scholarly journals Acute Effect of a Single Dose of Tomato Sofrito on Plasmatic Inflammatory Biomarkers in Healthy Men

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 851 ◽  
Author(s):  
Sara Hurtado-Barroso ◽  
Miriam Martínez-Huélamo ◽  
Jose Fernando Rinaldi de Alvarenga ◽  
Paola Quifer-Rada ◽  
Anna Vallverdú-Queralt ◽  
...  
Keyword(s):  
Single Dose ◽  
Bioactive Compounds ◽  
Acute Effect ◽  
Inflammatory Biomarkers ◽  
Positive Health ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Factor Α ◽  
Antioxidant Diet

Sofrito is a Mediterranean tomato-based sauce that typically also contains olive oil, onion, and garlic. The preparation of sofrito modifies the bioactive compounds (carotenoids and polyphenols) in the ingredients to more bioavailable forms, promoting cis-lycopene formation and polyphenol bioaccessibility. To evaluate the health benefits of this cooking technique, the effect of consuming an acute dose of sofrito on the inflammatory status was studied. In a clinical trial, 22 healthy male subjects consumed a single dose of sofrito (240 g/70 kg) after three days without ingesting any tomato products and following a low-antioxidant diet the day before the intervention. Plasma carotenoids and total polyphenol excretion (TPE) were evaluated, as well as the inflammatory biomarkers C-reactive protein (CRP), interleukin-6 (IL-6), interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α). After the sofrito intake, a significant decrease in CRP (p = 0.010) and TNF-α (p = 0.011) was observed, but only TNF-α was inversely correlated with an increase in TPE and plasma β-carotene (not the major carotenoid, lycopene). The positive health effects of this tomato-based product may be attributed not only to lycopene, but to the bioactive compounds of all the ingredients.

β-Carotene Concentration and Its Association with Inflammatory Biomarkers in Spanish Schoolchildren

2017 ◽  
Vol 71 (1-2) ◽  
pp. 80-87 ◽  
Author(s):  
Elena Rodríguez-Rodríguez ◽  
Ana M. López-Sobaler ◽  
Beatriz Navia ◽  
Pedro Andrés ◽  
Ana I. Jiménez-Ortega ◽  
...  
Keyword(s):  
High Sensitivity ◽  
Inflammatory Biomarkers ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Hs Crp ◽  
Α Level ◽  
Factor Α ◽  
Β Carotene ◽  
Necrosis Factor

Aim: To examine the correlation between inflammatory biomarkers and plasma β-carotene levels in children. Methods: A total of 564 Spanish schoolchildren aged 9-12 were observed and studied. Plasma β-carotene levels were assessed by HPLC. A β-carotene level <4.83 µg/dL (0.09 µmol/L) was considered deficient. Plasma tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by immunoenzyme assays. Serum high-sensitivity C-reactive protein (hs-CRP) was tested by immunonephelometry. Results: Subjects who were β-carotene-deficient (23.1% of the studied children) had higher IL-6 levels than subjects with normal β-carotene concentrations. The log-IL-6 and log-hs-CRP concentrations, but not the log-TNF-α level, were strongly and inversely related to the plasma log-β-carotene level (taking into account log-age, energy intake, log-triglycerides, gender, log-body mass index, log-β-carotene intake, energy from lipids and cholesterol as covariables). When the 3 inflammatory biomarkers were introduced into the regression model along with the corresponding covariables, only the log-IL-6 level was related to the plasma log-β-carotene level (β = -0.505 ± 0.078; p < 0.001). Conclusions: Inflammatory status, in particular IL-6 levels, appears to be negatively associated with plasma β-carotene levels in schoolchildren.

scholarly journals Randomized Controlled Trial for Promotion of Healthy Eating in Older Adults by Increasing Consumption of Plant-Based Foods: Effect on Inflammatory Biomarkers

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3753
Author(s):  
Andreas Nilsson ◽  
Antonio Cano ◽  
Oscar Bergens ◽  
Fawzi Kadi
Keyword(s):  
Older Adults ◽  
Controlled Trial ◽  
Activity Level ◽  
Inflammatory Biomarkers ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Chemokine Ligand ◽  
Factor Α

