Gavala A.,National and Kapodistrian University of Athens |
Myrianthefs P.,National and Kapodistrian University of Athens |
Venetsanou K.,National and Kapodistrian University of Athens |
Baltopoulos G.,National and Kapodistrian University of Athens |
Alevizopoulos G.,Agioi Anargyroi General Hospital
African Journal of Psychiatry (South Africa) | Year: 2015
Alcohol exposure is related to increased susceptibility to infections. We investigated the effect of acute exposure to alcohol on pro- and anti-inflammatory cytokine production in an ex-vivo model of whole blood stimulation with lipopolysacharide (LPS). Ten ml of whole blood were taken from 24 healthy volunteers (all men) aged 36.5 ± 1.4 years. Each sample was transferred into two tubes, without and with EDTA as anticoagulant, under sterile conditions. We had 14 groups: the control group in which whole blood was incubated without any other intervention, the LPS group in which whole blood was stimulated with LPS alone, and 12 alcohol groups with (6 groups) and without LPS stimulation (6 groups) using six different doses of alcohol (5, 12.5, 25, 50, 100 and 200mM). LPS (500pg) was added after pretreatment with alcohol for 10 minutes. Blood samples were diluted 1:10 in RPMI 1640 culture medium (100μl whole blood added in 900μl RPMI 1640), and then alcohol solution and LPS were added according to the study protocol for incubation period of 4 hours at 37°C. Cell culture supernatants were isolated with centrifugation at 1,800rpm, for 5 min at room temperature and stored at -70°C until measurements. Cytokine levels were determined in culture supernatant with the ELISA method. Alcohol had no effect on cytokine production when incubated with whole blood alone. TNF-α IL-6 and IL-10 significantly increased after LPS stimulation. Alcohol had no effect on IL-6 production after LPS challenge but significantly decreased TNF-α and IL-10 production in the presence of LPS challenge at 25mM to 200mM in a dose dependent manner. Conclusively TNF-α and IL-10 were significantly decreased after alcohol exposure in a dose depended manner in a model of whole blood stimulation with LPS exvivo expressing both suppression of pro- and anti-inflammatory response. © 2015 Gavala A, et al.
Papavasileiou M.V.,Sismanoglio General Hospital |
Karamanou A.G.,Sismanoglio General Hospital |
Kalogeropoulos P.,Agioi Anargyroi General Hospital |
Moustakas G.,Sismanoglio General Hospital |
And 2 more authors.
Journal of Human Hypertension | Year: 2016
Associations between high serum uric acid (SUA) levels and high blood pressure (BP), as well as between SUA levels and metabolic syndrome (MetS) have already been reported. The aim of the study was to investigate the relationship between the components of MetS with the SUA levels as also between SUA and apolipoproteins A1 and B (apoA1 and apoB) ratio in hypertensive patients. A total of 2577 consecutive hypertensive patients (1193 male and 1384 female) aged 57.5±13.3 years, were enrolled in our research. Samples were taken to measure SUA, glucose, triglycerides, high density lipoprotein (HDL-C), components of the MetS and apoA1 and apoB. The study population was divided into two groups: group A: SUA levels above normal range (men ≥7 mg dl -1, women ≥6 mg dl -1) and group B: SUA levels within normal range. In the overall study population, SUA levels showed a statistically significant correlation with waist circumference (WC; r=0.293, P<0.000), triglycerides (r=0.197, P<0.000), glucose (r=0.085, P<0.000), apoB/apoA1 (r=0.136, P<0.000) and HDL-C (r=-0.235, P<0,001). In newly diagnosed untreated hypertensive patients there was also a statistically significant correlation of SUA levels with WC (r=0.331, P<0.001), triglycerides (r=0.228, P<0.001) apoB/apoA1 ratio (r=0.202, P<0.001) and HDL-C (r=-0.278, P<0.001). In hyperurecemic hypertensives there was a statistically significant correlation between SUA levels with WC (r=0.168, P=0.007), apoB/apoA1 ratio (r=0.256, P=0.003) and HDL-C (r=-0.202, P<0.001). SUA levels correlate significantly with all the components of MetS, as well as with the risk factor apoB/apoA1 ratio, in hypertensive patients. © 2016 Macmillan Publishers Limited All rights reserved.