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Identification of (poly)phenol treatments that modulate the release of pro-inflammatory cytokines by human lymphocytes.

Ford CT, Richardson S, McArdle F, Lotito SB, Crozier A, McArdle A, Jackson MJ - Br. J. Nutr. (2016)

Bottom Line: We compared thirty-one (poly)phenols and six (poly)phenol mixtures for effects on pro-inflammatory cytokine release by Jurkat T-lymphocytes.A number of (poly)phenols significantly altered cytokine release from Jurkat cells (P<0·05), but H2O2 generation did not correlate with cytokine release.These results suggest that (poly)phenols derived from onions, turmeric, red grapes, green tea and açai berries may help reduce the release of pro-inflammatory mediators in people at risk of chronic inflammation.

View Article: PubMed Central - PubMed

Affiliation: 1Department of Musculoskeletal Biology,Institute of Ageing and Chronic Disease,University of Liverpool,Liverpool L7 8TX,UK.

ABSTRACT
Diets rich in fruits and vegetables (FV), which contain (poly)phenols, protect against age-related inflammation and chronic diseases. T-lymphocytes contribute to systemic cytokine production and are modulated by FV intake. Little is known about the relative potency of different (poly)phenols in modulating cytokine release by lymphocytes. We compared thirty-one (poly)phenols and six (poly)phenol mixtures for effects on pro-inflammatory cytokine release by Jurkat T-lymphocytes. Test compounds were incubated with Jurkat cells for 48 h at 1 and 30 µm, with or without phorbol ester treatment at 24 h to induce cytokine release. Three test compounds that reduced cytokine release were further incubated with primary lymphocytes at 0·2 and 1 µm for 24 h, with lipopolysaccharide added at 5 h. Cytokine release was measured, and generation of H2O2 by test compounds was determined to assess any potential correlations with cytokine release. A number of (poly)phenols significantly altered cytokine release from Jurkat cells (P<0·05), but H2O2 generation did not correlate with cytokine release. Resveratrol, isorhamnetin, curcumin, vanillic acid and specific (poly)phenol mixtures reduced pro-inflammatory cytokine release from T-lymphocytes, and there was evidence for interaction between (poly)phenols to further modulate cytokine release. The release of interferon-γ induced protein 10 by primary lymphocytes was significantly reduced following treatment with 1 µm isorhamnetin (P<0·05). These results suggest that (poly)phenols derived from onions, turmeric, red grapes, green tea and açai berries may help reduce the release of pro-inflammatory mediators in people at risk of chronic inflammation.

No MeSH data available.


Related in: MedlinePlus

Heat maps showing cytokine release by Jurkat CD4+ T-lymphocytesfollowing treatment with mixtures of four (poly)phenols at 1 or 30 µmol/l comparedwith vehicle controls (a), and mathematical averages of the effects on cytokinerelease following treatment with the individual compounds (b). Cells were incubatedwith (poly)phenol mixtures for 48 h, with or without the addition of 25 ng/mlphorbol myristoyl acetate and 5 µg/ml phytohaemagglutinin at the 24-h time point.The mixtures comprised the following: (1) catechol, phloroglucinol, 4-hydroxybenzoicacid and protocatechuic acid; (2) 4'-hydroxymandelic acid, 4-hydroxyphenylaceticacid, 5-(3'-hydroxyphenyl) propionic acid and 3-(4'-hydroxyphenyl) lactic acid; (3)(–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucosideand punicalagin; (4) dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; (5) caffeic acid, ferulic acid, isoferulicacid and isoferuloylglycine; and (6) hippuric acid, tyrosol, 4'-hydroxyhippuric acidand chlorogenic acid. * Mean value was significantly different between the‘expected’ response predicted by mathematically averaging the effects of treatmentwith individual compounds and the ‘observed’ response measured following treatmentwith the mixtures (P<0·05; one-way ANOVA with Tukey’spost hoc test).
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fig4: Heat maps showing cytokine release by Jurkat CD4+ T-lymphocytesfollowing treatment with mixtures of four (poly)phenols at 1 or 30 µmol/l comparedwith vehicle controls (a), and mathematical averages of the effects on cytokinerelease following treatment with the individual compounds (b). Cells were incubatedwith (poly)phenol mixtures for 48 h, with or without the addition of 25 ng/mlphorbol myristoyl acetate and 5 µg/ml phytohaemagglutinin at the 24-h time point.The mixtures comprised the following: (1) catechol, phloroglucinol, 4-hydroxybenzoicacid and protocatechuic acid; (2) 4'-hydroxymandelic acid, 4-hydroxyphenylaceticacid, 5-(3'-hydroxyphenyl) propionic acid and 3-(4'-hydroxyphenyl) lactic acid; (3)(–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucosideand punicalagin; (4) dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; (5) caffeic acid, ferulic acid, isoferulicacid and isoferuloylglycine; and (6) hippuric acid, tyrosol, 4'-hydroxyhippuric acidand chlorogenic acid. * Mean value was significantly different between the‘expected’ response predicted by mathematically averaging the effects of treatmentwith individual compounds and the ‘observed’ response measured following treatmentwith the mixtures (P<0·05; one-way ANOVA with Tukey’spost hoc test).

