Association between activation of phase 2 enzymes and down-regulation of dendritic cell maturation by c9,t11-conjugated linoleic acid

Paolo Bergamo, Francesco Maurano, Rossana D'Arienzo, Chella David, Mauro Rossi

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Antioxidant and cytoprotective enzymes (phase 2) exert protective activity against reactive oxygen species (ROS)-induced injury. We have recently shown how the beneficial effects of conjugated linoleic acid (CLA) in a mouse model of an autoimmune disease are parallel with the activation of phase 2 enzymes. In the present study we found that c9,t11-CLA isomer activates cytoprotective enzymes and down-regulates LPS- or gliadin-induced maturation in dendritic cells (DCs) obtained from a murine model of celiac disease. As expected, the enhancement of LPS-induced maturation (increased NFκB p65 nuclear translocation, CD86 expression and decreased CD11c+ cell number) was exacerbated by specific glutathione (GSH) inhibitor (buthionine sulphoximine; BSO). Conversely, the down-regulation of DC maturation by antioxidant N-acetylcysteine (NAC) was associated with the marked increase of intracellular thiol concentration. c9,t11-CLA activation of phase 2 enzymes in mouse DCs was observed first. Next, we found that the significant reduction of LPS- and gliadin-induced DC maturation in cultures pre-treated with c9,t11-CLA improved cellular redox status (decreased ROS and higher antioxidant defenses). Finally, the process of DC maturation triggered by gliadin, in contrast with that exhibited by LPS, was not associated with enhanced NFκB nuclear translocation and pro-inflammatory cytokines synthesis. These results demonstrate that c9,t11-CLA renders DCs more resistant to gliadin- or LPS-induced maturation, thus indicating that a cytoprotective mechanism elicited by c9,t11-CLA may modulate DC responsiveness.

Original languageEnglish (US)
Pages (from-to)181-190
Number of pages10
JournalImmunology Letters
Volume117
Issue number2
DOIs
StatePublished - May 15 2008

Fingerprint

Conjugated Linoleic Acids
Dendritic Cells
Down-Regulation
Gliadin
Enzymes
Antioxidants
Reactive Oxygen Species
Buthionine Sulfoximine
Acetylcysteine
Celiac Disease
Sulfhydryl Compounds
Autoimmune Diseases
Oxidation-Reduction
Glutathione
Cell Count
Cytokines
Wounds and Injuries

Keywords

  • Conjugated linoleic acid
  • Dendritic cells
  • Phase 2 enzymes

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Association between activation of phase 2 enzymes and down-regulation of dendritic cell maturation by c9,t11-conjugated linoleic acid. / Bergamo, Paolo; Maurano, Francesco; D'Arienzo, Rossana; David, Chella; Rossi, Mauro.

In: Immunology Letters, Vol. 117, No. 2, 15.05.2008, p. 181-190.

Research output: Contribution to journalArticle

Bergamo, Paolo ; Maurano, Francesco ; D'Arienzo, Rossana ; David, Chella ; Rossi, Mauro. / Association between activation of phase 2 enzymes and down-regulation of dendritic cell maturation by c9,t11-conjugated linoleic acid. In: Immunology Letters. 2008 ; Vol. 117, No. 2. pp. 181-190.
@article{8651289ef2ba4dd19ffe3eae884b6e73,
title = "Association between activation of phase 2 enzymes and down-regulation of dendritic cell maturation by c9,t11-conjugated linoleic acid",
abstract = "Antioxidant and cytoprotective enzymes (phase 2) exert protective activity against reactive oxygen species (ROS)-induced injury. We have recently shown how the beneficial effects of conjugated linoleic acid (CLA) in a mouse model of an autoimmune disease are parallel with the activation of phase 2 enzymes. In the present study we found that c9,t11-CLA isomer activates cytoprotective enzymes and down-regulates LPS- or gliadin-induced maturation in dendritic cells (DCs) obtained from a murine model of celiac disease. As expected, the enhancement of LPS-induced maturation (increased NFκB p65 nuclear translocation, CD86 expression and decreased CD11c+ cell number) was exacerbated by specific glutathione (GSH) inhibitor (buthionine sulphoximine; BSO). Conversely, the down-regulation of DC maturation by antioxidant N-acetylcysteine (NAC) was associated with the marked increase of intracellular thiol concentration. c9,t11-CLA activation of phase 2 enzymes in mouse DCs was observed first. Next, we found that the significant reduction of LPS- and gliadin-induced DC maturation in cultures pre-treated with c9,t11-CLA improved cellular redox status (decreased ROS and higher antioxidant defenses). Finally, the process of DC maturation triggered by gliadin, in contrast with that exhibited by LPS, was not associated with enhanced NFκB nuclear translocation and pro-inflammatory cytokines synthesis. These results demonstrate that c9,t11-CLA renders DCs more resistant to gliadin- or LPS-induced maturation, thus indicating that a cytoprotective mechanism elicited by c9,t11-CLA may modulate DC responsiveness.",
keywords = "Conjugated linoleic acid, Dendritic cells, Phase 2 enzymes",
author = "Paolo Bergamo and Francesco Maurano and Rossana D'Arienzo and Chella David and Mauro Rossi",
year = "2008",
month = "5",
day = "15",
doi = "10.1016/j.imlet.2008.02.001",
language = "English (US)",
volume = "117",
pages = "181--190",
journal = "Immunology Letters",
issn = "0165-2478",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Association between activation of phase 2 enzymes and down-regulation of dendritic cell maturation by c9,t11-conjugated linoleic acid

