scholarly journals Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

scholarly journals A Randomized Control Trial Study to Determine the Effect of Melatonin on Serum Levels of IL-1β and TNF-α in Patients with Multiple Sclerosis

2020 ◽  
Author(s):  
Masoomeh Yosefifard ◽  
Gholamhassan Vaezi ◽  
Ali Akbar Malekirad ◽  
Fardin Faraji ◽  
Vida Hojati
Keyword(s):  
Multiple Sclerosis ◽  
Interleukin 1 ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Treatment Groups ◽  
Tnf Α ◽  
Significant Difference ◽  
The Central Nervous System

Multiple sclerosis (MS) is the most common neurological disease that happens at a young age. MS is an inflammatory disease; associated with the demyelination of the central nervous system. Therefore, some inflammatory factors are effective in the mechanism and progression of the disease. Melatonin, as a multi-effect substance including anti-inflammatory effects, can reduce symptoms of MS in patients with a change in their inflammatory factors level. In this study, 50 MS patients who were referred to the MS Society of Markazi Province were randomly selected. All patients were treated with routine MS treatment (interferon) and were divided into control (25 placebo recipients) and treatment (25 recipients of 3 mg melatonin per day for 24 weeks) groups. Anthropometric data of patients including height, weight, and age were determined. Blood samples were collected after fasting in order to determine serum levels of interleukin 1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Then, samples were immediately centrifuged for serum separation and sera were transferred to a freezer at -80°C and serum levels of these factors were determined; using ELISA kit. The results of this study showed that there was no significant difference between the control and treatment groups in terms of serum levels of TNF-α. However, the level of IL-1β was significantly reduced in the treatment group compared to the control group, indicating that melatonin decreases this inflammatory substance. Our findings suggest a valuable strategy in the treatment of patients who suffer from MS

Effect of Resveratrol on NF-κB Activity in Rat Peritoneal Macrophages

2006 ◽  
Vol 34 (04) ◽  
pp. 623-630 ◽  
Author(s):  
Zhen-Hua Ma ◽  
Qing-Yong Ma ◽  
Lian-Cai Wang ◽  
Huan-Chen Sha ◽  
Sheng-Li Wu ◽  
...  
Keyword(s):  
Culture Medium ◽  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Inflammatory Factors ◽  
Future Application ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference

This study was to investigate the inhibitive effect of resveratrol (RESV) on nuclear factor kappa B (NF-κB) expression and activity induced by lipopolysaccharide (LPS) in rat peritoneal macrophages (PMA). Male Sprague-Dawley (SD) rats were randomly divided into 7 groups, including control group, LPS group and RESV I-V group. In the LPS group, PMA were incubated in DMEM containing LPS (10 μg/ml), whereas in control group, PMA were incubated in DMEM only. In the RESV I-V groups, PMA were incubated in DMEM containing LPS (10 μg/ml) and different concentrations of RESV. After 24 hours of incubation, NF-κB activity in PMA, and the levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1) and nitric oxide (NO) in the culture medium were measured. In the concentrations of 1.25-5 μg/ml, RESV had a dose- dependent inhibitive effect on NF-κB activity in PMA as well as the expressions of TNF-α, IL-1 and NO in the culture medium contrasted with the LPS group. There was no significant difference in the levels of these pro-inflammatory factors between the groups of 5 μg/ml and 10 μg/ml RESV. In conclusion, RESV has the potential for the future application of preventing inflammatory diseases involving PMA.

Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

2018 ◽  
Vol 44 (4) ◽  
pp. 530-538
Author(s):  
Aysun Çetin ◽  
İhsan Çetin ◽  
Semih Yılmaz ◽  
Ahmet Şen ◽  
Göktuğ Savaş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Paraoxonase 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Phenotypic Effect ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

scholarly journals Influence of Intra-Articular Administration of Trichostatin A on Autologous Osteochondral Transplantation in a Rabbit Model

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Huacheng Hou ◽  
Ke Zheng ◽  
Guanghu Wang ◽  
Shiro Ikegawa ◽  
Minghao Zheng ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Cartilage Repair ◽  
Trichostatin A ◽  
Interleukin 1 ◽  
Rabbit Model ◽  
Treated Group ◽  
Control Group ◽  
Osteochondral Transplantation ◽  
Autologous Osteochondral Transplantation ◽  
Significant Difference

Autologous osteochondral transplantation (AOT) is a method for articular cartilage repair. However, several disadvantages of this method have been reported, such as transplanted cartilage degeneration and the lack of a connection between the grafted and adjacent cartilage tissues. To evaluate the effect of intra-articular administration of trichostatin A (TSA) on AOT, we conducted a case control study in a rabbit model. International Cartilage Repair Society (ICRS) macroscopic scores, the modified O’Driscoll histology scores, and real-time PCR were utilized to evaluate the results. At 4 weeks, both macroscopic and histological assessments showed that there was no significant difference between the TSA and control groups. However, the mean macroscopic and histological scores for the TSA-treated group were significantly higher than the scores for the control group at 12 weeks. TSA was shown to directly reduce collagen type II (COL2), aggrecan, matrix metalloproteinase (MMP), and a disintegrin and metalloproteinase domain with thrombospondin motifs 5 (ADAMTS-5) expression and to simultaneously repress the upregulation of MMP-3, MMP-9, and MMP-13 levels induced by interleukin 1β(IL-1β) in chondrocytes. In conclusion, TSA protects AOT grafts from degeneration, which may provide a benefit in the repair of articular cartilage injury.

Proinflammatory cytokine levels in patients with conversion disorder

2013 ◽  
Vol 25 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Utkan Tiyekli ◽  
Okan Çalıyurt ◽  
Nimet Dilek Tiyekli
Keyword(s):  
Acute Phase ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Conversion Disorder ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
Cytokine Levels ◽  
As Stress

ObjectiveIt was aimed to evaluate the relationship between proinflammatory cytokine levels and conversion disorder both commonly known as stress regulated.MethodBaseline proinflammatory cytokine levels–[Tumour necrosis factor alpha (TNF‐α), Interleukin‐1 beta (IL‐1β), Interleukin‐6 (IL‐6)]–were evaluated with enzyme‐linked immunosorbent assay in 35 conversion disorder patients and 30 healthy controls. Possible changes in proinflammatory cytokine levels were evaluated again, after their acute phase in conversion disorder patients.ResultsStatistically significant decreased serum TNF‐α levels were obtained in acute phase of conversion disorder. Those levels increased after acute conversion phase. There were no statistically significant difference observed between groups in serum IL‐1β and (IL‐6) levels.ConclusionsStress associated with conversion disorder may suppress immune function in acute conversion phase and may have diagnostic and therapeutic value.

scholarly journals The Effect of Scaling and Root Planning on Salivary TNF-α and IL-1α Concentrations in Patients with Chronic Periodontitis

2017 ◽  
Vol 11 (1) ◽  
pp. 573-580 ◽  
Author(s):  
Masoome Eivazi ◽  
Negar Falahi ◽  
Nastaran Eivazi ◽  
Mohammad Ali Eivazi ◽  
Asad Vaisi Raygani ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Interleukin 1 ◽  
Negative Relationship ◽  
Inflammatory Factors ◽  
Control Group ◽  
Pocket Depth ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Root Planning ◽  
Scaling And Root Planning

Objective:Periodontitis is one of the main diseases in the oral cavity that causes tooth loss. The host immune response and inflammatory factors have important role in periodontal tissue. The current study was done with the objective to determine the effect of scaling and root planning on the salivary concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1-alpha (IL-1α).Methods:In this quasi-experimental clinical trial, 29 patients with chronic periodontitis and 29 healthy subjects without periodontitis were studied. Clinical examination findings and salivary TNF-α and IL-1α (using ELISA method) were compared before and after scaling, root planning.Results:Before starting treatment, salivary TNF-α and IL-1α concentrations were higher in healthy control group than in periodontitis group (P< 0.05). Non-surgical treatment increased the concentration of these two biomarkers in the saliva. However, increase in IL-1α concentration was not statistically significant (P= 0.056). There was a negative relationship between TNF-α and IL-1α levels with pocket depth and attachment loss (P< 0.05).Conclusion:Scaling and root planning improved periodontal disease indices and salivary TNF-α and IL-1α levels.