Mentions: To assess potential interactions between test compounds in modulating cytokine release,we prepared several mixtures of (poly)phenols: mixture 1 representing low-molecular weightcolonic catabolites such as catechol, phloroglucinol, 4-hydroxybenzoic acid andprotocatechuic acid; mixture 2 representing mid-molecular weight colonic catabolites suchas 4'-hydroxymandelic acid, 4'-hydroxyphenylacetic acid, 5-(3'-hydroxyphenyl) propionicacid and 3-(4'-hydroxyphenyl) lactic acid; mixture 3 representing a mixture of dietarypolyphenols such as (–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucoside andpunicalagin; mixture 4 representing polyphenols and high molecular weight hydroxycinnamatemetabolites, such as dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; mixture 5 representing a mixture of hydroxycinnamatederivatives derived from chlorogenic acid after the consumption of coffee, such as caffeicacid, ferulic acid, isoferulic acid and isoferuloylglycine; and mixture 6 representingcompounds derived from apple cider, such as hippuric acid, tyrosol, 4'-hydroxyhippuricacid and chlorogenic acid. We measured cytokine release from Jurkat CD4+T-lymphocytes following 48 h of incubation with each mixture at a total concentration of 1or 30 µmol/l, with or without stimulation with PMA/PHA at 24 h. For comparison, theresults previously obtained for cytokine release following treatment with each individualcompound were averaged to generate a prediction of the effects expected if there were nointeractions between compounds (i.e. a hypothesis that there were no synergisticeffects). The results illustrated in Fig. 4indicate that five of the six test mixtures significantly reduced pro-inflammatorycytokine release in comparison with results anticipated from simple addition of theeffects observed for individual compounds (P<0·05; one-way ANOVAwith Dunnett’s post hoc test).Fig. 4


Identification of (poly)phenol treatments that modulate the release of pro-inflammatory cytokines by human lymphocytes.

Ford CT, Richardson S, McArdle F, Lotito SB, Crozier A, McArdle A, Jackson MJ - Br. J. Nutr. (2016)