AU - Bergamo, Paolo

AU - Maurano, Francesco

AU - D'Arienzo, Rossana

AU - David, Chella

AU - Rossi, Mauro

PY - 2008/5/15

Y1 - 2008/5/15

N2 - Antioxidant and cytoprotective enzymes (phase 2) exert protective activity against reactive oxygen species (ROS)-induced injury. We have recently shown how the beneficial effects of conjugated linoleic acid (CLA) in a mouse model of an autoimmune disease are parallel with the activation of phase 2 enzymes. In the present study we found that c9,t11-CLA isomer activates cytoprotective enzymes and down-regulates LPS- or gliadin-induced maturation in dendritic cells (DCs) obtained from a murine model of celiac disease. As expected, the enhancement of LPS-induced maturation (increased NFκB p65 nuclear translocation, CD86 expression and decreased CD11c+ cell number) was exacerbated by specific glutathione (GSH) inhibitor (buthionine sulphoximine; BSO). Conversely, the down-regulation of DC maturation by antioxidant N-acetylcysteine (NAC) was associated with the marked increase of intracellular thiol concentration. c9,t11-CLA activation of phase 2 enzymes in mouse DCs was observed first. Next, we found that the significant reduction of LPS- and gliadin-induced DC maturation in cultures pre-treated with c9,t11-CLA improved cellular redox status (decreased ROS and higher antioxidant defenses). Finally, the process of DC maturation triggered by gliadin, in contrast with that exhibited by LPS, was not associated with enhanced NFκB nuclear translocation and pro-inflammatory cytokines synthesis. These results demonstrate that c9,t11-CLA renders DCs more resistant to gliadin- or LPS-induced maturation, thus indicating that a cytoprotective mechanism elicited by c9,t11-CLA may modulate DC responsiveness.

AB - Antioxidant and cytoprotective enzymes (phase 2) exert protective activity against reactive oxygen species (ROS)-induced injury. We have recently shown how the beneficial effects of conjugated linoleic acid (CLA) in a mouse model of an autoimmune disease are parallel with the activation of phase 2 enzymes. In the present study we found that c9,t11-CLA isomer activates cytoprotective enzymes and down-regulates LPS- or gliadin-induced maturation in dendritic cells (DCs) obtained from a murine model of celiac disease. As expected, the enhancement of LPS-induced maturation (increased NFκB p65 nuclear translocation, CD86 expression and decreased CD11c+ cell number) was exacerbated by specific glutathione (GSH) inhibitor (buthionine sulphoximine; BSO). Conversely, the down-regulation of DC maturation by antioxidant N-acetylcysteine (NAC) was associated with the marked increase of intracellular thiol concentration. c9,t11-CLA activation of phase 2 enzymes in mouse DCs was observed first. Next, we found that the significant reduction of LPS- and gliadin-induced DC maturation in cultures pre-treated with c9,t11-CLA improved cellular redox status (decreased ROS and higher antioxidant defenses). Finally, the process of DC maturation triggered by gliadin, in contrast with that exhibited by LPS, was not associated with enhanced NFκB nuclear translocation and pro-inflammatory cytokines synthesis. These results demonstrate that c9,t11-CLA renders DCs more resistant to gliadin- or LPS-induced maturation, thus indicating that a cytoprotective mechanism elicited by c9,t11-CLA may modulate DC responsiveness.

KW - Conjugated linoleic acid

KW - Dendritic cells

KW - Phase 2 enzymes

UR - http://www.scopus.com/inward/record.url?scp=41449091687&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=41449091687&partnerID=8YFLogxK

U2 - 10.1016/j.imlet.2008.02.001

DO - 10.1016/j.imlet.2008.02.001

M3 - Article

C2 - 18343507

AN - SCOPUS:41449091687

VL - 117

SP - 181

EP - 190

JO - Immunology Letters

JF - Immunology Letters

SN - 0165-2478

IS - 2

ER -