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A diet high in carotenoid-rich vegetables and fruits favorably impacts inflammation status by increasing plasma concentrations of IFN-α2 and decreasing MIP-1β and TNF-α in healthy individuals during a controlled feeding trial.
Jahns, L, Conrad, Z, Johnson, LK, Whigham, LD, Wu, D, Claycombe-Larson, KJ
Nutrition research (New York, N.Y.). 2018;:98-104
Abstract
The health benefits of vegetable and fruit (VF) intake include benefits for diseases that have an inflammatory component, although the relationship between VF intake and systemic inflammatory status is unclear due to the lack of comprehensive analysis of inflammatory markers in most studies. Therefore, our hypothesis was that the consumption of carotenoid-rich vegetables and fruits in the diet would have a beneficial effect on systemic inflammation status. In this study, we determined the association between varying doses of carotenoid-rich VF intake, plasma carotenoids, and a broad array of markers including 26 cytokines and high-sensitivity C-reactive protein. Data were derived from a single-arm controlled clinical feeding trial in which healthy, nonobese individuals received a low-carotenoid prescription for 6 weeks and then consumed a provided high-VF diet for 8 weeks. Proinflammatory cytokines and plasma carotenoids were measured at baseline, at 6 weeks, and at the end of the 8-week feeding period. Maximum likelihood estimation was used to calculate overall correlations between total plasma carotenoid concentrations and the cytokines. Plasma carotenoids decreased during the low-carotenoid treatment and increased during the feeding treatment. Of the inflammatory markers measured, we found increased plasma concentrations of interferon α-2 (P = .003) and decreased macrophage inflammatory protein-1β (P = .027) and tumor necrosis factor-α (P = .012) after consumption of the carotenoid-rich diet. These results indicate that consumption of VF may be important in the maintenance of beneficial inflammatory homeostasis.
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Assessment of local and systemic 25-hydroxy-vitamin D, RANKL, OPG, and TNF levels in patients with rheumatoid arthritis and periodontitis.
Balci Yuce, H, Gokturk, O, Aydemir Turkal, H, Inanir, A, Benli, I, Demir, O
Journal of oral science. 2017;(3):397-404
Abstract
The present study aimed to evaluate proinflammatory cytokine and vitamin D levels in rheumatoid arthritis (RA) and chronic periodontitis (CP) patients and healthy individuals before and after initial periodontal treatment. Overall, 17 CP patients with RA (RA + CP), 18 systemically healthy CP patients (CP), and 18 healthy controls (C) were included. Clinical periodontal measurements were recorded and gingival crevicular fluid (GCF) and blood samples were recorded. RA + CP and CP patients received nonsurgical periodontal treatment. Vitamin D, tumor necrosis factor (TNF)-α, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls (P < 0.05). Periodontal treatment improved clinical parameters in all periodontitis groups (P < 0.05). GCF vitamin D levels were higher in RA + CP and CP groups than in healthy controls, but these levels decreased in the RA + CP group after periodontal treatment (P < 0.05). Serum RANKL and GCF TNF-α levels in RA patients decreased after periodontal treatment (P < 0.05). Within the limitations of this study, the results suggested that GCF vitamin D levels are increased in RA patients and decrease after periodontal treatment; therefore, local vitamin D levels might be an important indicator of periodontal bone loss.
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Prospective assessment of body weight and body composition changes in patients with psoriasis receiving anti-TNF-α treatment.
Renzo, LD, Saraceno, R, Schipani, C, Rizzo, M, Bianchi, A, Noce, A, Esposito, M, Tiberti, S, Chimenti, S, DE Lorenzo, A
Dermatologic therapy. 2011;(4):446-51
Abstract
Tumor necrosis factor (TNF)-α is a pro-inflammatory cytokine associated with psoriasis pathogenesis. Anti-TNF-α therapies are effective in psoriasis. A significant weight gain has been reported in patients treated with anti-TNF-α agents. The aim of the present study was to evaluate the body composition changes in psoriatic patients receiving anti-TNF-α therapies according with disease phenotype. Forty patients affected with psoriasis were followed up for 24 weeks and divided into two groups: psoriasis vulgaris (PsO) and psoriatic arthritis (PsA). Anthropometric, blood biochemical, body composition parameters, resting metabolic rate, and disease activity indexes were measured at baseline and at week 24. After 24 weeks of anti-TNF-α administration, the disease activity indexes and concentration of inflammatory markers were significantly decreased. Seventy-five percent of PsO and 60% of PsA patients had an increase in body weight. Weight changes correlated with fat mass gain in the PsO group, and with fat and lean mass gain in the PsA group. In the present study, we demonstrated that a blockage of TNF-α bioactivity is related with fat and lean mass gain in both PsO and PsA subjects. The anti-TNF-α therapies could play a key role in the cross talk between adipose tissue and skeletal muscle, mediated by the reduction of TNF-α and interleukin-6 production.