To what extent the intake of fruit and vegetables (FV) influences inflammatory status remains elusive, particularly in older populations. The aim of the present study was to determine the effect of increased FV intake for 16 weeks on circulating biomarkers of inflammation in a population of older men and women. Sixty-six participants (65–70 years) randomly assigned to either FV or control (CON) groups were instructed to increase FV intake to five servings per day through nutritional counseling (FV) or to maintain habitual diet (CON). Dietary intake and physical activity level (PA) were determined using food frequency questionnaire and accelerometers, respectively, at the start and end of the intervention. C-reactive protein (CRP), interleukin 6 (IL-6), IL-18, macrophage inflammatory protein-1α (MIP-1α), MIP-1β, tumor necrosis factor-α (TNF-α), TNF-related apoptosis-inducing ligand (TRAIL), TNF-related activation-induced cytokine (TRANCE), and C-X3-C motif chemokine ligand-1 (CX3CL1, or fractalkine) were analyzed. The FV group significantly increased daily FV intake (from 2.2 ± 1.3 to 4.2 ± 1.8 servings/day), with no change in CON. Waist circumference and PA level were unchanged by the intervention. Interaction effects (time × group, p < 0.05) for TRAIL, TRANCE, and CX3CL1 denoting a significant decrease (p < 0.05) in FV but not in CON were observed. No corresponding effects on CRP, IL6, TNF-α, MIP-1α, and β and IL-18 were observed. The present study demonstrates the influence of increased FV consumption on levels of some inflammatory biomarkers in a population of older adults. Future work is warranted to examine the clinical implications of FV-induced alterations in these inflammatory biomarkers.

Body dissatisfaction predicts inflammatory status in asymptomatic healthy individuals

2016 ◽  
Vol 23 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Maša Černelič-Bizjak ◽  
Zala Jenko-Pražnikar
Keyword(s):  
Body Dissatisfaction ◽  
Inflammatory Biomarkers ◽  
Lifestyle Behaviour ◽  
Inflammatory Cytokine Production ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Circulating Levels ◽  
Necrosis Factor

Body dissatisfaction may play some role in the pathophysiology of chronic diseases. This study examined relations between body dissatisfaction and circulating levels of inflammatory biomarkers C-reactive protein, tumour necrosis factor-α, interleukin-6 and anti-inflammatory adiponectin, and to explore positive changes in relevant lifestyle behaviour after these associations. A total of 33 asymptomatic overweight men and women were evaluated at the baseline and after a 6-month lifestyle behaviour intervention. Body dissatisfaction emerged as an important predictor of pro- and anti-inflammatory biomarkers and may promote the production of inflammatory cytokines by reducing the level of anti-inflammatory and increasing the level of pro-inflammatory cytokine production.

Genetic Variation in TNF-α, its Relation with Inflammatory Biomarkers and Susceptibility to Rheumatoid Arthritis

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Khadiga Ahmed Ismail
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Functional Disability ◽  
Serum Levels ◽  
Amplification Refractory Mutation System ◽  
Reactive Protein ◽  
Tnf Α ◽  
Mutation System ◽  
Potential Factor ◽  
Factor Α

Background: Tumor necrosis Factor-α (TNF-α) is encoded and controlled by TNF-α gene, which is involved in rheumatoid arthritis (RA) susceptibility. This research aimed to identify genetic variations of TNF-α (G308A) and to establish its association with inflammatory markers in Rheumatoid Arthritis predisposition. Methods: In the present study, fifty RA patients and fifty volunteers were involved and evaluated for the C-reactive protein, rheumatoid factor, and TNF-α were estimated by ELISA, Erythrocyte Sedimentation Rate (ESR) by Wintergreen method and for TNF-α-308 G>A polymorphism by polymerase chain reaction with amplification refractory mutation system (PCR-ARMS). Results: The CRP, RF, ESR and TNF-α were significantly elevated in RA patients relative to controls. The serum level TNF-α was also significantly elevated in female patients and in patients ≥50 years. Analysis of TNF-308 gene polymorphism revealed that GG genotypes were more prevalent in RA patients than in the healthy individuals and that GG genotype may be a potential factor to RA. The G allele was more common in RA than in the control. Elevated TNF-α serum levels were significantly associated the GG genotype and functional disability in RA patients. Conclusion: TNF-α promoter 308polymorphism GG genotype may be considered as a risk factor for RA and the TNF-α serum level was significantly related to the functional disability in the disease.