Heat maps showing cytokine release by Jurkat CD4+ T-lymphocytesfollowing treatment with mixtures of four (poly)phenols at 1 or 30 µmol/l comparedwith vehicle controls (a), and mathematical averages of the effects on cytokinerelease following treatment with the individual compounds (b). Cells were incubatedwith (poly)phenol mixtures for 48 h, with or without the addition of 25 ng/mlphorbol myristoyl acetate and 5 µg/ml phytohaemagglutinin at the 24-h time point.The mixtures comprised the following: (1) catechol, phloroglucinol, 4-hydroxybenzoicacid and protocatechuic acid; (2) 4'-hydroxymandelic acid, 4-hydroxyphenylaceticacid, 5-(3'-hydroxyphenyl) propionic acid and 3-(4'-hydroxyphenyl) lactic acid; (3)(–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucosideand punicalagin; (4) dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; (5) caffeic acid, ferulic acid, isoferulicacid and isoferuloylglycine; and (6) hippuric acid, tyrosol, 4'-hydroxyhippuric acidand chlorogenic acid. * Mean value was significantly different between the‘expected’ response predicted by mathematically averaging the effects of treatmentwith individual compounds and the ‘observed’ response measured following treatmentwith the mixtures (P<0·05; one-way ANOVA with Tukey’spost hoc test).
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fig4: Heat maps showing cytokine release by Jurkat CD4+ T-lymphocytesfollowing treatment with mixtures of four (poly)phenols at 1 or 30 µmol/l comparedwith vehicle controls (a), and mathematical averages of the effects on cytokinerelease following treatment with the individual compounds (b). Cells were incubatedwith (poly)phenol mixtures for 48 h, with or without the addition of 25 ng/mlphorbol myristoyl acetate and 5 µg/ml phytohaemagglutinin at the 24-h time point.The mixtures comprised the following: (1) catechol, phloroglucinol, 4-hydroxybenzoicacid and protocatechuic acid; (2) 4'-hydroxymandelic acid, 4-hydroxyphenylaceticacid, 5-(3'-hydroxyphenyl) propionic acid and 3-(4'-hydroxyphenyl) lactic acid; (3)(–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucosideand punicalagin; (4) dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; (5) caffeic acid, ferulic acid, isoferulicacid and isoferuloylglycine; and (6) hippuric acid, tyrosol, 4'-hydroxyhippuric acidand chlorogenic acid. * Mean value was significantly different between the‘expected’ response predicted by mathematically averaging the effects of treatmentwith individual compounds and the ‘observed’ response measured following treatmentwith the mixtures (P<0·05; one-way ANOVA with Tukey’spost hoc test).
Mentions: To assess potential interactions between test compounds in modulating cytokine release,we prepared several mixtures of (poly)phenols: mixture 1 representing low-molecular weightcolonic catabolites such as catechol, phloroglucinol, 4-hydroxybenzoic acid andprotocatechuic acid; mixture 2 representing mid-molecular weight colonic catabolites suchas 4'-hydroxymandelic acid, 4'-hydroxyphenylacetic acid, 5-(3'-hydroxyphenyl) propionicacid and 3-(4'-hydroxyphenyl) lactic acid; mixture 3 representing a mixture of dietarypolyphenols such as (–)-epigallocatechin-3-O-gallate,pelargonidin-3-O-glucoside, cyanidin-3-O-glucoside andpunicalagin; mixture 4 representing polyphenols and high molecular weight hydroxycinnamatemetabolites, such as dihydroferulic acid, feruloylglycine, quercetin and3-O-methylquercetin; mixture 5 representing a mixture of hydroxycinnamatederivatives derived from chlorogenic acid after the consumption of coffee, such as caffeicacid, ferulic acid, isoferulic acid and isoferuloylglycine; and mixture 6 representingcompounds derived from apple cider, such as hippuric acid, tyrosol, 4'-hydroxyhippuricacid and chlorogenic acid. We measured cytokine release from Jurkat CD4+T-lymphocytes following 48 h of incubation with each mixture at a total concentration of 1or 30 µmol/l, with or without stimulation with PMA/PHA at 24 h. For comparison, theresults previously obtained for cytokine release following treatment with each individualcompound were averaged to generate a prediction of the effects expected if there were nointeractions between compounds (i.e. a hypothesis that there were no synergisticeffects). The results illustrated in Fig. 4indicate that five of the six test mixtures significantly reduced pro-inflammatorycytokine release in comparison with results anticipated from simple addition of theeffects observed for individual compounds (P<0·05; one-way ANOVAwith Dunnett’s post hoc test).Fig. 4

Bottom Line: We compared thirty-one (poly)phenols and six (poly)phenol mixtures for effects on pro-inflammatory cytokine release by Jurkat T-lymphocytes.A number of (poly)phenols significantly altered cytokine release from Jurkat cells (P<0·05), but H2O2 generation did not correlate with cytokine release.These results suggest that (poly)phenols derived from onions, turmeric, red grapes, green tea and açai berries may help reduce the release of pro-inflammatory mediators in people at risk of chronic inflammation.

View Article: PubMed Central - PubMed

Affiliation: 1Department of Musculoskeletal Biology,Institute of Ageing and Chronic Disease,University of Liverpool,Liverpool L7 8TX,UK.

ABSTRACT
Diets rich in fruits and vegetables (FV), which contain (poly)phenols, protect against age-related inflammation and chronic diseases. T-lymphocytes contribute to systemic cytokine production and are modulated by FV intake. Little is known about the relative potency of different (poly)phenols in modulating cytokine release by lymphocytes. We compared thirty-one (poly)phenols and six (poly)phenol mixtures for effects on pro-inflammatory cytokine release by Jurkat T-lymphocytes. Test compounds were incubated with Jurkat cells for 48 h at 1 and 30 µm, with or without phorbol ester treatment at 24 h to induce cytokine release. Three test compounds that reduced cytokine release were further incubated with primary lymphocytes at 0·2 and 1 µm for 24 h, with lipopolysaccharide added at 5 h. Cytokine release was measured, and generation of H2O2 by test compounds was determined to assess any potential correlations with cytokine release. A number of (poly)phenols significantly altered cytokine release from Jurkat cells (P<0·05), but H2O2 generation did not correlate with cytokine release. Resveratrol, isorhamnetin, curcumin, vanillic acid and specific (poly)phenol mixtures reduced pro-inflammatory cytokine release from T-lymphocytes, and there was evidence for interaction between (poly)phenols to further modulate cytokine release. The release of interferon-γ induced protein 10 by primary lymphocytes was significantly reduced following treatment with 1 µm isorhamnetin (P<0·05). These results suggest that (poly)phenols derived from onions, turmeric, red grapes, green tea and açai berries may help reduce the release of pro-inflammatory mediators in people at risk of chronic inflammation.

No MeSH data available.


Related in: MedlinePlus