Astaxanthin prevents lung injury due to hyperoxia and inflammation

2020 ◽  
Vol 23 ◽  
Author(s):  
Hasan Akduman ◽  
Cüneyt Tayman ◽  
Ufuk Çakir ◽  
Esra Çakir ◽  
Dilek Dilli ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Interleukin 1 ◽  
Survival Rates ◽  
Lipid Hydroperoxide ◽  
Treated Group ◽  
Lung Damage ◽  
Pregnant Rats ◽  
Necrosis Factor Alpha ◽  
Total Thiol ◽  
Tnf Α

Background/aim: We aimed to ascertain the effects of astaxanthin on the lungs of rat pups with bronchopulmonary dysplasia (BPD) induced by hyperoxia and lipopolysaccharide (LPS). Materials and methods: Forty-two newborn Wistar rats born to spontaneous pregnant rats were divided into three groups: Hyperoxia (95% O2) + lipopolysaccharide (LPS) group, hyperoxia + LPS + astaxhantin group and control: no treatment group (21% O2). Pups in the hyperoxia + LPS + astaxanthin group were given 100 mg/kg/day oral astaxanthin from the first day to the fifth day. Histopathologic and biochemical evaluations including glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), lipid hydroperoxide (LPO), 8-hydroxydeoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), myeloperoxidase (MPO), total thiol, tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL1β) and caspase-3 activities were performed. Results: A better survival rates and weight gain were demonstrated in the hyperoxia + LPS + astaxanthin group (p <0.001). In the histopathologic evaluation, the severity of lung damage was significantly reduced in the hyperoxia+LPS+astaxanthin group, as well as decreased apoptosis (ELİSA for caspase-3) (p <0.001). The biochemical analyses of lung tissues TAS, GSH, Total thiol levels were significantly higher in the astaxanthin treated group compared to hyperoxia + LPS group (p <0.05) while TOS, AOPP, LPO, 8-OHdG, MPO levels were significantly lower (p <0.001). In addition, unlike the hyperoxia + LPS group, TNF-α and IL-1β levels in lung tissue were significantly lower in the astaxanthin-treated group (p <0.001). Conclusion: Astaxanthin was shown to reduce lung damage caused by inflammation and hyperoxia with its antiinflammatory, anti-oxidant, anti-apoptotic properties and to protect the lung from severe destruction.

scholarly journals Suppression of Macrophage Activation with CNI-1493 Increases Survival in Infant Rats with Systemic Haemophilus influenzae Infection

2000 ◽  
Vol 68 (9) ◽  
pp. 5329-5334 ◽  
Author(s):  
Carl Granert ◽  
Hana Abdalla ◽  
Lars Lindquist ◽  
Asim Diab ◽  
Moiz Bakhiet ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Infant Rats ◽  
Cytokine Inhibition ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT CNI-1493, a potent macrophage deactivator, was used to treat infant rats systemically infected with Haemophilus influenzae type b (Hib). CNI-1493 was injected 1 h prior to bacterial inoculation and 24 h later and resulted in a 75 percent increased rate of survival compared to that for untreated controls. The effect of CNI-1493 on the inflammatory response was studied by immunohistochemical detection of individual tumor necrosis factor alpha (TNF-α)-, interleukin 1 beta (IL-1β)-, and gamma interferon (IFN-γ)-producing cells in the spleen. A significant reduction of the incidence of TNF-α- and IL-1β-expressing cells was found for CNI-1493-treated animals. IFN-γ expression was not suppressed by CNI-1493, indicating that cytokine inhibition was specific in macrophages. CNI-1493 significantly reduced the number of infiltrating granulocytes in the brain from that for controls. This study provides evidence that CNI-1493 protects against lethal Hib infection by deactivating the inflammatory cascade in infant rats.

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