streptozotocin +125 mg/ kg (b.w.) magnesium+300 mg/kg (b.w.) L-carnitine administered for 4 weeks. Liver and kidney malondialdehyde, 8-hydroxy-2’-deoxyguanosine, tumor necrosis factor alpha and interleukin-6 levels did not change in the magnesium, L-carnitine, and magnesium + L-carnitine groups compared to the control. The highest levels of malondialdehyde, 8-hydroxy-2’-deoxyguanosine, tumor necrosis factor alpha and interleukin-6 were determined only in the group with diabetes (Group 2). Lipid peroxidation, DNA damage, and cytokine levels were significantly reduced in diabetic animals with the administration of magnesium and L-carnitine separately or in combination. Based on the obtained results it can be concluded that magnesium and L-carnitine may have antidiabetic effects, especially in combination.


1994 ◽  
Vol 266 (4) ◽  
pp. C967-C974 ◽  
Author(s):  
J. E. Ensor ◽  
S. M. Wiener ◽  
K. A. McCrea ◽  
R. M. Viscardi ◽  
E. K. Crawford ◽  
...  

The pyrogenic cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) appear in the circulation during infections and injuries, but TNF-alpha and IL-6 are regulated differently in macrophages. We compared the effects of elevated temperatures within the usual febrile range on the expression of TNF-alpha and IL-6 in vitro in lipopolysaccharide (LPS)-stimulated human macrophages derived from peripheral blood monocytes (HuMoM phi). During an 18-h incubation at 37 degrees C with 5 ng/ml LPS, these cells released 5,030 +/- 1,460 pg TNF-alpha/10(6) cells (means +/- SE) and 1,380 +/- 280 pg IL-6/10(6) cells. In LPS-stimulated HuMoM phi incubated at 40 degrees C, TNF-alpha release was almost completely inhibited (76 +/- 76 pg TNF-alpha/10(6) cells; P < 0.01 compared with LPS-stimulated HuMoM phi at 37 degrees C), but release of IL-6 was preserved (1,600 +/- 780 pg IL-6/10(6) cells). Western and Northern analyses showed that levels of TNF-alpha mRNA and cell-associated and secreted TNF-alpha protein were decreased, but IL-6 expression was unchanged at 40 degrees C in LPS-stimulated macrophages. Incubating HuMoM phi at 40 degrees did not alter their viability after 18 h but induced a 75-fold increase in levels of the inducible heat-shock protein 72 (HSP-72) mRNA in the face of a 56% inhibition in total protein synthesis. Our results show that IL-6 expression persisted at incubation temperatures in the upper end of the physiological range that induced heat shock and attenuated the expression of functionally active TNF-alpha in LPS-stimulated HuMoM phi.


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