Seasonal variation in whole blood cytokine production after LPS stimulation in normal individuals

Myrianthefs, Pavlos; Karatzas, Stylianos; Venetsanou, Kyriaki; Grouzi, Elisabeth; Evagelopoulou, P; Boutzouka, Eleni; Fildissis, George; Spiliotopoulou, I; Baltopoulos, George

doi:10.1016/j.cyto.2003.08.005

Cited by 59 publications

(44 citation statements)

References 20 publications

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“…Studies accessing the roles of both TNFRs in the activity of TNF on edema reabsorption and formation would provide valuable information about the implicated mechanism. One possible explanation for the observation by others that under certain conditions TNF is able to stimulate edema reabsorption in an in situ flooded rat lung (13), whereas we found it not to do so in the time period in which the experiments were performed, could be explained by a variation in the presence of factors antagonizing receptor-mediated TNF actions in the treated animals, caused either by differences in the induction of inflammation due to the protocols used or by variations in basal levels of these agents (41,42).…”

Section: Discussionmentioning

confidence: 56%

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Braun

Hamacher

Morel³

et al. 2005

The Journal of Immunology

109

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Distinct from its receptor binding sites, TNF carries a lectin-like domain, situated at the tip of the molecule, which specifically binds oligosaccharides, such as N,N′-diacetylchitobiose. In view of the apparently conflicting data concerning TNF actions in pulmonary edema, we investigated the contribution of, on the one hand, the receptor binding sites and, in contrast, the lectin-like domain of the cytokine on pulmonary fluid reabsorption in in situ and in vivo flooded rat lungs. Receptor binding sites were blocked with the human soluble TNFR type 1 construct (sTNFR1), whereas the lectin-like domain was blunted with the oligosaccharide N,N′-diacetylchitobiose. We observed that in situ, TNF failed to stimulate alveolar liquid clearance, but did so together with the sTNFR1, and this activity was neutralized by N,N′-diacetylchitobiose. In vivo TNF inhibited liquid clearance, but activated it when complexed with the sTNFR1. A TNF-derived peptide mimic of the lectin-like domain activated fluid reabsorption in flooded lungs, and this activity was blunted by cotreatment with TNF. Our results thus indicate that in these models the receptor binding sites of TNF inhibit, whereas its lectin-like domain activates, edema reabsorption.

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Section: Discussionmentioning

confidence: 56%

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Braun

Hamacher

Morel³

et al. 2005

The Journal of Immunology

109

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“…Part of the explanation for an increase in adduct formation in summer may not be associated with input PAH at all, but may be due to interaction effects between PAH input and enzymatic activation that could change with season. Seasonal changes occur in endocrine function (Holdaway et al, 1997;Walker et al, 1997;Hansen et al, 2001); immune response (Maes and De Meyer, 2000;Nelson and Drazen, 2000;Myrianthefs et al, 2003); breast biology (Paradiso et al, 2001); and in enzyme inducibility, such as aryl hydrocarbon hydroxylase (AHH), which is an enzyme responsible for the metabolism of PAH like BaP (Paigen et al, 1981;Peluso et al, 1998;Gupta and Singh, 2004;Kiyohara and Hirohata, 1997).…”

Section: Discussionmentioning

confidence: 99%

Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

Shantakumar

Gammon

Eng

et al. 2005

J Expo Sci Environ Epidemiol

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The detection of polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human lymphocytes may be useful as a surrogate end point for individual cancer risk prediction. In this study, we examined the relationship between environmental sources of residential PAH, as well as other potential factors that may confound their association with cancer risk, and the detection of PAH-DNA adducts in a large population-based sample of adult women. Adult female residents of Long Island, New York, aged at least 20 years were identified from the general population between August 1996 and July 1997. Among 1556 women who completed a structured questionnaire, 941 donated sufficient blood (25 þ ml) to allow use of a competitive ELISA for measurement of PAH-DNA adducts in peripheral blood mononuclear cells. Ambient PAH exposure at the current residence was estimated using geographic modeling (n ¼ 796). Environmental home samples of dust (n ¼ 356) and soil (n ¼ 360) were collected on a random subset of long-term residents (15 þ years). Multivariable regression was conducted to obtain the best-fitting predictive models. Three separate models were constructed based on data from : (A) the questionnaire, including a dietary history; (B) environmental home samples; and (C) geographic modeling. Women who donated blood in summer and fall had increased odds of detectable PAH-DNA adducts (OR ¼ 2.65, 95% confidence interval (CI) ¼ 1.69, 4.17; OR ¼ 1.59, 95% CI ¼ 1.08, 2.32, respectively), as did current and past smokers (OR ¼ 1.50, 95% CI ¼ 1.00, 2.24; OR ¼ 1.46, 95% CI ¼ 1.05, 2.02, respectively). There were inconsistent associations between detectable PAH-DNA adducts and other known sources of residential PAH, such as grilled and smoked foods, or a summary measure of total dietary benzo-[a]-pyrene (BaP) intake during the year prior to the interview. Detectable PAH-DNA adducts were inversely associated with increased BaP levels in dust in the home, but positively associated with BaP levels in soil outside of the home, although CIs were wide. Ambient BaP estimates from the geographic model were not associated with detectable PAH-DNA adducts. These data suggest that PAH-DNA adducts detected in a population-based sample of adult women with ambient exposure levels reflect some key residential PAH exposure sources assessed in this study, such as cigarette smoking.

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“…Whole blood models explore a wide cell population in which the variety of cells is unknown. Although cytokine production, as measured in both whole blood and mononuclear cell cultures, is significantly correlated, changes in the number of viable cells -producing cytokines or changes in the ability of these cells to produce cytokines -could result in variations in cytokine production under either different circumstances or between different individuals leading to misinterpretation of findings [21,47].…”

Section: Discussionmentioning

confidence: 98%

“…In summary, whole blood culture assays retain all blood components and maintain normal operating environment for cell to cell interactions and there are also present circulating stimulatory and inhibitory mediators necessary for cell viability. Also, this method has been suggested to be most appropriate to study cytokine production in an environment that reproduces physiological phenomena, is very simple and quicker, less expensive and can be readily adapted to use in field studies [21,47].…”

Section: Discussionmentioning

confidence: 99%

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Alcohol Effects on TNF-ÃÂ± and IL-10 Production in an Ex-Vivo Model of Whole Blood Stimulated by LPS

Àlex¹,

Gavala²,

Myrianthefs³

et al. 2015

J Psychiatry

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Journal of Psychiatry AbstractAlcohol 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.Keywords: Alcohol; Cytokines; Lipopolysacharide; TNF-α; IL-6; IL-10 Abbreviations: LPS = lipopolysaccharide; TNF-α = Tumor necrosis factor-alpha; IL-6 = Interleukin-6; IL-10 = Interleukin-10

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Seasonal variation in whole blood cytokine production after LPS stimulation in normal individuals

Cited by 59 publications

References 20 publications

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

Alcohol Effects on TNF-ÃÂ± and IL-10 Production in an Ex-Vivo Model of Whole Blood Stimulated by LPS

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Seasonal variation in whole blood cytokine production after LPS stimulation in normal individuals

Cited by 59 publications

References 20 publications

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

Alcohol Effects on TNF-ÃÂ± and IL-10 Production in an Ex-Vivo Model of Whole Blood Stimulated by LPS

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Alcohol Effects on TNF-ÃÂ± and IL-10 Production in an Ex-Vivo Model of Whole Blood Stimulated by LPS