PMID- 26882889
OWN - NLM
STAT- MEDLINE
DCOM- 20160728
LR  - 20160314
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 296
DP  - 2016 Apr 1
TI  - Desert dust induces TLR signaling to trigger Th2-dominant lung allergic 
      inflammation via a MyD88-dependent signaling pathway.
PG  - 61-72
LID - S0041-008X(16)30033-3 [pii]
LID - 10.1016/j.taap.2016.02.011 [doi]
AB  - Asian sand dust (ASD) is known to exacerbate asthma, although its mechanism is 
      not yet well understood. In this study, when the effects on inflammatory response 
      by LPS present in ASD was investigated by measuring the gene expression of 
      cytokines and chemokines in RAW264.7 cells treated with ASD and/or polymyxin B 
      (PMB), the ASD effects were attenuated by PMB, but not completely. When an in 
      vitro study was performed using bone marrow-derived macrophages (BMDMs) from WT, 
      TLR2(-/-), TLR4(-/-), and MyD88(-/-) BALB/c mice and BMDMs from WT, TLR2(-/-), 
      TLR4(-/-), TLR2/4(-/-), TLR7/9(-/-), and MyD88(-/-) C57BL/6J mice, cytokine 
      (IL-6, IL-12) production in BMDMs was higher in ASD-stimulated TLR2(-/-) cells 
      than in TLR4(-/-) cells, whereas it was lower or undetectable in TLR2/4(-/-) and 
      MyD88(-/-) cells. These results suggest that ASD causes cytokine production 
      predominantly in a TLR4/MyD88-dependent pathway. When WT and TLRs 2(-/-), 4(-/-), 
      and MyD88(-/-) BALB/c mice were intratracheally challenged with OVA and/or ASD, 
      ASD caused exacerbation of lung eosinophilia along with Th2 cytokine and 
      eosinophil-relevant chemokine production. Serum OVA-specific IgE and IgG1 similar 
      to WT was observed in TLRs 2(-/-), 4(-/-) mice, but not in MyD88(-/-) mice. The 
      Th2 responses in TLR2(-/-) mice were attenuated remarkably by PMB. These results 
      indicate that ASD exacerbates lung eosinophilia in a MyD88-dependent pathway. 
      TLRs 2 and 4 signaling may be important in the increase in lung eosinophilia. 
      Also, the TLR4 ligand LPS and TLR2 ligand like beta-glucan may be strong candidates 
      for exacerbation of lung eosinophilia.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - He, Miao
AU  - He M
AD  - Environment and Non-communicable Disease Research Center, School of Public 
      Health, China Medical University, Shenyang 110122, China. Electronic address: 
      hemiao@mail.cmu.edu.cn.
FAU - Ichinose, Takamichi
AU  - Ichinose T
AD  - Department of Health Sciences, Oita University of Nursing and Health Sciences, 
      Oita 870-1201, Japan. Electronic address: ichinose@oita-nhs.ac.jp.
FAU - Song, Yuan
AU  - Song Y
AD  - Department of Immunology and Parasitology, School of Medicine, University of 
      Occupational and Environmental Health, Fukuoka 807-8555, Japan.
FAU - Yoshida, Yasuhiro
AU  - Yoshida Y
AD  - Department of Immunology and Parasitology, School of Medicine, University of 
      Occupational and Environmental Health, Fukuoka 807-8555, Japan.
FAU - Bekki, Kanae
AU  - Bekki K
AD  - Department of Environmental Health, National Institute of Public Health, Saitama 
      351-0197, Japan.
FAU - Arashidani, Keiichi
AU  - Arashidani K
AD  - Department of Immunology and Parasitology, School of Medicine, University of 
      Occupational and Environmental Health, Fukuoka 807-8555, Japan.
FAU - Yoshida, Seiichi
AU  - Yoshida S
AD  - Department of Health Sciences, Oita University of Nursing and Health Sciences, 
      Oita 870-1201, Japan.
FAU - Nishikawa, Masataka
AU  - Nishikawa M
AD  - Environmental Chemistry Division, National Institute for Environmental Studies, 
      Ibaraki 305-8506, Japan.
FAU - Takano, Hirohisa
AU  - Takano H
AD  - Environmental Health Division, Department of Environmental Engineering, Graduate 
      School of Engineering, Kyoto University, Kyoto 615-8530, Japan.
FAU - Shibamoto, Takayuki
AU  - Shibamoto T
AD  - Department of Environmental Toxicology, University of California, Davis, CA 
      95616, USA.
FAU - Sun, Guifan
AU  - Sun G
AD  - Environment and Non-communicable Disease Research Center, School of Public 
      Health, China Medical University, Shenyang 110122, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160213
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Dust)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Toll-Like Receptors)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - *Dust
MH  - Inflammation Mediators/immunology/*metabolism
MH  - Lung/immunology/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myeloid Differentiation Factor 88/immunology/*metabolism
MH  - Pulmonary Eosinophilia/chemically induced/immunology/*metabolism
MH  - Signal Transduction/physiology
MH  - Th2 Cells/*metabolism
MH  - Toll-Like Receptors/*deficiency/immunology
OTO - NOTNLM
OT  - Asthma
OT  - Desert dust
OT  - MyD88 deficiency
OT  - TLR deficiency
EDAT- 2016/02/18 06:00
MHDA- 2016/07/29 06:00
CRDT- 2016/02/18 06:00
PHST- 2015/09/22 00:00 [received]
PHST- 2016/01/19 00:00 [revised]
PHST- 2016/02/11 00:00 [accepted]
PHST- 2016/02/18 06:00 [entrez]
PHST- 2016/02/18 06:00 [pubmed]
PHST- 2016/07/29 06:00 [medline]
AID - S0041-008X(16)30033-3 [pii]
AID - 10.1016/j.taap.2016.02.011 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2016 Apr 1;296:61-72. doi: 10.1016/j.taap.2016.02.011. 
      Epub 2016 Feb 13.