TNF-α induced bronchial vasoconstriction

2000 ◽  
Vol 279 (3) ◽  
pp. H946-H951 ◽  
Author(s):  
Elizabeth M. Wagner
Keyword(s):  
Bronchial Artery ◽  
Autologous Blood ◽  
Inflammatory Status ◽  
Tnf Α ◽  
In Vitro Systems ◽  
Essential Function ◽  
Factor Α ◽  
Necrosis Factor ◽  
Airways Inflammation

The pro-inflammatory characteristics of tumor necrosis factor-α (TNF-α) have been extensively characterized in in vitro systems. Furthermore, this cytokine has been shown to play a pivotal role in airways inflammation in asthma. Since the airway vasculature also performs an essential function in inflammatory cell transit to the airways, experiments were performed to determine the effects of TNF-α on bronchial vascular resistance (BVR). In anesthetized, ventilated sheep, the bronchial artery (BA) was cannulated and perfused with autologous blood. BVR was defined as inflow pressure/flow and averaged 6.3 ± 0.2 mmHg · ml−1 · min−1 (±SE) for the 25 sheep studied. Recombinant human TNF-α (10 μg for 20 or 40 min) infused directly into the BA resulted in a significant decrease in BVR to 87% of baseline ( P < 0.05). This vasodilation was followed by a reversal of tone by 120 min and a sustained increase in BVR to 126% of baseline ( P < 0.05). Since others have shown TNF-α caused coronary vasoconstriction through endothelial release of endothelin-1 (ET-1), an ET-1 antagonist was used to block bronchial vasoconstriction. BQ-123, a selective ETA receptor antagonist, was delivered to the bronchial vasculature prior to TNF-α challenge. Attenuation of bronchial vasoconstriction was observed at 120 min ( P < 0.03). Thus TNF-α causes bronchial vasoconstriction by the secondary release of ET-1. Although TNF-α exerts pro-inflammatory actions on most cells of the airways, vasoactive properties of this cytokine likely further contribute to the inflammatory status of the airways.

scholarly journals Usporedba učinkovitosti i trogodišnjeg preživljenja TNF-α inhibitora u liječenju ankilozantnog spondilitisa

2020 ◽  
Vol 56 (1) ◽  
pp. 51-58
Author(s):  
Filip Mirić ◽  
Srđan Novak
Keyword(s):  
Ankylosing Spondylitis ◽  
Analogue Scale ◽  
Activity Index ◽  
Disease Activity Index ◽  
C Reactive Protein ◽  
Functional Index ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Cilj: Svrha rada bila je utvrditi i usporediti učinkovitost te preživljenje TNF-α (engl. tumor necrosis factor-α) inhibitora (adalimumab, golimumab, infliksimab) tijekom trogodišnjeg praćenja u liječenju ankilozantnog spondilitisa. Materijali i metode: Ovim retrospektivnim istraživanjem obuhvaćena je skupina od 29 ispitanika koji su primili prvi biološki lijek na Odjelu reumatologije i kliničke imunologije Kliničkog bolničkog centra Rijeka. Započeli su s biološkim lijekom u razdoblju od siječnja 2009. do lipnja 2015. godine i bili praćeni tri godine nakon početka terapije. Parametri kojima se pratila aktivnost bolesti bili su BASDAI (engl. Bath Ankylosing Spondylitis Disease Activity Index), BASFI (engl. Bath Ankylosing Spondylitis Functional Index), CRP (engl. C reactive protein) i VAS (engl. Visual Analogue Scale), a mjereni su prije početka terapije te nakon 3 i 36 mjeseci od njenog uvođenja. Rezultati: Od ukupno 29 ispitanika, 11 ih je bilo na adalimumabu, 10 na golimumabu, a 8 na infliksimabu. Analizirajući parametre uključene u ovo istraživanje (BASDAI, BASFI, CRP, VAS), ni u jednom promatranom periodu nije zabilježena statistički značajna razlika između ispitanika s obzirom na primijenjeni TNF-α inhibitor (svi p &gt; 0,05). Ukupno trogodišnje preživljenje TNF-α inhibitora iznosilo je 75,8 %. Kod ispitanika liječenih adalimumabom trogodišnje preživljenje iznosilo je 72,8 %, za golimumab 80 % te infliksimab 75 % (svi p &gt; 0,05). Zaključci: Uspoređujući ispitanike liječene adalimumabom, golimumabom i infliksimabom u prvoj liniji biološke terapije, naše istraživanje na malom broju ispitanika pokazalo je kako nema značajne razlike u njihovoj učinkovitosti i preživljenju.

