PMID- 29941462
OWN - NLM
STAT- MEDLINE
DCOM- 20190305
LR  - 20190305
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 86
IP  - 9
DP  - 2018 Sep
TI  - High Mobility Group Protein 1 Reverses Immune System Paralysis in Late-Phase 
      Sepsis.
LID - 10.1128/IAI.00455-18 [doi]
LID - e00455-18
AB  - High mobility group protein 1 (HMGB1) is considered to be the primary 
      inflammatory factor triggering immune paralysis in late-phase sepsis. In this 
      study, however, we wanted to explore the possibility of using HMGB1 to boost 
      local differentiation of bone marrow cells (BMCs) into regulatory dendritic cells 
      (DCs) in vivo, thereby inducing immune reversal in late-phase sepsis and 
      improving the prognosis. For this purpose, sepsis was induced by cecal ligation 
      and puncture (CLP). Mice were injected intraperitoneally with HMGB1 (10, 50, or 
      250 mug/kg of body weight) 7 days before CLP. BMCs and liver immune cells were 
      isolated at 0, 3, 5, and 7 days post-CLP. Mice were intranasally infected with 
      Pseudomonas aeruginosa 3 days post-CLP as a secondary pneumonia infection model. 
      BMCs and liver cells isolated from septic mice pretreated with HMGB1 were 
      adoptively transferred into CLP mice. GFP(+)-C57BL/6 and C3H/HeN-C3H/HeJ 
      parabiosis models were established. We found that HMGB1 pretreatment improved the 
      survival of sepsis and increased the numbers of BMCs and liver immune cells in 
      CLP mice. Furthermore, HMGB1 stimulation improved survival in the secondary 
      pneumonia infection model. HMGB1 increased the number as well as the percentage 
      of CD11c(-) CD45RB(high) DCs in septic BM and liver. Adoptive transfer of septic 
      cells pretreated with HMGB1 into CLP mice attenuated sepsis. HMGB1 enhanced the 
      redistribution of CD11c(-) CD45RB(high) DCs through TLR4 signaling in parabiosis 
      models. We conclude that HMGB1 triggers immune reversal through the mobilization, 
      redistribution, and local immune differentiation of BMCs, thereby compensating 
      for impaired immunity and leading to sufficient bacterial eradication.
CI  - Copyright (c) 2018 American Society for Microbiology.
FAU - Liu, Qing-Yang
AU  - Liu QY
AD  - Department of Translational Medicine and Nephrology, China Meitan General 
      Hospital, Beijing, China qingyangliu_ccm@sina.com xukaizhi195601@163.com.
AD  - Department of Microbiology and Immunology, Burns Institute, First Hospital 
      Affiliated to the Chinese PLA General Hospital, Beijing, China.
FAU - Wang, Yue-Xin
AU  - Wang YX
AD  - First Department of Orthopedics, Tangshan Worker's Hospital Affiliated to Hebei 
      Medical University, Tangshan, Hebei Province, China.
FAU - Wu, Zong-Sheng
AU  - Wu ZS
AD  - Department of Emergency, Zhongda Hospital Affiliated to Southeast University, 
      Nanjing, China.
FAU - Shi, Zhen-Wei
AU  - Shi ZW
AD  - Department of Translational Medicine and Nephrology, China Meitan General 
      Hospital, Beijing, China.
FAU - Wu, Xu
AU  - Wu X
AD  - Becton-Dickinson Biosciences, Beijing, China.
FAU - Chen, Xin
AU  - Chen X
AD  - Department of Oncology, Tongji Hospital of Tongji Medical College of Huazhong 
      University of Science and Technology, Wuhan, Hubei Province, China.
FAU - Yang, Zhao
AU  - Yang Z
AD  - College of Chemistry, Beijing Normal University, Beijing, China.
FAU - Xu, Kai-Zhi
AU  - Xu KZ
AD  - Department of Anesthesiology, Tangshan Worker's Hospital Affiliated to Hebei 
      Medical University, Tangshan, Hebei Province, China qingyangliu_ccm@sina.com 
      xukaizhi195601@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180822
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (HMGB1 Protein)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Bone Marrow Cells/immunology
MH  - Cecum
MH  - Cell Differentiation
MH  - Dendritic Cells/immunology
MH  - Disease Models, Animal
MH  - HMGB1 Protein/*immunology/*pharmacology
MH  - Ligation
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Parabiosis
MH  - Pneumonia/*immunology/microbiology
MH  - Pseudomonas Infections/blood/drug therapy
MH  - Pseudomonas aeruginosa/immunology
MH  - Sepsis/*drug therapy/*immunology/microbiology
MH  - Toll-Like Receptor 4/immunology
PMC - PMC6105879
OTO - NOTNLM
OT  - CD11c- CD45RBhigh dendritic cells
OT  - bone marrow cells
OT  - high mobility group protein 1
OT  - sepsis
EDAT- 2018/06/27 06:00
MHDA- 2019/03/06 06:00
PMCR- 2019/02/22
CRDT- 2018/06/27 06:00
PHST- 2018/06/14 00:00 [received]
PHST- 2018/06/19 00:00 [accepted]
PHST- 2018/06/27 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
PHST- 2018/06/27 06:00 [entrez]
PHST- 2019/02/22 00:00 [pmc-release]
AID - IAI.00455-18 [pii]
AID - 00455-18 [pii]
AID - 10.1128/IAI.00455-18 [doi]
PST - epublish
SO  - Infect Immun. 2018 Aug 22;86(9):e00455-18. doi: 10.1128/IAI.00455-18. Print 2018 
      Sep.