Acute effect of two exercise intensity programs on interleukin-6, interleukin-1 beta and tumor necrosis factor-α in female futsalists

2021 ◽  
pp. 1-8
Author(s):  
A. Zar ◽  
E. Ahmadi ◽  
D. Amani ◽  
R. Ramsbottom
Keyword(s):  
Exercise Intensity ◽  
High Intensity ◽  
Interleukin 1 ◽  
Acute Effect ◽  
Moderate Intensity ◽  
Exercise Session ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Duration, intensity, and type of exercise can affect serum cytokine levels and change inflammatory indices. The present study aimed to examine the acute effect of two different exercise intensity programs on levels of circulating interleukin (IL)-6, IL-1β and tumour necrosis factor-α (TNF-α) in athletes. Eleven female futsal players aged 20.6±1.2 years completed this cross-over study. Participants performed, either a MI (moderate intensity: 60-65%) or a HI (high intensity: 75-80% heart rate reserve) exercise program. The study was performed on different days separated by a 1-week washout period. Each session consisted of 30 min running, either MI or HI. Blood samples were taken before (Pre) and immediately after (Post) each exercise session from an antecubital vein by venous puncture in a seated position. A Student’s t-test (P<0.05) was used to examine any difference between Pre and Post values. The results showed that IL-6 (P=0.22), IL-1β (P=0.90) and TNF-α (P=0.63) serum concentrations were not significantly different after moderate-intensity exercise. Similarly, high-intensity exercise did not significantly change serum concentrations of TNF-α (P=0.63), and IL-1β (P=0.18). However, HI caused a significant increase in IL-6 (P=0.04). A significant correlation was observed only between IL-1β and IL-6 (r=-0.761, P=0.01) after MI exercise. Based on the findings of the present study, the intensity of exercise can affect some cytokines, such as IL-6 in female futsal players.

Influence of Carbohydrate Supplementation on Plasma Cytokine and Neutrophil Degranulation Responses to High Intensity Intermittent Exercise

2002 ◽  
Vol 12 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Nicolette C. Bishop ◽  
Michael Gleeson ◽  
Ceri W. Nicholas ◽  
Ajmol Ali
Keyword(s):  
High Intensity ◽  
Intermittent Exercise ◽  
Plasma Concentrations ◽  
Neutrophil Function ◽  
Moderate Intensity ◽  
Post Exercise ◽  
Carbohydrate Supplementation ◽  
Tnf Α ◽  
Neutrophil Degranulation ◽  
Factor Α

Ingesting carbohydrate (CHO) beverages during prolonged, continuous heavy exercise results in smaller changes in the plasma concentrations of several cytokines and attenuates a decline in neutrophil function. In contrast, ingesting CHO during prolonged intermittent exercise appears to have negligible influence on these responses, probably due to the overall moderate intensity of these intermittent exercise protocols. Therefore, we examined the effect of CHO ingestion on plasma interIeukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS)-stimuIated neutrophil degranulation responses to high-intensity intermittent running. Six trained male soccer players performed 2 exercise trials, 7 days apart, in a randomized, counterbalanced design. On each occasion, they completed six 15-min periods of intermittent running consisting of maximal sprinting interspersed with less intense periods of running and walking. Subjects consumed either CHO or artificially sweetened placebo(PLA) beverages immediately before and at 15-min intervals during the exercise. At 30 min post-exercise, CHO versus PLA was associated with a higher plasma glucose concentration (p< .01), a lower plasma cortisol and IL-6 concentration (p < .02), and fewer numbers of circulating neutrophils (p < .05). Following the exercise, LPS-stimulated elastase release per neutrophil fell 31 % below baseline values on the PLA trial (p = .06) compared with 11% on the CHO trial (p = .30). Plasma TNF-α concentration increased following the exercise (main effect of time, p < .001) but was not affected by CHO. These data indicate that CHO ingestion attenuates changes in plasma IL-6 concentration, neutrophil trafficking, and LPS-stimulated neutrophil degranulation in response to intermittent exercise that involves bouts of very high intensity exercise.

