PMID- 36580757
OWN - NLM
STAT- MEDLINE
DCOM- 20230208
LR  - 20230213
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 115
DP  - 2023 Feb
TI  - NF-kappaB p65 and SETDB1 expedite lipopolysaccharide-induced intestinal inflammation 
      in mice by inducing IRF7/NLR-dependent macrophage M1 polarization.
PG  - 109554
LID - S1567-5769(22)01039-6 [pii]
LID - 10.1016/j.intimp.2022.109554 [doi]
AB  - Macrophages exhibit distinct phenotypes that are pro-inflammatory (M1) or 
      anti-inflammatory (M2) in response to inflammation. In this study, we tried to 
      identify the roles and mechanisms of interferon regulatory factor 7 (IRF7) in 
      modulating the phenotypes of macrophages in lipopolysaccharide (LPS)-induced 
      intestinal inflammation. The mouse model of intestinal inflammation was induced 
      by lipopolysaccharide (LPS), and mouse bone marrow-derived macrophages (BMDMs) 
      and mouse intestinal epithelial cells were selected for experimental verification 
      in vitro. Results demonstrated that IRF7 was highly expressed in the mouse model 
      of intestinal inflammation, while IRF7 deficiency repressed macrophage M1 
      polarization and attenuated intestinal inflammation in mice. p65 and SET domain 
      bifurcated 1 (SETDB1) synergistically promoted histone 3 lysine 4 trimethylation 
      (H3K4me3) methylation to elevate IRF7 expression, which activated the Nod-like 
      receptor (NLR) pathway to induce macrophage M1 polarization. Through this 
      mechanism, IRF7 in BMDMs functioned to accelerate intestinal epithelial cell 
      apoptosis and their release of pro-inflammatory proteins. Furthermore, the 
      promoting effect of p65 and SETDB1 on LPS-induced intestinal inflammation was 
      validated in vivo. To sum up, NF-kappaB p65 and SETDB1 facilitated IRF7-mediated 
      macrophage M1 polarization, thereby aggravating the LPS-induced intestinal 
      inflammation. Hence, this study highlights the appealing value of these factors 
      as anti-inflammatory targets.
CI  - Copyright (c) 2022. Published by Elsevier B.V.
FAU - Chen, Li
AU  - Chen L
AD  - Department of Digestion, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China.
FAU - Dai, Maolin
AU  - Dai M
AD  - Department of Anesthesia, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China.
FAU - Zuo, Wei
AU  - Zuo W
AD  - Department of Digestion, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China.
FAU - Dai, Yongyu
AU  - Dai Y
AD  - Department of Digestion, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China.
FAU - Yang, Qiqi
AU  - Yang Q
AD  - Department of Digestion, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China.
FAU - Yu, Shuangjiang
AU  - Yu S
AD  - Department of Neurosurgery, The First Hospital Affiliated to Army Military 
      Medical University (Southwest Hospital), Chongqing 400038, PR China.
FAU - Huang, Min
AU  - Huang M
AD  - Department of Digestion, Affiliated Hospital of North Sichuan Medical College, 
      Nanchong 637000, PR China.
FAU - Liu, Hao
AU  - Liu H
AD  - Department of Digestion, Rongchang District People's Hospital of Chongqing, 
      Chongqing 402468, PR China. Electronic address: liuhao_rc@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20221227
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (NF-kappa B)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Interferon Regulatory Factor-7)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Irf7 protein, mouse)
RN  - EC 2.1.1.43 (SETDB1 protein, mouse)
RN  - EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *NF-kappa B/metabolism
MH  - *Lipopolysaccharides/pharmacology
MH  - Interferon Regulatory Factor-7/metabolism
MH  - PR-SET Domains
MH  - Macrophages
MH  - Inflammation/chemically induced/metabolism
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Histone-Lysine N-Methyltransferase/genetics/metabolism
OTO - NOTNLM
OT  - Interferon regulatory factor 7
OT  - Intestinal inflammation
OT  - Macrophage M1 polarization
OT  - NOD-like receptor signaling pathway
OT  - Nuclear factor kappa B p65
OT  - SET domain containing 1B
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- 2022/12/30 06:00
MHDA- 2023/02/09 06:00
CRDT- 2022/12/29 18:09
PHST- 2022/08/04 00:00 [received]
PHST- 2022/12/04 00:00 [revised]
PHST- 2022/12/04 00:00 [accepted]
PHST- 2022/12/30 06:00 [pubmed]
PHST- 2023/02/09 06:00 [medline]
PHST- 2022/12/29 18:09 [entrez]
AID - S1567-5769(22)01039-6 [pii]
AID - 10.1016/j.intimp.2022.109554 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2023 Feb;115:109554. doi: 10.1016/j.intimp.2022.109554. Epub 
      2022 Dec 27.