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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

Generation of H2O2 by (poly)phenols at 30 µmol/lconcentration in Roswell Park Memorial Institute (RPMI)-1640 medium containing 10 %fetal calf serum and phenol red (a), and relationships with Jurkat CD4+T-lymphocyte pro-inflammatory cytokine release and cell growth (b–e).H2O2 production was measured by a kinetic reaction betweeneach (poly)phenol incubated at 30 µmol/l with Amplex red reagent, which fluorescesfollowing reaction with H2O2 (a). Scatter plots wereconstructed for H2O2 production against Jurkat CD4+T-lymphocyte cytokine release (b=IL-2, c=IL-8, d=TNFα) or cellnumber (e) after 48 h of treatment, with or without phorbol 12-myristate 13-acetate(PMA)/phytohaemagglutinin (PHA) stimulation to induce cytokine release at the 24 htime point. A linear correlation was identified between H2O2production and IL-8 release in non-stimulated cells only (R2 0·3048; trend line shown in figure). 3MQ,3-O-methylquercetin; CAF, caffeic acid; CAT, catechol; CGA,chlorogenic acid; CUR, curcumin; CYA, cyanidin-3-O-glucoside; DHC,dihydrocaffeic acid; DFA, dihydroferulic acid; EPI,(–)-epigallocatechin-3-O-gallate; FER, ferulic acid; FLG,feruloylglycine; HBA, 4-hydroxybenzoic acid; HHA, 4'-hydroxyhippuric acid; HIP,hippuric acid; HMA, 4'-hydroxymandelic acid; HPA, 4'-hydroxyphenylacetic acid; HPC,homoprotocatechuic acid; HPL, 3-(4'-hydroxyphenyl)lactic acid; HPP,5-(3'-hydroxyphenyl)propionic acid; HVA, homovanillic acid; IFA, isoferulic acid;IFG, isoferuloylglycine; ISO, isorhamnetin; PCA, protocatechuic acid; PEL,pelargonidin-3-O-glucoside; PHL, phloroglucinol; PUN,punicalagin; PYR, pyrogallol; QUE, quercetin; RES, resveratrol; TYR, tyrosol; VAN,vanillic acid. Compounds are ordered from least (CAT) to highest (PUN) molecularweight along the x-axis. ■, Data from non-stimulated cells; ▲, datafrom PMA/PHA-stimulated cells.
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fig6: Generation of H2O2 by (poly)phenols at 30 µmol/lconcentration in Roswell Park Memorial Institute (RPMI)-1640 medium containing 10 %fetal calf serum and phenol red (a), and relationships with Jurkat CD4+T-lymphocyte pro-inflammatory cytokine release and cell growth (b–e).H2O2 production was measured by a kinetic reaction betweeneach (poly)phenol incubated at 30 µmol/l with Amplex red reagent, which fluorescesfollowing reaction with H2O2 (a). Scatter plots wereconstructed for H2O2 production against Jurkat CD4+T-lymphocyte cytokine release (b=IL-2, c=IL-8, d=TNFα) or cellnumber (e) after 48 h of treatment, with or without phorbol 12-myristate 13-acetate(PMA)/phytohaemagglutinin (PHA) stimulation to induce cytokine release at the 24 htime point. A linear correlation was identified between H2O2production and IL-8 release in non-stimulated cells only (R2 0·3048; trend line shown in figure). 3MQ,3-O-methylquercetin; CAF, caffeic acid; CAT, catechol; CGA,chlorogenic acid; CUR, curcumin; CYA, cyanidin-3-O-glucoside; DHC,dihydrocaffeic acid; DFA, dihydroferulic acid; EPI,(–)-epigallocatechin-3-O-gallate; FER, ferulic acid; FLG,feruloylglycine; HBA, 4-hydroxybenzoic acid; HHA, 4'-hydroxyhippuric acid; HIP,hippuric acid; HMA, 4'-hydroxymandelic acid; HPA, 4'-hydroxyphenylacetic acid; HPC,homoprotocatechuic acid; HPL, 3-(4'-hydroxyphenyl)lactic acid; HPP,5-(3'-hydroxyphenyl)propionic acid; HVA, homovanillic acid; IFA, isoferulic acid;IFG, isoferuloylglycine; ISO, isorhamnetin; PCA, protocatechuic acid; PEL,pelargonidin-3-O-glucoside; PHL, phloroglucinol; PUN,punicalagin; PYR, pyrogallol; QUE, quercetin; RES, resveratrol; TYR, tyrosol; VAN,vanillic acid. Compounds are ordered from least (CAT) to highest (PUN) molecularweight along the x-axis. ■, Data from non-stimulated cells; ▲, datafrom PMA/PHA-stimulated cells.

Mentions: Some (poly)phenols have been reported to generate H2O2 in cellculture media(16,17). To quantify H2O2 production, we conducted kineticspectrophotometry assays using Amplex red reagent, which is converted to fluorescentresorufin following oxidation by H2O2. Production ofH2O2 was detected for sixteen of the thirty-two test compounds(Fig. 6(a)). H2O2production was detected from the hydroxybenzene derivatives catechol and pyrogallol, thephenylacetic acid homoprotocatechuic acid, the hydroxycinnamates caffeic acid anddihydrocaffeic acid, and the ellagitannin punicalagin, whereas other test compoundsproduced no detectable levels of H2O2. Comparisons were also made toassess the effects of phenol red in the culture media, which showed that rates ofH2O2 production were 24 (sem 2) % lower in RPMI-1640medium containing phenol red than in RPMI-1640 medium without phenol red (data not shownin detail).Fig. 6