Tumor Necrosis Factor-α −308 Genotypes Influence Inflammatory Activity and TNF-α Serum Concentrations in Children with Juvenile Idiopathic Arthritis

2009 ◽  
Vol 36 (4) ◽  
pp. 837-842 ◽  
Author(s):  
ANA FILIPA MOURÃO ◽  
JOANA CAETANO-LOPES ◽  
PAULA COSTA ◽  
HELENA CANHÃO ◽  
MARIA JOSÉ SANTOS ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inflammatory Activity ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Considering the relevance of tumor necrosis factor-α (TNF-α) in the pathophysiology of juvenile idiopathic arthritis (JIA), it is likely that polymorphisms in its promoter area may be relevant in disease susceptibility and activity. We investigated if clinical measures of JIA activity and TNF-α serum concentrations were associated with TNF-α −308 genotypes.Methods.Portuguese patients with JIA in 5 pediatric rheumatology centers were recruited consecutively, along with a control group of healthy subjects. Demographic and clinical data and blood samples were collected from each patient. DNA was extracted for analysis of TNF-α gene promoter polymorphisms at position −308 by restriction fragment-length polymorphism.Results.One hundred fourteen patients and 117 controls were evaluated; 57% of patients presented the oligoarticular subtype, 25% the polyarticular subtype, 8% the systemic subtype, and 9% had enthesitis-related arthritis and 5% psoriatic arthritis. Twenty-four percent of the patients presented the −308 GA/AA genotypes and 76% the −308 GG genotype, similar to findings in controls. Patients with the −308 GA/AA genotype had higher degree of functional impairment, erythrocyte sedimentation rate, 100-mm visual analog scale score for disease activity, and TNF-α levels compared to those with the −308 GG genotype.Conclusion.TNF-α −308 GA/AA genotypes were found to be related to higher inflammatory activity and worse measures of disease activity in Portuguese patients with JIA. They were not associated with susceptibility to JIA.

Tumor necrosis factor-α and interleukin-1 β levels in recurrent and persistent otitis media with effusion

2002 ◽  
Vol 126 (4) ◽  
pp. 417-422 ◽  
Author(s):  
Sertac Yetiser ◽  
Bulent Satar ◽  
Atilla Gumusgun ◽  
Faruk Unal ◽  
Yalcin Ozkaptan
Keyword(s):  
Tumor Necrosis Factor ◽  
Otitis Media ◽  
Tumor Necrosis ◽  
Otitis Media With Effusion ◽  
Interleukin 1 ◽  
Tertiary Referral Center ◽  
Adenoid Tissue ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

OBJECTIVE: Based on interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in effusions, our goals were to specify either recurrent or persistent otitis media with effusion (OME) is a mid stage in the development of chronic disease and to identify the factors that have an influence on cytokine levels. STUDY DESIGN: Samples from groups with recurrent (n = 15) and persistent (n = 39) OME were essayed for IL-1 β and TNF-α. Children were also grouped with respect to age, sex, quality of effusion, and the presence of pharyngeal adenoid tissue. SETTING: Tertiary referral center. RESULTS: In recurrent and persistent OME groups, IL-1β was higher than TNF-α ( P < 0.01). IL-β was higher in recurrent OME than in persistent OME ( P < 0.05). CONCLUSION: Recurrent OME seems to be closer to the chronic stage of the disease relative to persistent OME in terms of higher IL-1 β levels. Each exacerbation of acute disease in recurrent otitis media is likely to be mediated by IL-1 β. SIGNIFICANCE: We were able to clarify that recurrent OME is a stage that occurs before chronic OME. Therefore, the prevention of acute attacks in recurrent disease would also impede long-term damage to the middle ear.

