PMID- 34062371
OWN - NLM
STAT- MEDLINE
DCOM- 20211231
LR  - 20211231
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 97
DP  - 2021 Aug
TI  - A20 functions as a negative regulator in macrophage for DSS-induced colitis.
PG  - 107804
LID - S1567-5769(21)00440-9 [pii]
LID - 10.1016/j.intimp.2021.107804 [doi]
AB  - The function of A20 as a deubiquitinating enzyme in inflammatory diseases and 
      autoimmune diseases has been reported, we therefore aimed to investigate the 
      potential effects of A20 in macrophages and dextran sodium sulfate (DSS)-induced 
      colitis mouse model. Colitis mouse model was induced by DSS treatment. 
      Tnfaip3(fl/fl) mice were crossed with Lyz2-Cre mice to generate A20 myeloid 
      cell-conditional knockout mice. The expression levels of indicated cytokines were 
      analyzed by quantitative reverse transcriptase real-time polymerase chain 
      reaction and enzyme-linked immunosorbent assay. Phosphorylated and total protein 
      levels in nuclear factor kappa B (NF-kappaB) signaling pathway were detected by 
      Western blot. In the bone marrow of mice, A20 deficiency did not affect 
      macrophage development. In bone marrow-derived macrophages (BMDMs) after 
      lipopolysaccharide (LPS) treatment, A20 deficiency enhanced pro-inflammatory 
      cytokine expression. A20 deficiency in macrophages led to severe symptoms of 
      DSS-induced colitis in mice. A20 deficiency enhanced the NF-kappaB signaling pathway 
      activity in BMDMs. The effects of A20 deficiency in DSS-induced colitis were 
      suppressed by NF-kappaB pathway inhibition. A20/inhibitor of NF-kappaB kinase 2 
      (IKKbeta)-double knockout mice were resistant to DSS-induced colitis. A20 suppresses 
      pro-inflammatory cytokine expression in macrophages through the NF-kappaB signal 
      pathway and alleviates the pathogenesis of DSS-induced colitis in mice.
CI  - Copyright (c) 2021 Elsevier B.V. All rights reserved.
FAU - Pu, Tian
AU  - Pu T
AD  - Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou 
      University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan, China.
FAU - Liu, Wenzheng
AU  - Liu W
AD  - Department of Gastroenterology, Peking University Third Hospital, No. 49 Huayuan 
      North Road, Beijing 100191, China.
FAU - Wu, Yijun
AU  - Wu Y
AD  - Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou 
      University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan, China.
FAU - Zhao, Ye
AU  - Zhao Y
AD  - Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou 
      University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan, China. Electronic 
      address: fcczhaoy@zzu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20210529
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 9042-14-2 (Dextran Sulfate)
RN  - EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
RN  - EC 3.4.22.- (Tnfaip3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Colitis/chemically induced/*immunology/pathology
MH  - Colon/immunology/pathology
MH  - Dextran Sulfate/administration & dosage/toxicity
MH  - Disease Models, Animal
MH  - Humans
MH  - Intestinal Mucosa/immunology/pathology
MH  - Macrophages/*immunology/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Primary Cell Culture
MH  - Tumor Necrosis Factor alpha-Induced Protein 3/genetics/*metabolism
OTO - NOTNLM
OT  - A20
OT  - DSS-induced colitis
OT  - Macrophage
OT  - NF-kappaB
EDAT- 2021/06/02 06:00
MHDA- 2022/01/01 06:00
CRDT- 2021/06/01 20:18
PHST- 2021/02/08 00:00 [received]
PHST- 2021/04/13 00:00 [revised]
PHST- 2021/05/19 00:00 [accepted]
PHST- 2021/06/02 06:00 [pubmed]
PHST- 2022/01/01 06:00 [medline]
PHST- 2021/06/01 20:18 [entrez]
AID - S1567-5769(21)00440-9 [pii]
AID - 10.1016/j.intimp.2021.107804 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2021 Aug;97:107804. doi: 10.1016/j.intimp.2021.107804. Epub 
      2021 May 29.