PMID- 28419838
OWN - NLM
STAT- MEDLINE
DCOM- 20170619
LR  - 20171128
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 487
IP  - 2
DP  - 2017 May 27
TI  - Peptidoglycan accelerates granulopoiesis through a TLR2- and MyD88-dependent 
      pathway.
PG  - 419-425
LID - S0006-291X(17)30753-2 [pii]
LID - 10.1016/j.bbrc.2017.04.077 [doi]
AB  - Granulopoiesis is accelerated during Gram-negative bacterial infection through 
      activation of toll-like receptor 4 (TLR4). In this study, we tested whether 
      activation of TLR2 promotes granulopoiesis by using the well-known TLR2 agonist, 
      peptidoglycan (PGN). Neutrophils in bone marrow and spleen, and plasma 
      granulocyte colony-stimulating factor (G-CSF) were increased in mice that had 
      received intraperitoneal PGN administration. Incorporation of BrdU into bone 
      marrow neutrophils increased, demonstrating that PGN accelerated granulopoiesis. 
      Treatment of bone marrow cells (BMCs) with PGN increased neutrophils in vitro and 
      promoted the secretion of G-CSF from Ly-6G(-)Ly-6C(+) monocytes. The accelerated 
      granulopoiesis caused by PGN was not seen in TLR2-deficient and MyD88-deficient 
      BMCs. Additionally, PGN induced G-CSF production in human umbilical vein 
      endothelial cells. These findings demonstrate that PGN promotes the secretion of 
      G-CSF from monocytes and endothelial cells, leading to the acceleration of 
      granulopoiesis. Our results illustrate that bacterial recognition by TLR2 
      facilitates granulopoiesis during Gram-positive bacterial infection.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Takehara, Masaya
AU  - Takehara M
AD  - Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri 
      University, Yamashiro-cho, Tokushima 770-8514, Japan. Electronic address: 
      mtakehara@ph.bunri-u.ac.jp.
FAU - Seike, Soshi
AU  - Seike S
AD  - Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri 
      University, Yamashiro-cho, Tokushima 770-8514, Japan.
FAU - Takagishi, Teruhisa
AU  - Takagishi T
AD  - Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri 
      University, Yamashiro-cho, Tokushima 770-8514, Japan.
FAU - Kobayashi, Keiko
AU  - Kobayashi K
AD  - Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri 
      University, Yamashiro-cho, Tokushima 770-8514, Japan.
FAU - Nagahama, Masahiro
AU  - Nagahama M
AD  - Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri 
      University, Yamashiro-cho, Tokushima 770-8514, Japan. Electronic address: 
      nagahama@ph.bunri-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170415
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Peptidoglycan)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Granulocytes/drug effects/*physiology
MH  - Hematopoiesis/drug effects/*physiology
MH  - Mice
MH  - Myeloid Differentiation Factor 88/*metabolism
MH  - Peptidoglycan/*pharmacology
MH  - Signal Transduction/drug effects/physiology
MH  - Toll-Like Receptor 2/*metabolism
OTO - NOTNLM
OT  - Colony-stimulating factor
OT  - Granulopoiesis
OT  - Peptidoglycan
OT  - Toll-like receptors
EDAT- 2017/04/19 06:00
MHDA- 2017/06/20 06:00
CRDT- 2017/04/19 06:00
PHST- 2017/04/10 00:00 [received]
PHST- 2017/04/14 00:00 [accepted]
PHST- 2017/04/19 06:00 [pubmed]
PHST- 2017/06/20 06:00 [medline]
PHST- 2017/04/19 06:00 [entrez]
AID - S0006-291X(17)30753-2 [pii]
AID - 10.1016/j.bbrc.2017.04.077 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2017 May 27;487(2):419-425. doi: 
      10.1016/j.bbrc.2017.04.077. Epub 2017 Apr 15.