scholarly journals Impacts of different intensities of exercise on inflammation and hypoxia markers in low altitude

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Fatih Baygutalp ◽  
Yusuf Buzdağlı ◽  
Murat Ozan ◽  
Mitat Koz ◽  
Nurcan Kılıç Baygutalp ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Maximal Oxygen Consumption ◽  
Interleukin 10 ◽  
Bicycle Ergometer ◽  
Exercise Session ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Rest Condition ◽  
Low Altitude ◽  
Hypoxia Markers

Abstract Background This study aims to determine and compare the effects of exercise modalities with different intensities on the secretion of key inflammation and hypoxia markers in amateur athletes. Methods Twenty-three athletes with a mean age of 20.1 years, living at low altitude (1850 m) participated in this study. The participants' maximal oxygen consumption values (VO2 max) were determined with an incremental cycle exercise test as 54.15 ± 6.14 mL kg min−1. Athletes performed four protocols: at rest, 50% VO2 max, 75% VO2 max and 100% VO2 max (until exhaustion) with one-week intervals. 50% VO2 max, 75% VO2 max sessions were performed continuously for 30 min on a bicycle ergometer and 100% VO2 max session was performed by cycling until exhaustion. Blood samples were obtained at rest and immediately after each exercise session. Serum tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), interleukin-10 (IL-10), and hypoxia inducible factor-1 alpha (HIF-1α) levels were measured. Results There were significant differences in serum TNF-α levels in 75% VO2 max and 100% VO2 max sessions (489.03 ± 368.37 and 472.70 ± 365.21 ng/L, respectively) compared to rest conditions (331.65 ± 293.52 ng/L). Serum CRP levels of 50% VO2 max and 75% VO2 max sessions (1.19 ± 0.50; 1.07 ± 0.52 mg/L) were significantly higher than the rest condition (0.74 ± 0.35 mg/L). There were significant differences in serum IL-10 levels of rest condition and 50% VO2 max; 50% VO2 max, and 100% VO2 max sessions (328.09 ± 128.87; 446.36 ± 142.84; 347.44 ± 135.69; 324.88 ± 168.06 pg/mL). Serum HIF-1α levels were significantly higher in 75% VO2 max session compared to rest (1.26 ± 0.16; 1.08 ± 0.19 ng/mL) (P < 0.05 for all comparisons). Conclusions Both inflammatory and anti-inflammatory pathway is induced on different exercise intensities. Exercise protocols performed until exhaustion may lead to activation of inflammatory pathways and hypoxia-induced damage.

scholarly journals A Defect in Interleukin-10 Leads to Enhanced Malarial Disease in Plasmodium chabaudi chabaudi Infection in Mice

1999 ◽  
Vol 67 (9) ◽  
pp. 4435-4442 ◽  
Author(s):  
Ching Li ◽  
Inés Corraliza ◽  
Jean Langhorne
Keyword(s):  
Body Weight ◽  
Knockout Mice ◽  
Interleukin 10 ◽  
Plasmodium Chabaudi ◽  
Double Knockout ◽  
Direct Stimulation ◽  
Necrosis Factor Alpha ◽  
Glucose Levels ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT Infection of interleukin-10 (IL-10)-nonexpressing (IL-10−/−) mice with Plasmodium chabaudi chabaudi (AS) leads to exacerbated pathology in female mice and death in a proportion of them. Hypoglycemia, hypothermia, and loss in body weight were significantly greater in female IL-10−/−mice than in male knockout mice and all wild-type (WT) mice during the acute phase of infection. At this time, both female and male IL-10−/− mice produced more gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and IL-12p40 mRNA than their respective WT counterparts. Inactivation of IFN-γ in IL-10−/− mice by the injection of anti-IFN-γ antibodies or by the generation of IL-10−/− IFN-γ receptor−/− double-knockout mice resulted in reduced mortality but did not affect body weight, temperature, or blood glucose levels. The data suggest that IFN-γ-independent pathways may be responsible for these pathological features of P. chabaudimalaria and may be due to direct stimulation of TNF-α by the parasite. Since male and female knockout mice both produce more inflammatory cytokines than their WT counterparts, it is likely that the mortality seen in females is due to the nature or magnitude of the response to these cytokines rather than the amount of IFN-γ or TNF-α produced.

scholarly journals High Coping Self-Efficacy Associated With Lower Sweat Inflammatory Cytokines in Adults: A Pilot Study

