PMID- 35816944
OWN - NLM
STAT- MEDLINE
DCOM- 20220817
LR  - 20220817
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 110
DP  - 2022 Sep
TI  - Sodium butyrate attenuates bovine mammary epithelial cell injury by inhibiting 
      the formation of neutrophil extracellular traps.
PG  - 109009
LID - S1567-5769(22)00493-3 [pii]
LID - 10.1016/j.intimp.2022.109009 [doi]
AB  - Neutrophil extracellular traps (NETs) are an important means by which the body 
      fights against exogenous bacteria. However, studies have shown that excessive 
      NETs release can damage other cells. Accumulating evidence has shown that butyric 
      acid can alleviate the inflammatory response of cells. However, the effect of 
      butyric acid on Staphylococcus aureus-induced NETs formation and its underlying 
      mechanism are still unclear. In this study, western blotting, immunofluorescence 
      and CCK-8 assays were used to examine the effect of NETs formation by sodium 
      butyrate (NaB). The results showed that NaB suppressed the release of S. 
      aureus-induced NETs formation, as indicated by decreases in the levels of DNA, 
      histones, myeloperoxidase, and neutrophil elastase. S. aureus can induce 
      autophagy, and autophagy plays a key role in the formation of NETs. Our data 
      showed that NaB activated mammalian target of rapamycin (mTOR) and the kinases 
      protein kinase B (AKT) and unc-51 like kinase 1 (ULK1) at Ser757 and inhibited 
      AMP-activated protein kinase (AMPK). To explore whether NaB inhibited the 
      formation of NETs by inhibiting autophagy, we added 3-methyladenine (autophagy 
      inhibitor) (3-MA, 5 mM) to bovine neutrophils, and the results showed that 3-MA 
      significantly inhibited NETs release. Furthermore, we found that NETs and their 
      component histones exhibited significantly increased the cytotoxic effects on 
      bovine mammary epithelial cells (BMECs), indicating that NETs and their component 
      histones play a key role in BMEC damage. In conclusion, NaB can reduce the 
      excessive formation of NETs by inhibiting autophagy, thus reducing the damaging 
      effect of NETs on BMECs.
CI  - Copyright (c) 2022 Elsevier B.V. All rights reserved.
FAU - Li, Yuhang
AU  - Li Y
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: yhli9915@mails.jlu.edu.cn.
FAU - Liu, Juxiong
AU  - Liu J
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: juxiong@jlu.edu.cn.
FAU - Cui, Yueyao
AU  - Cui Y
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: cuiyy9918@mails.jlu.edu.cn.
FAU - Cao, Yu
AU  - Cao Y
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: 1015009909@qq.com.
FAU - Xu, Ping
AU  - Xu P
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: xuping20@mails.jlu.edu.cn.
FAU - Kan, Xingchi
AU  - Kan X
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: kanxingchi@outlook.com.
FAU - Guo, Wenjin
AU  - Guo W
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: guowenjin@jlu.edu.cn.
FAU - Fu, Shoupeng
AU  - Fu S
AD  - College of Veterinary Medicine, Jilin University, Changchun 130062, China. 
      Electronic address: fushoupeng@jlu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20220708
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Histones)
RN  - 107-92-6 (Butyric Acid)
SB  - IM
MH  - Animals
MH  - Butyric Acid/pharmacology
MH  - Cattle
MH  - Epithelial Cells/metabolism
MH  - *Extracellular Traps
MH  - Histones/metabolism
MH  - Mammals
MH  - Neutrophils
MH  - Staphylococcus aureus/metabolism
OTO - NOTNLM
OT  - Autophagy
OT  - BMECs
OT  - NaB
OT  - Neutrophil extracellular traps
OT  - S. aureus
EDAT- 2022/07/12 06:00
MHDA- 2022/08/18 06:00
CRDT- 2022/07/11 18:28
PHST- 2022/05/09 00:00 [received]
PHST- 2022/06/13 00:00 [revised]
PHST- 2022/06/25 00:00 [accepted]
PHST- 2022/07/12 06:00 [pubmed]
PHST- 2022/08/18 06:00 [medline]
PHST- 2022/07/11 18:28 [entrez]
AID - S1567-5769(22)00493-3 [pii]
AID - 10.1016/j.intimp.2022.109009 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2022 Sep;110:109009. doi: 10.1016/j.intimp.2022.109009. Epub 
      2022 Jul 8.