Predisposition to Hyperthyroidism May Be Influenced by Functional TNF-α, IL-1, IL-6, and IL-10 Polymorphisms: A Meta-Analysis

2020 ◽  
Vol 181 (12) ◽  
pp. 956-965
Author(s):  
Hong Ma ◽  
Ting Tan ◽  
Jie Wu ◽  
Juan Chen ◽  
Xiaohong Zhang
Keyword(s):  
Meta Analysis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Asian Origin ◽  
Tnf Α ◽  
Caucasian Origin ◽  
Meta Analyses ◽  
Factor Α ◽  
Necrosis Factor

<b><i>Background:</i></b> Predisposition to hyperthyroidism may be influenced by functional gene polymorphisms in tumor necrosis factor-α (<i>TNF-α</i>), interleukin-1 (<i>IL-1</i>), interleukin-4 (<i>IL-4</i>), interleukin-6 (<i>IL-6</i>), and interleukin-10 (<i>IL-10</i>). However, the results of the studies published so far remain discrepant, so we conducted a meta-analysis to more robustly investigate relationships between <i>TNF-α</i>/<i>IL-1/IL-4/IL-6/IL-10</i> polymorphisms and predisposition to hyperthyroidism. <b><i>Methods:</i></b> A comprehensive literature retrieval from PubMed, Embase, Web of Science, WanFang, VIP, and CNKI was endorsed by the authors, and 38 studies were found to be eligible for pooled meta-analyses. <b><i>Results:</i></b> We found that genotypic frequencies of <i>TNF-α</i> −308 G/A, <i>IL-1A</i> −889 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, <i>IL-10</i> −819 C/T, and <i>IL-10</i> −1082 A/G polymorphisms among cases were significantly different from those among controls. Moreover, we also found that genotypic frequencies of <i>TNF-α</i> −308 G/A and <i>IL-6</i> −174 G/C polymorphisms among cases of Caucasian origin were significantly different from those among Caucasian controls, and genotypic frequencies of <i>IL-1A</i> −889 C/T, <i>IL-1B</i> −511 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, and <i>IL-10</i> −1,082 A/G polymorphisms among cases of Asian origin were also significantly different from those among Asian controls. <b><i>Conclusions:</i></b> This meta-analysis suggests that <i>TNF-α</i> −308 G/A, <i>IL-1A</i> −889 C/T, <i>IL-1B</i> −511 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, <i>IL-10</i> −819 C/T, and <i>IL-10</i> −1,082 A/G polymorphisms may influence predisposition to hyperthyroidism in certain ethnic groups.

The Augmented Productions of Neopterin and Cytokines from Macrophages/monocytes in vitro

Pteridines ◽  
1996 ◽  
Vol 7 (3) ◽  
pp. 72-76
Author(s):  
Tadashi Lizuka ◽  
Mitsuyo Sasaki ◽  
Hitomi Kamisako ◽  
Ko Oishi ◽  
Shigeru Uemura ◽  
...  
Keyword(s):  
Kawasaki Disease ◽  
Interleukin 1 ◽  
Poly I:C ◽  
Recombinant Interferon ◽  
Preliminary Examination ◽  
Tnf Α ◽  
Ifn Γ ◽  
Factor Α ◽  
Necrosis Factor

Summary In Kawasaki disease patients, increases in excretion of urinary neopterin coincided with fever and monocytosis in peripheral blood. We examined the products of neopterin, tumor necrosis factor-α (TNFα) and Interleukin-1 β (1L-1β) from healthy adult macrophages/monocytes (Mφ>/M), after stimulation with several activators to obtain some understanding of Kawasaki disease. Upon stimulation with either lipopolysaccharide (LPS) or polyinosinate-polycytidylate (Poly I:C), the Mφ/M released neopterin and pyogenic products (TNF-α or 1L-1β). The release of neopterin was eliminated by the addition of the anti-interferon-y antibody. The production of both TNF-α, 1L-1β and neopterin from Mφ/M upon stimulation of LPS was augmented in a co-culture with low dose recombinant interferon-y (rIFN-γ). Upon stimulation with rIFN-γ alone, however, the Mφ/M released neopterin but not the pyogenic products. A preliminary examination failed to detect. any difference in the response of the Mφ/M in adults annd children after stimulation with LPS. We concluded that some endotoxins could trigger the onset of Kawasaki disease and that endogenous IFN-γ can play an important role in the abnormality of Kawasaki disease patients

scholarly journals BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy

2020 ◽  
Author(s):  
Zetao Ma ◽  
Deli Wang ◽  
Jian Weng ◽  
Sheng Zhang ◽  
Yuanshi Zhang
Keyword(s):  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Related Protein ◽  
Interacting Protein ◽  
Tnf Α ◽  
Adenovirus E1b ◽  
Factor Α ◽  
Related Proteins ◽  
Necrosis Factor ◽  
Proinflammatory Factors

