PMID- 32222356
OWN - NLM
STAT- MEDLINE
DCOM- 20210906
LR  - 20210906
IS  - 1879-0089 (Electronic)
IS  - 0145-305X (Print)
IS  - 0145-305X (Linking)
VI  - 108
DP  - 2020 Jul
TI  - Notch signaling contributes to the expression of inflammatory cytokines induced 
      by highly pathogenic porcine reproductive and respiratory syndrome virus 
      (HP-PRRSV) infection in porcine alveolar macrophages.
PG  - 103690
LID - S0145-305X(19)30551-8 [pii]
LID - 10.1016/j.dci.2020.103690 [doi]
AB  - Notch signaling, an evolutionarily conserved signal pathway has emerged as a key 
      signal pathway to regulate host immune response but the contribution of Notch 
      signaling to immune response in pigs remains unknown. Infection of porcine 
      alveolar macrophages (PAM) with porcine reproductive and respiratory syndrome 
      virus (PRRSV) triggers expression of Jagged1 mRNA, suggesting that Notch 
      signaling might play a role in the immune response to PRRSV infection. To further 
      explore it, we examined the expression profile of Notch molecules in PAM 
      following a highly pathogenic PRRSV (HP-PRRSV) strain infection. We demonstrated 
      that HP-PRRSV infection resulted in the induction of Notch ligands (Jagged1, 
      Dll3, Dll4), the transcription factor RBP-J, and the target gene Hes1, consistent 
      with activation of Notch signaling. Next, using DAPT treatment and the knockdown 
      of RBP-J illustrated that inhibition of activation of Notch signaling attenuated 
      induction of the inflammatory cytokines (TNF-alpha and IL-1beta) instead of viral 
      replication in PAM during HP-PRRSV infection. Furthermore, the knockdown of 
      Jagged1, the most induced ligand not only inhibited activation of Notch 
      signaling, but also reduced the expression of inflammatory cytokines without any 
      influence in viral replication. Moreover, our data revealed that several 
      signaling including NF-kappaB, MAPK and Notch signaling contributed to the induction 
      of Jagged1 in PAM during HP-PRRSV infection. In summary, these findings reveal 
      that Notch as an important signaling pathway could contribute to the regulation 
      of inflammatory response induced by HP-PRRSV infection.
CI  - Copyright (c) 2020 Elsevier Ltd. All rights reserved.
FAU - Lu, Yan
AU  - Lu Y
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Zhang, Yanbing
AU  - Zhang Y
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Xiang, Xiao
AU  - Xiang X
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Sharma, Mona
AU  - Sharma M
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Liu, Ke
AU  - Liu K
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Wei, Jianchao
AU  - Wei J
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Shao, Donghua
AU  - Shao D
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Li, Beibei
AU  - Li B
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Tong, Guangzhi
AU  - Tong G
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China.
FAU - Olszewski, Michal A
AU  - Olszewski MA
AD  - Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, 
      University of Michigan Medical School, Ann Arbor, MI, USA; VA Ann Arbor 
      Healthcare System, Ann Arbor, MI, USA.
FAU - Ma, Zhiyong
AU  - Ma Z
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China. Electronic address: zhiyongma@shvri.ac.cn.
FAU - Qiu, Yafeng
AU  - Qiu Y
AD  - Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 
      China. Electronic address: yafengq@shvri.ac.cn.
LA  - eng
GR  - I01 BX000656/BX/BLRD VA/United States
GR  - IK6 BX003615/BX/BLRD VA/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200325
PL  - United States
TA  - Dev Comp Immunol
JT  - Developmental and comparative immunology
JID - 7708205
RN  - 0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Jagged-1 Protein)
RN  - 0 (Receptors, Notch)
RN  - 0 (Transcription Factor HES-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Immunoglobulin J Recombination Signal Sequence-Binding 
      Protein/genetics/metabolism
MH  - Interleukin-1beta/metabolism
MH  - Jagged-1 Protein/metabolism
MH  - Macrophages, Alveolar/*immunology/metabolism
MH  - Male
MH  - Porcine Reproductive and Respiratory Syndrome/*immunology/virology
MH  - Porcine respiratory and reproductive syndrome virus/immunology
MH  - Primary Cell Culture
MH  - Receptors, Notch/*metabolism
MH  - Signal Transduction/genetics/immunology
MH  - Sus scrofa/*immunology/virology
MH  - Swine
MH  - Transcription Factor HES-1/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Virus Replication/immunology
PMC - PMC7765342
MID - NIHMS1655974
OTO - NOTNLM
OT  - HP-PRRSV
OT  - Inflammatory response
OT  - Notch signaling
OT  - Porcine alveolar macrophages
EDAT- 2020/03/31 06:00
MHDA- 2021/09/07 06:00
PMCR- 2021/01/01
CRDT- 2020/03/31 06:00
PHST- 2019/11/06 00:00 [received]
PHST- 2020/02/28 00:00 [revised]
PHST- 2020/03/23 00:00 [accepted]
PHST- 2020/03/31 06:00 [pubmed]
PHST- 2021/09/07 06:00 [medline]
PHST- 2020/03/31 06:00 [entrez]
PHST- 2021/01/01 00:00 [pmc-release]
AID - S0145-305X(19)30551-8 [pii]
AID - 10.1016/j.dci.2020.103690 [doi]
PST - ppublish
SO  - Dev Comp Immunol. 2020 Jul;108:103690. doi: 10.1016/j.dci.2020.103690. Epub 2020 
      Mar 25.