PMID- 30628485
OWN - NLM
STAT- MEDLINE
DCOM- 20191230
LR  - 20200930
IS  - 1522-1504 (Electronic)
IS  - 1040-0605 (Print)
IS  - 1040-0605 (Linking)
VI  - 316
IP  - 3
DP  - 2019 Mar 1
TI  - Apoptosis signal-regulating kinase-1 promotes inflammasome priming in 
      macrophages.
PG  - L418-L427
LID - 10.1152/ajplung.00199.2018 [doi]
AB  - We previously showed that mice deficient in apoptosis signal-regulating kinase-1 
      (ASK1) were partially protected against ventilator-induced lung injury. Because 
      ASK1 can promote both cell death and inflammation, we hypothesized that ASK1 
      activation regulates inflammasome-mediated inflammation. Mice deficient in ASK1 
      expression (ASK1(-/-)) exhibited significantly less inflammation and lung injury 
      (as measured by neutrophil infiltration, IL-6, and IL-1beta) in response to 
      treatment with inhaled lipopolysaccharide (LPS) compared with wild-type (WT) 
      mice. To determine whether this proinflammatory response was mediated by ASK1, we 
      investigated inflammasome-mediated responses to LPS in primary macrophages and 
      bone marrow-derived macrophages (BMDMs) from WT and ASK1(-/-) mice, as well as 
      the mouse alveolar macrophage cell line MH-S. Cells were treated with LPS alone 
      for priming or LPS followed by ATP for activation. When macrophages were 
      stimulated with LPS followed by ATP to activate the inflammasome, we found a 
      significant increase in secreted IL-1beta from WT cells compared with ASK1-deficient 
      cells. LPS priming stimulated an increase in NOD-like receptor 3 (NLRP3) and 
      pro-IL-1beta in WT BMDMs, but expression of NLRP3 was significantly decreased in 
      ASK1(-/-) BMDMs. Subsequent ATP treatment stimulated an increase in cleaved 
      caspase-1 and IL-1beta in WT BMDMs compared with ASK1(-/-) BMDMs. Similarly, 
      treatment of MH-S cells with LPS + ATP caused an increase in both cleaved 
      caspase-1 and IL-1beta that was diminished by the ASK-1 inhibitor NQDI1. These 
      results demonstrate, for the first time, that ASK1 promotes inflammasome priming.
FAU - Immanuel, Camille N
AU  - Immanuel CN
AD  - Division of Pediatric Critical Care, Department of Pediatrics, Children's 
      Foundation Research Institute at Le Bonheur Children's Hospital, University of 
      Tennessee Health Sciences , Memphis, Tennessee.
AD  - Department of Physiology, University of Kentucky , Lexington, Kentucky.
FAU - Teng, Bin
AU  - Teng B
AD  - Department of Physiology, University of Tennessee Health Science Center , 
      Memphis, Tennessee.
FAU - Dong, Brittany
AU  - Dong B
AD  - Department of Physiology, University of Kentucky , Lexington, Kentucky.
FAU - Gordon, Elizabeth M
AU  - Gordon EM
AD  - Department of Physiology, University of Kentucky , Lexington, Kentucky.
FAU - Kennedy, Joseph A
AU  - Kennedy JA
AD  - Department of Physiology, University of Tennessee Health Science Center , 
      Memphis, Tennessee.
FAU - Luellen, Charlean
AU  - Luellen C
AD  - Department of Physiology, University of Tennessee Health Science Center , 
      Memphis, Tennessee.
FAU - Schwingshackl, Andreas
AU  - Schwingshackl A
AD  - Department of Pediatrics, Mattel Children's Hospital at the University of 
      California , Los Angeles, California.
FAU - Cormier, Stephania A
AU  - Cormier SA
AD  - Department of Biological Sciences, Louisiana State University , Baton Rouge, 
      Louisiana.
FAU - Fitzpatrick, Elizabeth A
AU  - Fitzpatrick EA
AD  - Department of Microbiology, Immunology, and Biochemistry, University of Tennessee 
      Health Science Center , Memphis, Tennessee.
FAU - Waters, Christopher M
AU  - Waters CM
AD  - Department of Physiology, University of Kentucky , Lexington, Kentucky.
LA  - eng
GR  - K08 HL118118/HL/NHLBI NIH HHS/United States
GR  - R01 AI090059/AI/NIAID NIH HHS/United States
GR  - P42 ES013648/ES/NIEHS NIH HHS/United States
GR  - R01 HL131526/HL/NHLBI NIH HHS/United States
GR  - R01 HL123540/HL/NHLBI NIH HHS/United States
GR  - R01 ES015050/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20190110
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - 0 (Carrier Proteins)
RN  - 0 (Inflammasomes)
RN  - 0 (Lipopolysaccharides)
RN  - EC 2.7.11.25 (MAP Kinase Kinase Kinase 5)
RN  - EC 2.7.11.25 (Map3k5 protein, mouse)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Carrier Proteins/metabolism
MH  - Cell Line
MH  - Inflammasomes/*drug effects/metabolism
MH  - Inflammation/drug therapy/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - MAP Kinase Kinase Kinase 5/drug effects/*metabolism
MH  - Macrophages/*drug effects/metabolism
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Neutrophil Infiltration/drug effects
MH  - Signal Transduction/drug effects
PMC - PMC6459294
OTO - NOTNLM
OT  - LPS priming
OT  - acute respiratory distress syndrome
OT  - apoptosis signal regulating kinase-1
OT  - lung inflammation
COIS- No conflicts of interest, financial or otherwise, are declared by the authors.
EDAT- 2019/01/11 06:00
MHDA- 2019/12/31 06:00
PMCR- 2020/03/01
CRDT- 2019/01/11 06:00
PHST- 2019/01/11 06:00 [pubmed]
PHST- 2019/12/31 06:00 [medline]
PHST- 2019/01/11 06:00 [entrez]
PHST- 2020/03/01 00:00 [pmc-release]
AID - L-00199-2018 [pii]
AID - 10.1152/ajplung.00199.2018 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2019 Mar 1;316(3):L418-L427. doi: 
      10.1152/ajplung.00199.2018. Epub 2019 Jan 10.