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The effect of anti-TNF agent on oxidation status in patients with ankylosing spondylitis.
Karkucak, M, Capkin, E, Alver, A, Akyuz, A, Kiris, A, Ak, E, Topbas, M, Tosun, M
Clinical rheumatology. 2010;(3):303-7
Abstract
The aim of this study was to comparatively evaluate oxidative status of ankylosing spondylitis (AS) patients receiving anti-tumor necrosis factor (TNF) or non-steroid anti-inflammatory drugs (NSAID). Forty-seven patients with AS and 27 healthy controls were enrolled. Of these, 23 were on anti-TNF (group 1) and 24 on NSAIDs (group 2). Groups 1 and 2 were consisted of matched patients with respect to age, gender, body mass index, disease duration, C-reactive protein, erythrocyte sedimentation rate, total cholesterol, and Bath Ankylosing Spondylitis Disease Activity Index. Mean duration of treatment for patients in group 1 was 12.6 +/- 6.8 months. Serum total antioxidative status (TAS) and total oxidative status (TOS) levels were determined using new automated methods. Oxidative stress index (OSI) was calculated. The groups' carotid intima-media thicknesses (IMT-C) were also measured using ultrasonography. Group 1 had the highest TAS and lowest TOS levels. The TOS levels of group 1 was lower than the control, while group 2 being higher than controls. The difference in TOS levels between group 1 and group 2 was statistically significant (p = 0.040). OSI values were highest in group 2 and lowest in group 1. There was no significant correlation between oxidant/antioxidant parameters and IMT-C for group 1 (r = -0.30, p = 0.198 for OSI; r = 0.22, p = 0.366 for TAS; r = -0.22, p = 0.361 for TOS). This is the first study to evaluate total oxidative/antioxidative status in patients with AS on anti-TNF agent. These results clearly indicate positive effects of anti-TNF treatment on oxidative status of AS patients. The limited effects of NSAIDs compared with controls may be due to excess impaired oxidative status in the patients in this study.
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The effect of montelukast on soluble interleukin-2 receptor and tumor necrosis factor alpha in pediatric asthma.
Can, M, Yüksel, B, Demirtaş, S, Tomaç, N
Allergy and asthma proceedings. 2006;(4):383-6
Abstract
Proinflammatory cytokines such as tumor necrosis factor (TNF) alpha and soluble interleukin 2 receptor (sIL-2R) are very important mediators in induction of inflammatory response in lung. The aim of this study was to investigate anti-inflammatory response of cysteinyl leukotriene receptor antagonist montelukast on macrophage and T-cell activation by sIL-2R and TNF-alpha in mild atopic asthmatic children. Fifteen children with mild-to-moderate atopic asthma and 15 nonatopic children as control, enrolled in the study. Asthmatic children were treated with montelukast, 5-mg tablets, for 1 month. Lung function test forced expiratory volume in 1 second (FEV1) was performed before and after treatment. Serum TNF-alpha, sIL-2R, and eosinophil cationic protein levels were determined in the control group and in asthmatic children before and after treatment. The mean eosinophil cationic protein value was significantly decreased (33.1 +/- 14.8 and 22.2 +/- 12.1; p < 0.05) and FEV1 was significantly increased (86.9 +/- 20.9 and 102.1 +/- 12.7; p < 0.05) after 1 month treatment with montelukast. The mean serum IL-2R levels were significantly higher in the before treatment group than in the after treatment group (1061.9 +/- 491 and 794 +/- 230.9; p < 0.05) or in control subjects (581.1 +/- 123; p < 0.01). The mean serum TNF-alpha level was higher in the before treatment group than in the after treatment group and control group (7.30 +/- 3.93, 5.20 +/- 1.46, and 4.95 +/- 1.27; p < 0.05). There was a significant correlation between TNF-alpha and sIL-2R in patients before montelukast treatment (r = 0.674; p < 0.01). This study indicates that montelukast improves clinical parameters and shows anti-inflammatory response by decreasing serum sIL-2R and TNF-alpha levels.
