PMID- 20851496
OWN - NLM
STAT- MEDLINE
DCOM- 20110815
LR  - 20181201
IS  - 1878-3279 (Electronic)
IS  - 0171-2985 (Linking)
VI  - 216
IP  - 3
DP  - 2011 Mar
TI  - The short chain fatty acid sodium butyrate regulates the induction of CD1a in 
      developing dendritic cells.
PG  - 275-84
LID - 10.1016/j.imbio.2010.07.004 [doi]
AB  - Dendritic cells (DCs) are professional antigen-presenting cells with attributes 
      for priming/activating T cells and mediating immune responses. Considering the 
      importance of DCs in the initiation of immune responses, it will be of interest 
      to study their mechanisms of regulation. Histone-modifying enzymes, such as 
      histone deacetylases (HDACs), are critical in controlling chromatin organization. 
      The aim of our study was to investigate DC differentiation under the influence of 
      sodium butyrate (NaB), a short chain fatty acid that is a histone deacetylase 
      inhibitor. Monocytes from healthy individuals were differentiated into immature 
      DCs with IL-4 and GM-CSF in the presence or absence of NaB. DC differentiation 
      was evaluated by CD14 and CD1a expression by flow cytometry. We observed that 
      monocytes stimulated to differentiate in the presence of NaB displayed colony 
      formation and dendritic cell morphology, lost CD14 and showed decreased secretion 
      of IL-1beta. The acquisition of CD1a, however, was impaired. Being a natural short 
      chain fatty acid, NaB may regulate CD1a acquisition independently of its HDAC 
      inhibitory activity. We observed that the addition of peroxisome 
      proliferator-activated receptor gamma (PPAR-gamma) antagonist (GW9662) did not reverse 
      NaB effect, suggesting this was not the pathway involved. On the other hand, CD1a 
      can also be induced by toll like receptors 2 (TLR 2) agonists, such as Pam3Cys, 
      and NaB inhibited this effect. Our data suggest that the histone deacetylase 
      inhibitor NaB instead of impairing DC differentiation inhibits the acquisition of 
      CD1a induced both by cytokines and by TLR 2 agonist stimulus. Furthermore, this 
      occurs at the transcriptional level as NaB led to a decrease in mRNA levels of 
      CD1a and upregulation of CD1d.
CI  - Copyright (c) 2010 Elsevier GmbH. All rights reserved.
FAU - Nascimento, Clarissa Rodrigues
AU  - Nascimento CR
AD  - Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de 
      Janeiro, Brazil.
FAU - Freire-de-Lima, Celio G
AU  - Freire-de-Lima CG
FAU - da Silva de Oliveira, Andreia
AU  - da Silva de Oliveira A
FAU - Rumjanek, Franklin D
AU  - Rumjanek FD
FAU - Rumjanek, Vivian M
AU  - Rumjanek VM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100819
PL  - Netherlands
TA  - Immunobiology
JT  - Immunobiology
JID - 8002742
RN  - 0 (2-chloro-5-nitrobenzanilide)
RN  - 0 (Anilides)
RN  - 0 (Antigens, CD1)
RN  - 0 (Antigens, CD1d)
RN  - 0 (Butyrates)
RN  - 0 (CD1a antigen)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (PPAR gamma)
RN  - 0 (RNA, Messenger)
RN  - 0 (Toll-Like Receptor 2)
RN  - 207137-56-2 (Interleukin-4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Anilides/pharmacology
MH  - Antigens, CD1/*genetics
MH  - Antigens, CD1d/genetics
MH  - Butyrates/*pharmacology
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Dendritic Cells/*metabolism
MH  - Flow Cytometry
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
MH  - Histone Deacetylases/metabolism
MH  - Humans
MH  - Interleukin-1beta/metabolism
MH  - Interleukin-4/pharmacology
MH  - Lipopolysaccharide Receptors/genetics
MH  - Monocytes/drug effects
MH  - PPAR gamma/antagonists & inhibitors
MH  - RNA, Messenger/genetics/metabolism
MH  - Toll-Like Receptor 2/agonists/*metabolism
EDAT- 2010/09/21 06:00
MHDA- 2011/08/16 06:00
CRDT- 2010/09/21 06:00
PHST- 2010/02/25 00:00 [received]
PHST- 2010/07/07 00:00 [revised]
PHST- 2010/07/09 00:00 [accepted]
PHST- 2010/09/21 06:00 [entrez]
PHST- 2010/09/21 06:00 [pubmed]
PHST- 2011/08/16 06:00 [medline]
AID - S0171-2985(10)00137-3 [pii]
AID - 10.1016/j.imbio.2010.07.004 [doi]
PST - ppublish
SO  - Immunobiology. 2011 Mar;216(3):275-84. doi: 10.1016/j.imbio.2010.07.004. Epub 
      2010 Aug 19.