PMID- 30919933
OWN - NLM
STAT- MEDLINE
DCOM- 20200421
LR  - 20200801
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 197
IP  - 2
DP  - 2019 Aug
TI  - High fructose-induced metabolic changes enhance inflammation in human dendritic 
      cells.
PG  - 237-249
LID - 10.1111/cei.13299 [doi]
AB  - Dendritic cells (DCs) are critical antigen-presenting cells which are the 
      initiators and regulators of the immune response. Numerous studies support the 
      idea that dietary sugars influence DC functions. Increased consumption of 
      fructose has been thought to be the leading cause of metabolic disorders. 
      Although evidence supports their association with immune dysfunction, the 
      specific mechanisms are not well understood. Fructose is one of the main dietary 
      sugars in our diet. Therefore, here we compared the effect of fructose and 
      glucose on the functions of human DCs. High levels of D-fructose compared to 
      D-glucose led to activation of DCs in vitro by promoting interleukin (IL)-6 and 
      IL-1beta production. Moreover, fructose exposed DCs also induced interferon (IFN)-gamma 
      secretion from T cells. Proinflammatory response of DCs in high fructose 
      environment was found to be independent of the major known metabolic regulators 
      or glycolytic control. Instead, DC activation on acute exposure to fructose was 
      via activation of receptor for advanced glycation end product (RAGE) in response 
      to increased accumulation of advanced glycation end products (AGE). However, 
      chronic exposure of DCs to high fructose environment induced a shift towards 
      glycolysis compared to glucose cultured DCs. Further investigations revealed that 
      the AGEs formed by fructose induced increased levels of inflammatory cytokines in 
      DCs compared to AGEs from glucose. In summary, understanding the link between 
      metabolic changes and fructose-induced DC activation compared to glucose has 
      broad implications for immune dysfunction associated with metabolic disorders.
CI  - (c) 2019 British Society for Immunology.
FAU - Jaiswal, N
AU  - Jaiswal N
AD  - Division of Basic and Clinical Immunology, Department of Medicine, University of 
      California, Irvine, Irvine, CA, USA.
FAU - Agrawal, S
AU  - Agrawal S
AD  - Division of Basic and Clinical Immunology, Department of Medicine, University of 
      California, Irvine, Irvine, CA, USA.
FAU - Agrawal, A
AU  - Agrawal A
AUID- ORCID: 0000-0002-3323-9152
AD  - Division of Basic and Clinical Immunology, Department of Medicine, University of 
      California, Irvine, Irvine, CA, USA.
LA  - eng
GR  - R01 AG045216/AG/NIA NIH HHS/United States
GR  - UL1 TR000153/TR/NCATS NIH HHS/United States
GR  - UL1 TR001414/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20190415
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Dietary Sugars)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (IFNG protein, human)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 30237-26-4 (Fructose)
RN  - 82115-62-6 (Interferon-gamma)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adult
MH  - Dendritic Cells/immunology/*metabolism
MH  - Dietary Sugars/*adverse effects/pharmacology
MH  - Fructose/*adverse effects/pharmacology
MH  - Glucose/*adverse effects/pharmacology
MH  - Glycation End Products, Advanced/metabolism
MH  - Humans
MH  - Immune System Diseases/chemically induced
MH  - Inflammation/*chemically induced/immunology
MH  - Interferon-gamma/metabolism
MH  - Muscle, Skeletal/pathology
MH  - Reactive Oxygen Species/metabolism
MH  - Receptor for Advanced Glycation End Products/metabolism
MH  - T-Lymphocytes/immunology
MH  - Young Adult
PMC - PMC6642875
OTO - NOTNLM
OT  - AGE-RAGE
OT  - dendritic cells
OT  - fructose
OT  - glucose
OT  - inflammation
COIS- The authors have declared that no conflicts of interest exist.
EDAT- 2019/03/29 06:00
MHDA- 2020/04/22 06:00
PMCR- 2020/08/01
CRDT- 2019/03/29 06:00
PHST- 2019/03/25 00:00 [accepted]
PHST- 2019/03/29 06:00 [pubmed]
PHST- 2020/04/22 06:00 [medline]
PHST- 2019/03/29 06:00 [entrez]
PHST- 2020/08/01 00:00 [pmc-release]
AID - CEI13299 [pii]
AID - 10.1111/cei.13299 [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2019 Aug;197(2):237-249. doi: 10.1111/cei.13299. Epub 2019 Apr 
      15.