2019 ◽  
Vol 22 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Melissa Hladek ◽  
Jessica Gill ◽  
Chen Lai ◽  
Kate Lorig ◽  
Sarah Szanton
Keyword(s):  
Chronic Disease ◽  
Pilot Study ◽  
Self Efficacy ◽  
Emotional Regulation ◽  
Longitudinal Research ◽  
Interleukin 10 ◽  
Cross Sectional Study ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Tnf Α

Introduction/Background: Chronic diseases, like diabetes and heart disease, are considered inflammatory conditions with elevated levels of the proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) and the anti-inflammatory cytokine interleukin-10 (IL-10). Disease progression is not consistent from person to person. Psychosocial factors are hypothesized to play a modifying role. Self-efficacy, the confidence in one’s ability to perform well in a specific life domain or at a specific task, is associated with better health outcomes. Coping self-efficacy is confidence in one’s ability to handle life’s problems through emotional regulation, problem-solving, and social support. Little is known about associations between coping self-efficacy and inflammation. Aim: The purpose of this pilot study was to examine associations between coping self-efficacy and IL-6, IL-10, and TNF-α levels. Method: This was a cross-sectional study conducted over two visits. Sociodemographic variables, chronic disease count, body mass index (BMI), and coping self-efficacy were collected. Inflammatory markers were collected via sweat using the sweat patch, a noninvasive collection device. Results: Higher TNF-α and IL-10 levels were significantly associated with low coping self-efficacy (β = −.03, p = .028; β = −.017, p = .007, respectively) after adjustment for age, sex, race, BMI, and chronic disease count. IL-6 trended toward significance after adjustment as well (β = −.22, p = .054). Conclusions: This pilot study showed that high coping self-efficacy was associated with lower IL-6, IL-10, and TNF-α levels, indicating a potential buffering effect of high coping self-efficacy. Further longitudinal research with larger sample sizes is needed.

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

Biologia ◽  
2007 ◽  
Vol 62 (3) ◽  
Author(s):  
Albena Alexandrova ◽  
Elena Bandžuchová ◽  
Anton Kebis ◽  
Marián Kukan ◽  
Daniel Kuba
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Matrix Metalloproteinase ◽  
Oxidative Dna Damage ◽  
Interleukin 10 ◽  
Matrix Metalloproteinase 2 ◽  
Necrosis Factor Alpha ◽  
Tissue Samples ◽  
Tnf Α ◽  
Rat Livers

AbstractCopper is known to induce oxidative stress in a number of models. It was shown that many pathophysiological events were associated with oxidative stress. Further, oxidative stress can increase gene expression of cytokines and of metalloproteinases. We previously found that copper toxic effects in isolated perfused rat livers were associated with significant oxidative stress (as assessed by lipid peroxidation, protein oxidation and oxidative DNA damage, particularly at concentration of 0.03 mM of Cu2+ in the perfusate). Here we investigated gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10); matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in frozen liver tissue samples by the real-time PCR assay. Compared to controls, copper at concentration of 0.01 mM did not affect gene expression of TNF-α, IL-10, MMP-2 and MMP-9, whereas copper at concentration of 0.03 mM significantly decreased gene expression of all the four TNF-α, IL-10, MMP-2 and MMP-9 by 69%, 81%, 43%, and 62%, respectively. These results suggest that copper-induced oxidative stress in the isolated rat liver can lead to the suppression of gene expression. Because TNF-α and metalloproteinases are involved also in liver regeneration, the suppression of these genes by copper may be one of the mechanisms by which acute intoxication of animals and humans with copper may impair regenerative capability of the liver.

scholarly journals Cinnamon and Eucalyptus Oils Suppress the Inflammation Induced by Lipopolysaccharide In Vivo

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7410
Author(s):  
Chen Zhao ◽  
Yuwei Cao ◽  
Zhuo Zhang ◽  
Dechao Nie ◽  
Yanling Li
Keyword(s):  
Tissue Injury ◽  
Body Weight Gain ◽  
Animal Health ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Cinnamon Oil ◽  
Eucalyptus Oil ◽  
Tnf Α ◽  
Anti Inflammatory

Inflammation caused by bacterial lipopolysaccharide (LPS) disrupts epithelial homeostasis and threatens both human and animal health. Therefore, the discovery and development of new anti-inflammatory drugs is urgently required. Plant-derived essential oils (EOs) have good antioxidant and anti-inflammatory activities. Thus, this study aims to screen and evaluate the effects of cinnamon oil and eucalyptus oil on anti-inflammatory activities. The associated evaluation indicators include body weight gain, visceral edema coefficient, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), nitrogen monoxide (NO), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), Urea, Crea, ALT, TLR4, MyD88, NF-κB, IκB-α, iNOS, and Mn-SOD. In addition, tissue injury was determined by H&E staining. The results revealed that cinnamon oil and eucalyptus oil suppressed inflammation by decreasing SOD, TNF-α, and NF-κB levels. We also found that cinnamon oil increased the level of GSH-Px, MDA, and Mn-SOD, as well as the visceral edema coefficient of the kidney and liver. Altogether, these findings illustrated that cinnamon oil and eucalyptus oil exhibited wide antioxidant and anti-inflammatory activities against LPS-induced inflammation.