Abstract Background: Inflammation and apoptosis of chondrocytes are the pathological basis of osteoarthritis. Autophagy could alleviate the symptoms of inflammation and apoptosis. Previous study has shown that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) can induce the occurrence and development of autophagy. However, it is unknown whether autophagy induced by BNIP3 can alleviate the inflammation and apoptosis of chondrocytes. Methods: We used the lentivirus to construct the overexpression BNIP3 chondrocytes. Next, the lipopolysaccharide (LPS) was used to stimulate these cells to simulate the physiological environment of osteoarthritis. After that, the enzyme-linked immunosorbent assays (ELISA) were performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) and the flow cytometry was performed to detect the apoptosis rates of chondrocytes. At last, the expression of autophagy related proteins was detected with the western blotting. Results: The expression of BNIP3 was suppressed after treatment with LPS. However, overexpression of BNIP3 inhibited the secretion of proinflammatory factors (TNF-α, IL-1β and IL-6) and decreased the apoptosis of chondrocytes. Furthermore, overexpression of BNIP3 led to the upregulation of autophagy related proteins expression including little computer 3 (LC3), autophagy-related protein 7 (ATG7) and Beclin-1. Application of autophagy inhibitor recovered the expression of proinflammatory factors and apoptosis rates of chondrocytes. Conclusions: BNIP3 decreased the LPS induced inflammation and apoptosis of chondrocytes by activating the autophagy.

Regulation of Murine Protein C Gene Expression In Vivo: Effects of Tumor Necrosis Factor-α, Interleukin-1, and Transforming Growth Factor-β

1999 ◽  
Vol 82 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
Takayoshi Shimokawa ◽  
Tetsuhito Kojima ◽  
David Loskutoff ◽  
Hidehiko Saito ◽  
Koji Yamamoto
Keyword(s):  
Growth Factor ◽  
Protein C ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Transforming Growth Factor Β ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

SummaryProtein C is a precursor of the anticoagulant serine protease, activated protein C, which inhibits coagulation factors Va and VIIIa. Although the liver appears to be the primary site of protein C synthesis, we previously demonstrated that the kidney and male reproductive organs also expressed abundant protein C mRNA in the mouse. In the present study, we further investigated the effects of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and transforming growth factor-β (TGF-β) on the expression of protein C mRNA in the principal producing organs, i.e., the liver, kidney, and testis. Both quantitative reverse transcription-PCR assay and in situ hybridization analysis revealed that TNF-α decreased protein C mRNA expression in the liver, kidney, and testis. IL-1 also down-regulated protein C mRNA expression in the liver and testis, but not in the kidney. In contrast, TGF-β unchanged the expression level of protein C mRNA in these three organs. These observations suggest that TNF-α and IL-1 may contribute to an increase in the procoagulant potential by down-regulation of protein C synthesis in the tissues during inflammatory processes.

scholarly journals Release of tumour necrosis factor alpha into bronchial alveolar lavage fluid following antigen challenge in passively sensitized guinea-pigs

1992 ◽  
Vol 1 (6) ◽  
pp. 425-428 ◽  
Author(s):  
D. E. Kelly ◽  
M. Denis ◽  
D. F. Biggs
Keyword(s):  
Tumour Necrosis Factor ◽  
Guinea Pigs ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Lavage Fluid ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Bronchial Alveolar Lavage ◽  
Necrosis Factor