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Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis.
Popa, C, Netea, MG, Radstake, T, Van der Meer, JW, Stalenhoef, AF, van Riel, PL, Barerra, P
Annals of the rheumatic diseases. 2005;(2):303-5
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Abstract
BACKGROUND Tumour necrosis factor (TNF) is known to increase the concentrations of interleukin (IL) 6 and C reactive protein (CRP) and to induce proatherogenic changes in the lipid profile and may increase the cardiovascular risk of patients with rheumatoid arthritis (RA) and other inflammatory disorders. OBJECTIVE To assess whether anti-TNF therapy modifies the cardiovascular risk profile in patients with RA. METHODS The lipoprotein spectrum and the inflammation markers CRP and IL6 were investigated in 33 patients with RA treated with human anti-TNF monoclonal antibodies (D2E7, adalimumab, Humira) and 13 patients with RA given placebo, before and after 2 weeks' treatment. RESULTS In the anti-TNF treated group, the mean (SD) concentrations of HDL-cholesterol were significantly higher after 2 weeks' treatment (0.86 (0.30) mmol/l v 0.98 (0.33) mmol/l, p<0.01), whereas LDL and triglyceride levels were not significantly changed. Additionally, a significant decrease in CRP (86.1 (54.4) mg/l v 35.4 (35.0) mg/l, p<0.0001), and IL6 (88.3 (60.5) pg/ml v 42.3 (40.7) pg/ml, p<0.001) concentrations was seen in this group. No changes in lipid profile, IL6, or CRP levels were seen in the placebo group. CONCLUSIONS TNF neutralisation with monoclonal anti-TNF antibodies increased HDL-cholesterol levels and decreased CRP and IL6 levels after 2 weeks. Therefore this treatment may improve the cardiovascular risk profile of patients with RA.
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Peripheral blood mononuclear cell expression of toll-like receptors and relation to cytokine levels in cirrhosis.
Riordan, SM, Skinner, N, Nagree, A, McCallum, H, McIver, CJ, Kurtovic, J, Hamilton, JA, Bengmark, S, Williams, R, Visvanathan, K
Hepatology (Baltimore, Md.). 2003;(5):1154-64
Abstract
Activation of macrophages by endotoxin is assumed responsible for increased circulating tumor necrosis factor alpha (TNF-alpha) and soluble TNF receptor (sTNFR) levels in cirrhosis. Relevant to this is expression of Toll-like receptor (TLR) 4 and TLR2, which is critically involved in production of TNF-alpha in response to endotoxin and Gram-positive microbial stimuli, respectively. The first studies on this in cirrhosis are reported here. In 36 cirrhotic patients and 32 controls, we measured (1) circulating endotoxin, TNF-alpha, and sTNFR levels; (2) peripheral blood mononuclear cell (PBMC) expression of TLR4 and TLR2, and (3) in vitro TNF-alpha production by PBMCs stimulated with endotoxin or Staphylococcus aureus enterotoxin B (SEB). PBMC expression of TLR2, circulating TNF-alpha levels, and in vitro TNF-alpha production were reassessed after supplementation with a synbiotic regimen known to increase intestinal levels of Gram-positive bacteria. Endotoxin, TNF-alpha, and sTNFR levels were significantly increased in cirrhosis. Endotoxin levels did not correlate significantly with other parameters. PBMC expression of TLR2 but not TLR4 was significantly up-regulated in cirrhosis and correlated significantly with serum TNF-alpha and sTNFR levels. In vitro TNF-alpha production by PBMCs stimulated by SEB was significantly blunted. Supplementation with the synbiotic regimen resulted in significant up-regulation of PBMC expression of TLR2. Serum TNF-alpha levels were further increased and in vitro TNF-alpha production further reduced in most patients. In conclusion, up-regulation of PBMC expression of TLR2 but not TLR4 occurs in cirrhosis, which implies, contrary to previous assumptions, an important stimulatory role for Gram-positive microbial components but not endotoxin. TLR2 likely contributes to increased circulating TNF-alpha and sTNFR levels in cirrhosis.