Clinical, Virological, and Immunological Profiles of DENV, ZIKV, and/or CHIKV-Infected Brazilian Patients

Intervirology ◽  
2020 ◽  
Vol 63 (1-6) ◽  
pp. 33-45
Author(s):  
Juan Camilo Sánchez-Arcila ◽  
Jessica Badolato-Correa ◽  
Thiara Manuele Alves de Souza ◽  
Iury Amâncio Paiva ◽  
Luciana Santos Barbosa ◽  
...  
Keyword(s):  
Viral Load ◽  
Inverse Correlation ◽  
Interleukin 10 ◽  
Serum Samples ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Infected Adult ◽  
Chemokine Ligand ◽  
And Migration

<b><i>Background:</i></b> Arboviruses co-circulating within a population that are transmitted by the same vector have the potential to cause coinfections. Coinfections with dengue virus (DENV), Zika virus (ZIKV), and chikungunya virus (CHIKV) have been occurring in Brazil, but it is not well-understood how human responses vary during mono- or coinfections and whether they play different roles in pathogenesis. <b><i>Methods:</i></b> We investigated the clinical, virological, and immunological status during patients’ acute infections, focusing on the CCL/CXC chemokines, proinflammatory, as well as anti-inflammatory cytokines levels quantified by ELISAs. Viral load was determined by qRT-PCR in serum samples from 116 acute DENV, ZIKV, CHIKV, DENV/ZIKV, and CHIKV/ZIKV-infected adult patients from Brazil. <b><i>Results:</i></b> Most of the acute patients displayed fever, headache, prostration, and myalgia, regardless of the type of arbovirus infection. Zika viral load was higher in CHIKV/ZIKV coinfected patients compared with ZIKV or DENV/ZIKV infections. All infected individuals presented increased concentrations of C-X-C motif chemokine ligand 10/interferon protein-10 (CXCL10/IP-10), C-C motif chemokine ligand 2/monocyte chemoattractant protein-1 (CCL2/MCP-1), and tumor necrosis factor alpha (TNF-α) compared to healthy donors. Interestingly, the ZIKV group separated from CHIKV/ZIKV due to higher levels of interleukin-10 (IL-10) and lower levels of TNF-α. While DENV/ZIKV differentiated from CHIKV due to their higher levels of CCL2/MCP-1, in CHIKV- and CHIKV/ZIKV-infected patients, levels of CXC10/IP-10, CCL2/MCP-1, and migration inhibitory factor (MIF) were associated with CHIKV viral load. By contrast, in DENV/ZIKV- and CHIKV/ZIKV-infected patients, levels of CXCL10/IP-10, CCL2/MCP-1, and TNF-α showed a significant inverse correlation with ZIKV viral load. <b><i>Conclusions:</i></b> From all the circulating mediators measured, we detected differences of IL-10, TNF-α, and CCL2/MCP-1 between arbovirus groups. We hypothesize that CXC10/IP-10, CCL2/MCP-1, and MIF in the CHIKV-infected group could regulate the CHIKV viral load, while CXC10/IP-10, CCL2/MCP-1, and TNF-α in DENV/ZIKV, and CHIKV/ZIKV groups, could regulate ZIKV viral load.

scholarly journals Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis

2002 ◽  
Vol 70 (6) ◽  
pp. 2862-2868 ◽  
Author(s):  
Manuela Puliti ◽  
Christina von Hunolstein ◽  
Claudie Verwaerde ◽  
Francesco Bistoni ◽  
Graziella Orefici ◽  
...  
Keyword(s):  
Systemic Infection ◽  
Interleukin 10 ◽  
Dose Dependence ◽  
Necrosis Factor Alpha ◽  
Clear Cut ◽  
Type Iv ◽  
Clinical Observations ◽  
Tnf Α ◽  
Group B