scholarly journals Flow-Mediated Vasodilation Is Not Attenuated in Hypertensive Pregnancies Despite Biochemical Signs of Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Heli Saarelainen ◽  
Henna Kärkkäinen ◽  
Pirjo Valtonen ◽  
Kari Punnonen ◽  
Tomi Laitinen ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Brachial Artery ◽  
Normal Pregnancy ◽  
Hypertensive Disorder ◽  
Reactive Protein ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Factor Α ◽  
Artery Flow ◽  
Flow Mediated Vasodilation

Background. Our objective was to evaluate endothelial function and markers of inflammation during and after pregnancy in normal pregnancies compared to pregnancies complicated with hypertension or preeclampsia (PE). Methods and Results. We measured endothelium-dependent brachial artery flow-mediated vasodilation (FMD) and high sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α) in 32 women with normal pregnancy and in 28 women whose pregnancy was complicated with hypertensive disorder in the second half of pregnancy and minimum 3-month postpartum. Enhancement of endothelial function was greater in hypertensive than normal pregnancies, the mean FMD% being 11.0% versus 8.8% during pregnancy (P=0.194) and 8.0% versus 7.9% postpartum (P=0.978). Concentrations of markers of inflammation were markedly increased in pregnant hypertensive group compared to those after delivery (hsCRP 4.5 versus 0.80 mg/L, P=0.023, IL-6 2.1 versus 1.2 pg/mL, P=0.006; TNF-α 1.9 versus 1.5 pg/mL, P=0.030). There were no statistically significant associations between the markers of inflammation and FMD. Conclusions. Brachial artery FMD was not attenuated in the third trimester hypertensive pregnancies compared to normal pregnancies, whereas circulating concentrations of hsCRP and IL-6 and TNF-α reacted to hypertensive complications.

Acute Immunomodulatory Effects of Fentanyl and its Three New Analogues in Swiss Albino Mice

2017 ◽  
Vol 3 (1) ◽  
pp. 24 ◽  
Author(s):  
Shiv Kumar Yadav ◽  
Rahul Bhattacharya
Keyword(s):  
Pain Management ◽  
Opioid Receptor ◽  
Inflammatory Cytokines ◽  
Opioid Analgesic ◽  
Interleukin 10 ◽  
Acute Effect ◽  
Post Exposure ◽  
Tnf Α ◽  
Pre Treatment ◽  
Factor Α

Fentanyl is a potent synthetic opioid analgesic. However, due to its several limitations, new analogues are being synthesised for better pain management. We have earlier reported the synthesis and bio-efficacy of fentanyl and its eight new analogues (1-8) in mice. Among eight analogues tested, N-(1-(2-phenoxyethyl)-4-piperidinyl)propionanilide (2), N-isopropyl-3-(4-(N-phenylpropionamido)piperidin-1-yl)propanamide (5), and N-t-butyl-3-(4-(N-phenylpropionamido)piperidin-1-yl)propanamide (6) were found to be more effective and less toxic compared to fentanyl. Therapeutic efficacy of fentanyl and its analogues are known to be compromised due to many adverse effects, including alterations in the immune system. Therefore, the present study was undertaken to assess the acute effect of fentanyl and its three analogues (2, 5, and 6) on plasma levels of different pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and anti-inflammatory cytokines such as interleukin-10 (IL-10) at different time points. Mice were intraperitoneally treated with 0.50 LD50 of the compounds and cytokines were measured 1 h, 2 h, 4 h, and 24 h post-exposure. Compared to control, none of the treatments produced any change in TNF-α and IL-1β levels. However, IL-6 levels were significantly elevated between 1 h to 2 h post-exposure in fentanyl and analogue 2 treated groups. Further, IL-10 levels were found to be significantly increased in fentanyl, analogue 2, and 6 treated groups at 1 h and 2 h post-exposure. Pre-treatment of naltrexone (opioid receptor antagonist) blocked the effects of fentanyl, confirming that its effects were opioid receptor- dependent. However, effect of naltrexone on analogue 2 and 6 was not conclusively evidenced, indicating that immunomodulatory changes caused by the analogues could have some additional implications as well. The present study reveals undesirable effects of fentanyl and its new analogues on cytokines homeostasis, thereby limiting their use in pain management.

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