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Pentoxiphylline reduces nitric oxide production among patients with HIV infection.
Wanchu, A, Khullar, M, Bhatnagar, A, Sud, A, Bambery, P, Singh, S
Immunology letters. 2000;(2):121-5
Abstract
Tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) levels are elevated among patients with human immunodeficiency virus (HIV) infection. TNF-alpha is known to lower NO production. In this study we used a TNF-alpha inhibitor, pentoxiphylline, to treat patients with HIV infection who were free of opportunistic infections and see if NO production was altered with this drug. NO production was determined by spectrophotometric analysis using nitrite and citrulline as surrogate markers and TNF-alpha levels were determined by ELISA before and after 4 weeks of the treatment. Nineteen patients (ten males, mean age 36.6+/-5.2 years) and 16 age and sex matched healthy controls were studied. Mean CD4 counts of patients were 206.5 mm(3). Nitrite level among patients at recruitment was 99.7+/-26.5 nmol/ml (range 50-167 nmol/ml) and was significantly higher than 46.4+/-16.2 nmol/ml; the value of healthy controls (P<0.05). Patient levels declined significantly to 44. 2+/-19.7 nmol/ml (range 10-106.6 nmol/ml) following 4 weeks of therapy (P<0.01). Citrulline level at recruitment was 810.8+/-425.8 nmol/ml (range 366.6-1888.7 nmol/ml), which was significantly higher than 488.6+/-224.5 nmol/ml, the level of controls (P<0.01). There was a statistically significant decrease in these levels among patients to 533.6+/-299.5 nmol/ml (range 250-163.4 nmol/ml) after 4 weeks of therapy (P<0.01). TNF-alpha levels showed a significant decline in the OD values from 0.34+/-0.22 at the start of therapy to 0.24+/-0.18 (P<0.05). We conclude that the use of pentoxiphylline is associated with decrease in TNF-alpha levels and NO production.
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Sodium nitroprusside in patients with compromised left ventricular function undergoing coronary bypass: reduction of cardiac proinflammatory substances.
Massoudy, P, Zahler, S, Freyholdt, T, Henze, R, Barankay, A, Becker, BF, Braun, SL, Meisner, H
The Journal of thoracic and cardiovascular surgery. 2000;(3):566-74
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Abstract
OBJECTIVE The aim of the present study was to investigate whether the nitric oxide donor sodium nitroprusside can reduce the cardiac inflammatory response during coronary artery bypass grafting in patients with severely compromised left ventricular function. METHODS Patients (n = 30) were assigned to receive placebo or sodium nitroprusside (0.5 microg. kg(-1). min(-1)) for the first 60 minutes of reperfusion. Interleukin 6, interleukin 8, and tumor necrosis factor alpha levels; platelet adhesion molecule CD41 and CD62 levels; and CD11b on leukocytes were determined in the radial artery and coronary sinus before cardiopulmonary bypass and during reperfusion (1, 5, 10, 35, and 75 minutes). RESULTS At 1 minute of reperfusion, coronary venous levels of CD41-positive polymorphonuclear leukocytes were 8% lower than arterial levels in the placebo group and 18% higher in the sodium nitroprusside group (P =.021). At 5 minutes of reperfusion, the respective levels were 29% and 1% for interleukin 6 (P =.015), -5% and 20% for CD41-positive monocytes (P =.032), and -2% and 16% for CD11b-positive monocytes (P =.038). At 10 minutes of reperfusion, these levels were -14% and 21% for CD41-positive monocytes (P =.006). At 35 minutes of reperfusion, these levels were -13% and 7% for CD41-positive monocytes (P =.017), -41% and 23% for CD11b-positive monocytes (P =.001), and 7% and 25% for CD62-positive platelets (P =. 041). At 75 minutes of reperfusion, the levels were 15% and -7% for tumor necrosis factor alpha (P =.025) and -10% and 10% for CD62-positive platelets (P =.041). CONCLUSIONS Transcardiac production of proinflammatory cytokines is reduced in patients undergoing coronary artery bypass grafting treated with the nitric oxide donor sodium nitroprusside. At the same time, less activated leukocytes and platelets are retained in the coronary circulation.