ABSTRACT Intravenous inoculation of CD-1 mice with 107 CFU of type IV group B Streptococcus (GBS) results in a high incidence of diffuse septic arthritis , associated with high levels of systemic and local production of interleukin-1β (IL-1β) and IL-6. In this study, the role of the anti-inflammatory cytokine IL-10 in the evolution of GBS systemic infection and arthritis was evaluated. IL-10 production was evident in sera and joints of GBS-infected mice. Neutralization of endogenous IL-10 by administration of anti-IL-10 antibodies (1 mg/mouse) at the time of infection resulted in worsening of articular lesions and 60% mortality associated with early sustained production of IL-6, IL-1β, and tumor necrosis factor alpha (TNF-α). The effect of IL-10 supplementation was assessed by administering IL-10 (100, 200, or 400 ng/mouse) once a day for 5 days, starting 1 h after infection. Treatment with IL-10 had a beneficial effect on GBS arthritis, and there was a clear-cut dose dependence. The decrease in pathology was associated with a significant reduction in IL-6, IL-1β, and TNF-α production. Histological findings showed limited periarticular inflammation and a few-cell influx in the articular cavity of IL-10-treated mice, confirming clinical observations. In conclusion, this study provides further information concerning the role of IL-10 in regulating the immune response and inflammation and calls attention to the potential therapeutic use of IL-10 in GBS arthritis.

scholarly journals Autocrine and Exocrine Regulation of Interleukin-10 Production in THP-1 Cells Stimulated with Borrelia burgdorferi Lipoproteins

2002 ◽  
Vol 70 (4) ◽  
pp. 1881-1888 ◽  
Author(s):  
Guillermo H. Giambartolomei ◽  
Vida A. Dennis ◽  
Barbara L. Lasater ◽  
P. K. Murthy ◽  
Mario T. Philipp
Keyword(s):  
Borrelia Burgdorferi ◽  
Interleukin 10 ◽  
Feedback Mechanism ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Necrosis Factor Alpha ◽  
Negative Feedback Mechanism ◽  
Human Monocytic Cell Line ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT We have recently demonstrated that interleukin-10 (IL-10), produced by THP-1 monocytes in response to Borrelia burgdorferi lipoproteins, dampens the production of concomitantly elicited inflammatory cytokines. Thus, IL-10 could potentially down-regulate inflammatory and microbicidal effector mechanisms of the innate immune response to a B. burgdorferi infection, facilitating the establishment of the spirochete. To understand the mechanism(s) implicated in the regulation of the synthesis and release of IL-10 during early infection, we investigated the autocrine effects of IL-6, IL-12, tumor necrosis factor alpha (TNF-α), and IL-10 itself, as well as the exocrine effect of IFN-γ on the production of macrophage-derived IL-10 with lipoprotein as a stimulant. In addition, in view of the differences in the receptor and signal transduction pathways of lipopolysaccharide (LPS) and bacterial lipoproteins, we also investigated the effects described above with LPS as a stimulant. The THP-1 human monocytic cell line and purified recombinant lipidated OspA (L-OspA) were used as the model target cell and stimulant, respectively. TNF-α increased the production of IL-10, as elicited by lipoproteins. The production of IL-10 by THP-1 cells stimulated with L-OspA was autoregulated by a negative feedback mechanism involving the IL-10 receptor (IL-10R). Exogenous IFN-γ significantly inhibited the production of IL-10. Both autocrine (IL-10) and exocrine (IFN-γ) inhibition of IL-10 production resulted in an increase in the production of the proinflammatory cytokines IL-6 and IL-12. The same results were obtained when the stimulant was LPS. The results further illustrate that IL-10 may play a pivotal role in Lyme disease pathogenesis. Moreover, the regulation of its production with lipoprotein as a stimulant is indistinguishable from that observed when LPS acts as a stimulant.

Effects of eccentric treadmill exercise on inflammatory gene expression in human skeletal muscle

2009 ◽  
Vol 34 (4) ◽  
pp. 745-753 ◽  
Author(s):  
Thomas W. Buford ◽  
Matthew B. Cooke ◽  
Brian D. Shelmadine ◽  
Geoffrey M. Hudson ◽  
Liz Redd ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Soreness ◽  
Vastus Lateralis ◽  
Maximal Oxygen Consumption ◽  
Housekeeping Gene ◽  
Necrosis Factor Alpha ◽  
Muscle Gene Expression ◽  
Tnf Α