Five groups of ten female guinea-pigs were passively sensitized against ovalbumin (OA) (n = 9) or control guinea-pig serum (n = 1). 24 h later, they received mepyramine (0.5 mg/kg, i.p.) and 30 min later inhaled aerosols of: (A) OA (2 in 0.9% saline, 8 min, n = 4/9); (B) saline (40 min, n = 4/9); (C) LPS (40 min, Escherichia coli 0111:B4, 150 ng/kg in PBS, n = 1/9); and (D) the control animal was treated as in (C) (n = 1). Their tracheas were cannulated under pentobarbital anaesthesia and bronchial alveolar lavage (BAL) was performed with 2 × 5 ml PBS containing BSA (1%) (n = 1 group), or BSA (1%) and aprotinin (1000 KIU/ml) (n = 4 groups), at 30, 60, 90 or 120 min post-inhalations. BAL fluids recovered were centrifuged, the supernatants recovered and frozen until assayed for tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6). No TNF-α could be detected unless aprotinin was present in the lavaging solution. BAL fluid from OA-sensitized and control animals that had inhaled LPS contained high levels of TNF-α that peaked at 90 min. BAL fluid from OA sensitized animals that inhaled OA aerosols contained no detectable TNF-α at 30 min, but it was found in increasing amounts at 60, 90 and 120 min; TNF-α was not detected in fluid from any of the animals that inhaled saline. As BAL fluids were toxic to the cells used in the assays, neither IL-1 nor IL-6 could be measured. We conclude that the monokine TNF-α is released into BAL fluid following anaphylactic challenge of passively sensitized guinea-pigs. The presence of the antiprotease, aprotinin, in the lavaging solution is essential for the detection and measurement of TNF-α in BAL fluid.

scholarly journals Tumour necrosis factor α (TNF-α), interleukin-6 (IL-6) and their soluble receptors (sTNF-α-Rp55 and slL-6R) serum levels in systemic lupus erythematodes

1996 ◽  
Vol 5 (6) ◽  
pp. 435-441 ◽  
Author(s):  
E. Robak ◽  
A. Sysa-Jędrzejowska ◽  
T. Robak ◽  
H. Stępień ◽  
A. Woźniacka ◽  
...  
Keyword(s):  
Tumour Necrosis ◽  
Serum Levels ◽  
Serum Concentrations ◽  
Tumour Necrosis Factor Α ◽  
Systemic Lupus ◽  
Soluble Receptors ◽  
Normal Individuals ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We investigated a possible association between serum concentrations of tumour necrosis factor α (TNF-α), interleukin-6 (IL-6) and their soluble receptors (sTNF-α-Rp55 and sIL-6R) using an enzyme-linked immunosorbent assay (ELISA) in 55 patients with systemic lupus erythematodes (SLE) and 16 healthy controls. We also examined a possible association between the serum levels of these peptides and SLE activity, as well as TNF-α and IL-6 concentrations and the levels of their soluble receptors. The median concentrations of TNF-α, sTNF-α-Rp55 and IL-6 were significantly higher in SLE patients than in normal individuals. In contrast, there was no difference between the serum level of sIL-6R in both groups. We found positive correlations between the serum concentrations of TNF-α and IL-6 as well as their soluble receptors and disease activity. There were also correlations between TNF-α and sTNF-α-Rp55 as well as IL-6 and sIL-6R serum levels in SLE patients but there were no such correlations in the normal control group. In conclusion, an increase in the serum levels of TNF-α, sTNF-α-Rp55 and IL-6 may become useful markers for SLE activity. Patients with SLE have sIL-6R serum concentration similar to that as in normal individuals. However, it correlates with disease activity and the level of IL-6.

Differential Effects of Interleukin 1-α (IL-1α) or Tumor Necrosis Factor-α (TNF-α) on Motility of Human Melanoma Cell Lines on Fibronectin

1994 ◽  
Vol 102 (6) ◽  
pp. 898-905 ◽  
Author(s):  
Sybren K Dekker ◽  
Jacqueline Vink ◽  
Bert Jan Vermeer ◽  
Jan A Bruijn ◽  
Martin C Mihm ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1 ◽  
Human Melanoma ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Melanoma Cell Lines
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