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)

Generation of H2O2 by (poly)phenols at 30 µmol/lconcentration in Roswell Park Memorial Institute (RPMI)-1640 medium containing 10 %fetal calf serum and phenol red (a), and relationships with Jurkat CD4+T-lymphocyte pro-inflammatory cytokine release and cell growth (b–e).H2O2 production was measured by a kinetic reaction betweeneach (poly)phenol incubated at 30 µmol/l with Amplex red reagent, which fluorescesfollowing reaction with H2O2 (a). Scatter plots wereconstructed for H2O2 production against Jurkat CD4+T-lymphocyte cytokine release (b=IL-2, c=IL-8, d=TNFα) or cellnumber (e) after 48 h of treatment, with or without phorbol 12-myristate 13-acetate(PMA)/phytohaemagglutinin (PHA) stimulation to induce cytokine release at the 24 htime point. A linear correlation was identified between H2O2production and IL-8 release in non-stimulated cells only (R2 0·3048; trend line shown in figure). 3MQ,3-O-methylquercetin; CAF, caffeic acid; CAT, catechol; CGA,chlorogenic acid; CUR, curcumin; CYA, cyanidin-3-O-glucoside; DHC,dihydrocaffeic acid; DFA, dihydroferulic acid; EPI,(–)-epigallocatechin-3-O-gallate; FER, ferulic acid; FLG,feruloylglycine; HBA, 4-hydroxybenzoic acid; HHA, 4'-hydroxyhippuric acid; HIP,hippuric acid; HMA, 4'-hydroxymandelic acid; HPA, 4'-hydroxyphenylacetic acid; HPC,homoprotocatechuic acid; HPL, 3-(4'-hydroxyphenyl)lactic acid; HPP,5-(3'-hydroxyphenyl)propionic acid; HVA, homovanillic acid; IFA, isoferulic acid;IFG, isoferuloylglycine; ISO, isorhamnetin; PCA, protocatechuic acid; PEL,pelargonidin-3-O-glucoside; PHL, phloroglucinol; PUN,punicalagin; PYR, pyrogallol; QUE, quercetin; RES, resveratrol; TYR, tyrosol; VAN,vanillic acid. Compounds are ordered from least (CAT) to highest (PUN) molecularweight along the x-axis. ■, Data from non-stimulated cells; ▲, datafrom PMA/PHA-stimulated cells.
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fig6: Generation of H2O2 by (poly)phenols at 30 µmol/lconcentration in Roswell Park Memorial Institute (RPMI)-1640 medium containing 10 %fetal calf serum and phenol red (a), and relationships with Jurkat CD4+T-lymphocyte pro-inflammatory cytokine release and cell growth (b–e).H2O2 production was measured by a kinetic reaction betweeneach (poly)phenol incubated at 30 µmol/l with Amplex red reagent, which fluorescesfollowing reaction with H2O2 (a). Scatter plots wereconstructed for H2O2 production against Jurkat CD4+T-lymphocyte cytokine release (b=IL-2, c=IL-8, d=TNFα) or cellnumber (e) after 48 h of treatment, with or without phorbol 12-myristate 13-acetate(PMA)/phytohaemagglutinin (PHA) stimulation to induce cytokine release at the 24 htime point. A linear correlation was identified between H2O2production and IL-8 release in non-stimulated cells only (R2 0·3048; trend line shown in figure). 3MQ,3-O-methylquercetin; CAF, caffeic acid; CAT, catechol; CGA,chlorogenic acid; CUR, curcumin; CYA, cyanidin-3-O-glucoside; DHC,dihydrocaffeic acid; DFA, dihydroferulic acid; EPI,(–)-epigallocatechin-3-O-gallate; FER, ferulic acid; FLG,feruloylglycine; HBA, 4-hydroxybenzoic acid; HHA, 4'-hydroxyhippuric acid; HIP,hippuric acid; HMA, 4'-hydroxymandelic acid; HPA, 4'-hydroxyphenylacetic acid; HPC,homoprotocatechuic acid; HPL, 3-(4'-hydroxyphenyl)lactic acid; HPP,5-(3'-hydroxyphenyl)propionic acid; HVA, homovanillic acid; IFA, isoferulic acid;IFG, isoferuloylglycine; ISO, isorhamnetin; PCA, protocatechuic acid; PEL,pelargonidin-3-O-glucoside; PHL, phloroglucinol; PUN,punicalagin; PYR, pyrogallol; QUE, quercetin; RES, resveratrol; TYR, tyrosol; VAN,vanillic acid. Compounds are ordered from least (CAT) to highest (PUN) molecularweight along the x-axis. ■, Data from non-stimulated cells; ▲, datafrom PMA/PHA-stimulated cells.
Mentions: Some (poly)phenols have been reported to generate H2O2 in cellculture media(16,17). To quantify H2O2 production, we conducted kineticspectrophotometry assays using Amplex red reagent, which is converted to fluorescentresorufin following oxidation by H2O2. Production ofH2O2 was detected for sixteen of the thirty-two test compounds(Fig. 6(a)). H2O2production was detected from the hydroxybenzene derivatives catechol and pyrogallol, thephenylacetic acid homoprotocatechuic acid, the hydroxycinnamates caffeic acid anddihydrocaffeic acid, and the ellagitannin punicalagin, whereas other test compoundsproduced no detectable levels of H2O2. Comparisons were also made toassess the effects of phenol red in the culture media, which showed that rates ofH2O2 production were 24 (sem 2) % lower in RPMI-1640medium containing phenol red than in RPMI-1640 medium without phenol red (data not shownin detail).Fig. 6

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