PMID- 22412931
OWN - NLM
STAT- MEDLINE
DCOM- 20120802
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 3
DP  - 2012
TI  - Butyrate attenuates lipopolysaccharide-induced inflammation in intestinal cells 
      and Crohn's mucosa through modulation of antioxidant defense machinery.
PG  - e32841
LID - 10.1371/journal.pone.0032841 [doi]
LID - e32841
AB  - Oxidative stress plays an important role in the pathogenesis of inflammatory 
      bowel disease (IBD), including Crohn's disease (CrD). High levels of Reactive 
      Oxygen Species (ROS) induce the activation of the redox-sensitive nuclear 
      transcription factor kappa-B (NF-kappaB), which in turn triggers the inflammatory 
      mediators. Butyrate decreases pro-inflammatory cytokine expression by the lamina 
      propria mononuclear cells in CrD patients via inhibition of NF-kappaB activation, but 
      how it reduces inflammation is still unclear. We suggest that butyrate controls 
      ROS mediated NF-kappaB activation and thus mucosal inflammation in intestinal 
      epithelial cells and in CrD colonic mucosa by triggering intracellular 
      antioxidant defense systems. Intestinal epithelial Caco-2 cells and colonic 
      mucosa from 14 patients with CrD and 12 controls were challenged with or without 
      lipopolysaccaride from Escherichia coli (EC-LPS) in presence or absence of 
      butyrate for 4 and 24 h. The effects of butyrate on oxidative stress, p42/44 MAP 
      kinase phosphorylation, p65-NF-kappaB activation and mucosal inflammation were 
      investigated by real time PCR, western blot and confocal microscopy. Our results 
      suggest that EC-LPS challenge induces a decrease in 
      Gluthation-S-Transferase-alpha (GSTA1/A2) mRNA levels, protein expression and 
      catalytic activity; enhanced levels of ROS induced by EC-LPS challenge mediates 
      p65-NF-kappaB activation and inflammatory response in Caco-2 cells and in CrD colonic 
      mucosa. Furthermore butyrate treatment was seen to restore GSTA1/A2 mRNA levels, 
      protein expression and catalytic activity and to control NF-kappaB activation, COX-2, 
      ICAM-1 and the release of pro-inflammatory cytokine. In conclusion, butyrate 
      rescues the redox machinery and controls the intracellular ROS balance thus 
      switching off EC-LPS induced inflammatory response in intestinal epithelial cells 
      and in CrD colonic mucosa.
FAU - Russo, Ilaria
AU  - Russo I
AD  - Department of Clinical and Experimental Medicine, Federico II University of 
      Naples, Napoli, Italy.
FAU - Luciani, Alessandro
AU  - Luciani A
FAU - De Cicco, Paola
AU  - De Cicco P
FAU - Troncone, Edoardo
AU  - Troncone E
FAU - Ciacci, Carolina
AU  - Ciacci C
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20120306
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antioxidants)
RN  - 0 (Butyrates)
RN  - 0 (Isoenzymes)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - EC 2.5.1.18 (glutathione S-transferase alpha)
SB  - IM
RIN - PLoS One. 2019 Oct 30;14(10):e0224849. PMID: 31665196
MH  - Adolescent
MH  - Adult
MH  - Antioxidants/*metabolism
MH  - Butyrates/*pharmacology
MH  - Catalysis/drug effects
MH  - Cell Line
MH  - Crohn Disease/*immunology/pathology
MH  - Enzyme Activation/drug effects
MH  - Gene Expression/drug effects
MH  - Glutathione Transferase/genetics
MH  - Humans
MH  - Intestinal Mucosa/drug effects/*immunology/pathology
MH  - Isoenzymes/genetics
MH  - Lipopolysaccharides/*immunology
MH  - NF-kappa B/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress
MH  - RNA, Messenger/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Young Adult
PMC - PMC3295784
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/03/14 06:00
MHDA- 2012/08/03 06:00
PMCR- 2012/03/06
CRDT- 2012/03/14 06:00
PHST- 2011/11/10 00:00 [received]
PHST- 2012/01/31 00:00 [accepted]
PHST- 2012/03/14 06:00 [entrez]
PHST- 2012/03/14 06:00 [pubmed]
PHST- 2012/08/03 06:00 [medline]
PHST- 2012/03/06 00:00 [pmc-release]
AID - PONE-D-11-22454 [pii]
AID - 10.1371/journal.pone.0032841 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(3):e32841. doi: 10.1371/journal.pone.0032841. Epub 2012 Mar 6.