PMID- 28939441
OWN - NLM
STAT- MEDLINE
DCOM- 20180629
LR  - 20201209
IS  - 1618-0607 (Electronic)
IS  - 1438-4221 (Linking)
VI  - 307
IP  - 8
DP  - 2017 Dec
TI  - Caspase-11 deficiency impairs neutrophil recruitment and bacterial clearance in 
      the early stage of pulmonary Klebsiella pneumoniae infection.
PG  - 490-496
LID - S1438-4221(17)30250-3 [pii]
LID - 10.1016/j.ijmm.2017.09.012 [doi]
AB  - Klebsiella pneumoniae (K. pneumoniae) is a gram-negative pathogen, and Klebsiella 
      pneumonia is one of the most common nosocomial infections. Canonical NLRP3 and 
      NLRC4 inflammasome was found involved in innate immune response against K. 
      pneumoniae, but the role of caspase-11 in K. pneumoniae infection remains 
      undefined. It was shown that Caspase-11 knockout blocked K. pneumoniae-induced 
      IL-1alpha and IL-1beta secretion and pyroptosis of bone marrow-derived macrophages 
      (BMDMs). Furthermore, caspase-11(-/-) mice exhibited impaired neutrophil 
      recruitment and bacterial clearance in the early stage of K. pneumoniae 
      infection, accompanied by a reduction in IL-1alpha production. Moreover, IL-1alpha 
      neutralizing antibody pretreatment was found to inhibit neutrophil recruitment 
      and bacterial clearance of wild-type mice. Together, these data suggest that 
      caspase-11/IL-1alpha pathway plays an important role in defending against K. 
      pneumoniae by recruiting neutrophils in the early stage of infection.
CI  - Copyright (c) 2017. Published by Elsevier GmbH.
FAU - Wang, Jian
AU  - Wang J
AD  - Department of Pathogen Biology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Shao, Yue
AU  - Shao Y
AD  - Department of Pathophysiology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Pathophysiology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Li, Shengjun
AU  - Li S
AD  - Department of Immunology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Xin, Na
AU  - Xin N
AD  - Department of Pathophysiology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Xie, Fang
AU  - Xie F
AD  - Department of Pathogen Biology, College of Basic Medical Science, China Medical 
      University, Shenyang, China.
FAU - Zhao, Chenghai
AU  - Zhao C
AD  - Department of Pathophysiology, College of Basic Medical Science, China Medical 
      University, Shenyang, China. Electronic address: zhaochenghai1@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20170912
PL  - Germany
TA  - Int J Med Microbiol
JT  - International journal of medical microbiology : IJMM
JID - 100898849
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Interleukin-1alpha)
RN  - 0 (Interleukin-1beta)
RN  - EC 3.4.22.- (Casp4 protein, mouse)
RN  - EC 3.4.22.- (Caspases)
RN  - EC 3.4.22.- (Caspases, Initiator)
SB  - IM
MH  - Animals
MH  - Caspases/*deficiency
MH  - Caspases, Initiator
MH  - Interleukin-1alpha/*metabolism
MH  - Interleukin-1beta/metabolism
MH  - Klebsiella Infections/*immunology/pathology
MH  - Klebsiella pneumoniae/*immunology
MH  - Macrophages/immunology
MH  - Mice, Knockout
MH  - *Neutrophil Infiltration
MH  - Pneumonia, Bacterial/*immunology/pathology
MH  - Pyroptosis
OTO - NOTNLM
OT  - Caspase-11
OT  - IL-1alpha
OT  - IL-1beta
OT  - Klebsiella pneumoniae
EDAT- 2017/09/25 06:00
MHDA- 2018/06/30 06:00
CRDT- 2017/09/24 06:00
PHST- 2017/05/25 00:00 [received]
PHST- 2017/09/04 00:00 [revised]
PHST- 2017/09/11 00:00 [accepted]
PHST- 2017/09/25 06:00 [pubmed]
PHST- 2018/06/30 06:00 [medline]
PHST- 2017/09/24 06:00 [entrez]
AID - S1438-4221(17)30250-3 [pii]
AID - 10.1016/j.ijmm.2017.09.012 [doi]
PST - ppublish
SO  - Int J Med Microbiol. 2017 Dec;307(8):490-496. doi: 10.1016/j.ijmm.2017.09.012. 
      Epub 2017 Sep 12.