PMID- 29531017
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20181211
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 38
IP  - 2
DP  - 2018 Apr 27
TI  - Activation of M1 macrophages plays a critical role in the initiation of acute 
      lung injury.
LID - BSR20171555 [pii]
LID - 10.1042/BSR20171555 [doi]
AB  - The goal of the present study was to investigate the role of M1 macrophages in 
      acute lung injury (ALI). To address this, we used lipopolysaccharide 
      (LPS)-treated wild-type and CD11b-DTR mice, and examined their M1 macrophage 
      levels, and the extent of their inflammation and pulmonary injuries. In addition, 
      we evaluated pulmonary function by measuring the expressions of SP-A and SP-B in 
      infiltrated M1 macrophages. Finally, we co-cultured the mouse type II-like 
      alveolar epithelial cells (AT-II) and mouse pulmonary microvascular endothelial 
      cells (PMECs) with M1 macrophages in the presence of TNF-alpha or H(2)O(2) and 
      assessed them for viability and apoptosis. After LPS treatment, we observed that 
      the number of pulmonary M1/M2 macrophages and the serum levels of interleukin-1beta 
      (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and reactive oxygen species (ROS) 
      significantly increased. Furthermore, the increase in cytokines was accompanied 
      with the initiation of lung injury indicated by the decreased levels of SP-A and 
      SP-B. In macrophage-depleted CD11b-DTR mice, ALI was attenuated, serum levels of 
      IL-1beta, TNF-alpha and ROS were reduced, and lung levels of monocyte chemoattractant 
      protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) were decreased. 
      After administering TNF-alpha and H(2)O(2), the proapoptotic effect of M1 macrophages 
      on AT-II or PMECs significantly increased, the cell viabilities significantly 
      decreased, and apoptosis significantly increased. Our results suggest that M1 
      macrophages are recruited to the lungs where they significantly contribute to an 
      increase in TNF-alpha and ROS production, thus initiating ALI.
CI  - (c) 2018 The Author(s).
FAU - Lu, Hui-Lun
AU  - Lu HL
AD  - Department of Respiratory Medicine, The Second People's Hospital of Longgang 
      District, Shenzhen, China.
FAU - Huang, Xin-Yan
AU  - Huang XY
AD  - The Division of Pulmonary and Critical Care Medicine,The First Affiliated 
      Hospital of Sun Yat-sen University; Institute of Respiratory Diseases of Sun 
      Yat-sen University, Guanzhou, China.
FAU - Luo, Yi-Feng
AU  - Luo YF
AD  - The Division of Pulmonary and Critical Care Medicine,The First Affiliated 
      Hospital of Sun Yat-sen University; Institute of Respiratory Diseases of Sun 
      Yat-sen University, Guanzhou, China.
FAU - Tan, Wei-Ping
AU  - Tan WP
AD  - The Division of Pulmonary and Critical Care Medicine,The First Affiliated 
      Hospital of Sun Yat-sen University; Institute of Respiratory Diseases of Sun 
      Yat-sen University, Guanzhou, China.
FAU - Chen, Pei-Fen
AU  - Chen PF
AD  - The Second Department of Internal Medicine, The Third People's Hospital of 
      Shenzhen, China.
FAU - Guo, Yu-Biao
AU  - Guo YB
AD  - The Division of Pulmonary and Critical Care Medicine,The First Affiliated 
      Hospital of Sun Yat-sen University; Institute of Respiratory Diseases of Sun 
      Yat-sen University, Guanzhou, China guoyubiao@hotmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180427
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Pulmonary Surfactant-Associated Protein A)
SB  - IM
MH  - Acute Lung Injury/chemically induced/*immunology/pathology
MH  - Animals
MH  - Cytokines/immunology
MH  - Lipopolysaccharides/toxicity
MH  - *Macrophage Activation
MH  - Macrophages/*immunology/pathology
MH  - Male
MH  - Mice
MH  - Pulmonary Surfactant-Associated Protein A/immunology
PMC - PMC5920144
OTO - NOTNLM
OT  - Acute lung injury
OT  - Inflammation
OT  - M1 macrohpages
OT  - Reactive oxygen species
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2018/03/14 06:00
MHDA- 2018/12/12 06:00
PMCR- 2018/04/27
CRDT- 2018/03/14 06:00
PHST- 2017/11/17 00:00 [received]
PHST- 2018/03/09 00:00 [revised]
PHST- 2018/03/09 00:00 [accepted]
PHST- 2018/03/14 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2018/03/14 06:00 [entrez]
PHST- 2018/04/27 00:00 [pmc-release]
AID - BSR20171555 [pii]
AID - 10.1042/BSR20171555 [doi]
PST - epublish
SO  - Biosci Rep. 2018 Apr 27;38(2):BSR20171555. doi: 10.1042/BSR20171555. Print 2018 
      Apr 27.