PMID- 31138763
OWN - NLM
STAT- MEDLINE
DCOM- 20200807
LR  - 20200807
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 39
IP  - 6
DP  - 2019 Jun 28
TI  - Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung 
      injury via NF-kappaB signaling in bone marrow-derived macrophages.
LID - BSR20181888 [pii]
LID - 10.1042/BSR20181888 [doi]
AB  - Acute lung injury (ALI) is an acute inflammatory disease. Leukocyte 
      immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based 
      inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various 
      pathological processes. However, the function of LILRB4 in ALI remains largely 
      unknown. The aim of the present study was to explore the role of LILRB4 in ALI. 
      LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone 
      marrow cell transplantation was used to identify the cell source of the LILRB4 
      deficiency-aggravated inflammatory response in ALI. The effect on ALI was 
      analyzed by pathological and molecular analyses. Our results indicated that 
      LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can 
      enhance lung inflammation. According to the results of our bone marrow transplant 
      model, LILRB4 regulates the occurrence and development of ALI by bone 
      marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The 
      observed inflammation was mainly due to BMDM-induced NF-kappaB signaling. In 
      conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental 
      role in ALI-associated BMDM activation by prompting the NF-kappaB signal pathway.
CI  - (c) 2019 The Author(s).
FAU - Qiu, Tao
AU  - Qiu T
AUID- ORCID: 0000-0002-1410-7795
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Zhou, Jiangqiao
AU  - Zhou J
AUID- ORCID: 0000-0002-6118-0020
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Wang, Tianyu
AU  - Wang T
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Chen, Zhongbao
AU  - Chen Z
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Ma, Xiaoxiong
AU  - Ma X
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Zhang, Long
AU  - Zhang L
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China.
FAU - Zou, Jilin
AU  - Zou J
AD  - Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan 
      University, Wuhan 430060, China zhoujq@whu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190614
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (LILRB4 protein, human)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NF-kappa B)
RN  - 0 (RELA protein, human)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Transcription Factor RelA)
SB  - IM
MH  - Acute Lung Injury/chemically induced/genetics/pathology/*therapy
MH  - Animals
MH  - Bone Marrow Cells/cytology
MH  - *Bone Marrow Transplantation
MH  - Female
MH  - Gene Expression Regulation/genetics
MH  - Humans
MH  - Immunoreceptor Tyrosine-Based Activation Motif/genetics
MH  - Lipopolysaccharides/toxicity
MH  - Macrophages/metabolism/pathology
MH  - Male
MH  - Membrane Glycoproteins/*genetics
MH  - Mice
MH  - Mice, Knockout
MH  - NF-kappa B/genetics
MH  - Pneumonia/genetics/pathology/*therapy
MH  - Receptors, Immunologic/*genetics
MH  - Signal Transduction/genetics
MH  - Transcription Factor RelA/genetics
PMC - PMC6566464
OTO - NOTNLM
OT  - LILRB4
OT  - acute lung injury
OT  - lung
OT  - macrophage
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2019/05/30 06:00
MHDA- 2020/08/08 06:00
PMCR- 2019/06/14
CRDT- 2019/05/30 06:00
PHST- 2018/10/14 00:00 [received]
PHST- 2019/05/17 00:00 [revised]
PHST- 2019/05/22 00:00 [accepted]
PHST- 2019/05/30 06:00 [pubmed]
PHST- 2020/08/08 06:00 [medline]
PHST- 2019/05/30 06:00 [entrez]
PHST- 2019/06/14 00:00 [pmc-release]
AID - BSR20181888 [pii]
AID - 10.1042/BSR20181888 [doi]
PST - epublish
SO  - Biosci Rep. 2019 Jun 14;39(6):BSR20181888. doi: 10.1042/BSR20181888. Print 2019 
      Jun 28.