The present study examined the skeletal muscle expression of several genes related to the inflammatory process before and after a bout of downhill running. Twenty-nine males between the ages of 18 and 35 years performed a 45-min downhill (–17.5%) treadmill protocol at 60% of maximal oxygen consumption. Venous bloods samples and muscle biopsy samples from the vastus lateralis were donated prior to and at 3-h and 24-h postexercise, along with ratings of perceived muscle soreness. Serum creatine kinase (CK) was determined, as was skeletal muscle gene expression of interleukin (IL)-6, IL-8, IL-12 (p35), tumor necrosis factor-alpha (TNF-α), IL-1β, cyclooxygenase 2 (COX2), and nuclear factor kappa B (NFkB) (p105/p50). Gene expression was analyzed using RT-PCR and compared with a standard housekeeping gene (β-actin). Data were analyzed for statistical differences using multivariate analysis of variance with univariate follow-up. In addition, Pearson correlations were conducted to determine if any significant relationship exists between any of these transcripts and both CK and muscle soreness. Significant (p < 0.05) up-regulations in IL-6, IL-8, and COX2 mRNA expression were observed compared with baseline, whereas no significant changes for IL-12, IL-1β, TNF-α, or NFkB were noted. Significant increases in IL-6 mRNA were observed at 3 h (p < 0.001) and 24 h (p = 0.043), whereas significant increases in IL-8 (p = 0.001) and COX2 (p = 0.046) mRNA were observed at 3-h postexercise. In addition, muscle soreness was significantly correlated with IL-8 at 24 h (r = –0.370; p = 0.048), whereas CK was significantly related to NFkB at baseline (r = –0.460; p = 0.012). These data indicate that increases in the mRNA expression of IL-6, IL-8, and COX2 occur in the vastus lateralis as a result of damaging eccentric exercise in young, recreationally trained males. Further, it appears that IL-8 transcription may play some role in inhibiting postexercise muscle soreness, possibly through regulation of angiogenesis.

scholarly journals Innate Lung Defenses and Compromised Pseudomonas aeruginosa Clearance in the Malnourished Mouse Model of Respiratory Infections in Cystic Fibrosis

2000 ◽  
Vol 68 (4) ◽  
pp. 2142-2147 ◽  
Author(s):  
H. Yu ◽  
S. Z. Nasr ◽  
V. Deretic
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Knockout Mice ◽  
Respiratory Infections ◽  
Bacterial Colonization ◽  
Interleukin 10 ◽  
High Morbidity ◽  
Necrosis Factor Alpha ◽  
Pulmonary Clearance ◽  
Tnf Α

ABSTRACT Cystic fibrosis (CF) is characterized by dysfunction of the digestive and respiratory tracts resulting in generalized malnutrition and chronic respiratory infections. Chronic lung infections withPseudomonas aeruginosa, intense neutrophil-dominated airway inflammation, and progressive lung disease are the major cause of high morbidity and mortality in CF. Here we investigated the effects of malnutrition in CF on innate lung defenses, susceptibility to P. aeruginosa colonization, and associated inflammation, using aerosol models of acute and chronic infections in normal, malnourished, and transgenic mice. CFTRm1Unc−/− knockout mice displayed body weight variations and showed variable pulmonary clearance of P. aeruginosa. This variability was not detected in bitransgenicCFTRm1Unc−/− (FABP-hCFTR) mice in which the intestinal defect had been corrected. Diet-induced protein calorie malnutrition in C57BL/6J mice resulted in impaired pulmonary clearance of P. aeruginosa. Tumor necrosis factor alpha (TNF-α) and nitrite levels detected upon exposure to P. aeruginosaaerosols were lower in the lungs of the malnourished C57BL/6J mice relative than in lungs of mice fed a normal diet. The role of TNF-α and reactive nitrogen intermediates in P. aeruginosaclearance was tested in TNF-α and inducible nitric oxide synthase (iNOS) knockout mice. P. aeruginosa clearance was diminished in transgenic TNF-α- and iNOS-deficient mice. In contrast to the effects of TNF-α and iNOS, gamma interferon knockout mice retained a full capacity to eliminate P. aeruginosafrom the lung. Malnutrition also contributed to excessive inflammation in C57BL/6J mice upon chronic challenge with P. aeruginosa. The repeatedly infected malnourished host did not produce interleukin-10, a major anti-inflammatory cytokine absent or diminished in the bronchoalveolar fluids of CF patients. These results are consistent with a model in which defective CFTR in the intestinal tract leads to nutritional deficiency which in turn contributes to compromised innate lung defenses, bacterial colonization, and excessive inflammation in the CF respiratory tract.

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