PMID- 32703418
OWN - NLM
STAT- MEDLINE
DCOM- 20210210
LR  - 20210210
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 529
IP  - 2
DP  - 2020 Aug 20
TI  - Trans-unsaturated fatty acid activates NLRP3 inflammasome in macrophages and 
      exacerbates intestinal inflammation in mice.
PG  - 243-250
LID - S0006-291X(20)31199-2 [pii]
LID - 10.1016/j.bbrc.2020.06.005 [doi]
AB  - Higher consumption of trans fatty acid (TFA) is a risk factor for several 
      inflammatory diseases including inflammatory bowel disease (IBD). However, the 
      detailed mechanisms by which TFA intake affects IBD pathology remain unclear. We 
      demonstrate here that elaidate, a trans-isomer of oleate, enhances interleukin 
      (IL)-1beta production through the activation of NLRP3 inflammasome in mouse bone 
      marrow-derived macrophages (BMDMs). Oleate has no effect on IL-1beta production. 
      Elaidate also induces oxidative stress and activates endoplasmic reticulum stress 
      in BMDMs. The elaidate-induced IL-1beta production is suppressed by co-treatments 
      with antioxidants and a chemical chaperone. Furthermore, we analyze the effects 
      of elaidate administration on intestinal inflammation using 2,4,6-trinitrobenzene 
      sulfonic acid (TNBS)-induced colitis model in mice. Increased colonic damage and 
      myeloperoxidase activity after TNBS treatment are elevated by elaidate 
      administration. Also, TNBS treatment induces IL-1beta production in colonic mucosa; 
      elaidate administration enhances the induction. We believe that these data reveal 
      some mechanisms by which the TFA intake is associated with increased risk for 
      IBD.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Higashimura, Yasuki
AU  - Higashimura Y
AD  - Department of Food Science, Ishikawa Prefectural University, Nonoichi, Ishikawa, 
      921-8836, Japan; Molecular Gastroenterology and Hepatology, Graduate School of 
      Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 
      602-8566, Japan. Electronic address: yasuki@ishikawa-pu.ac.jp.
FAU - Tanaka, Yumiko
AU  - Tanaka Y
AD  - Department of Food Science, Ishikawa Prefectural University, Nonoichi, Ishikawa, 
      921-8836, Japan.
FAU - Takagi, Tomohisa
AU  - Takagi T
AD  - Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
FAU - Uchiyama, Kazuhiko
AU  - Uchiyama K
AD  - Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
FAU - Mizushima, Katsura
AU  - Mizushima K
AD  - Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
FAU - Niki, Etsuo
AU  - Niki E
AD  - Research Center for Advanced Science and Technology, The University of Tokyo, 
      Meguro, Tokyo, 153-0041, Japan.
FAU - Naito, Yuji
AU  - Naito Y
AD  - Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kyoto, Kyoto, 602-8566, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200622
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Inflammasomes)
RN  - 0 (Interleukin-1beta)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Trans Fatty Acids)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Colitis/*metabolism/pathology
MH  - Inflammasomes/*metabolism
MH  - Inflammation/metabolism/pathology
MH  - Interleukin-1beta/metabolism
MH  - Intestines/pathology
MH  - Macrophages/metabolism/*pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism
MH  - Trans Fatty Acids/*metabolism
OTO - NOTNLM
OT  - Colon
OT  - Elaidate
OT  - Endoplasmic reticulum stress
OT  - Interleukin-1beta
OT  - Reactive oxygen species
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/07/25 06:00
MHDA- 2021/02/11 06:00
CRDT- 2020/07/25 06:00
PHST- 2020/05/27 00:00 [received]
PHST- 2020/06/02 00:00 [accepted]
PHST- 2020/07/25 06:00 [entrez]
PHST- 2020/07/25 06:00 [pubmed]
PHST- 2021/02/11 06:00 [medline]
AID - S0006-291X(20)31199-2 [pii]
AID - 10.1016/j.bbrc.2020.06.005 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2020 Aug 20;529(2):243-250. doi: 
      10.1016/j.bbrc.2020.06.005. Epub 2020 Jun 22.