PMID- 23896513
OWN - NLM
STAT- MEDLINE
DCOM- 20131210
LR  - 20131021
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 272
IP  - 3
DP  - 2013 Nov 1
TI  - Effects of two Asian sand dusts transported from the dust source regions of Inner 
      Mongolia and northeast China on murine lung eosinophilia.
PG  - 647-55
LID - S0041-008X(13)00313-X [pii]
LID - 10.1016/j.taap.2013.07.010 [doi]
AB  - The quality and quantity of toxic materials adsorbed onto Asian sand dust (ASD) 
      are different based on dust source regions and passage routes. The aggravating 
      effects of two ASDs (ASD1 and ASD2) transported from the source regions of Inner 
      Mongolia and northeast China on lung eosinophilia were compared to clarify the 
      role of toxic materials in ASD. The ASDs contained different amounts of 
      lipopolysaccharides (LPS) and beta-glucan (ASD1<ASD2) and SiO2 (ASD1>ASD2). CD-1 
      mice were instilled intratracheally with ASD1, ASD2 and/or ovalbumin (OVA) four 
      times at 2-week intervals. ASD1 and ASD2 enhanced eosinophil recruitment induced 
      by OVA in the submucosa of the airway, with goblet cell proliferation in the 
      bronchial epithelium. ASD1 and ASD2 synergistically increased OVA-induced 
      eosinophil-relevant cytokines interleukin-5 (IL-5), IL-13 (ASD1<ASD2) and 
      chemokine eotaxin (ASD1>ASD2) in bronchoalveolar lavage fluid. ASD2 aggravating 
      effects on lung eosinophilia were greater than ASD1. The role of LPS and beta-glucan 
      in ASD2 on the production of pro-inflammatory mediators was assessed using in 
      vitro bone marrow-derived macrophages (BMDMs) from wild type, Toll-like receptor 
      2-deficient (TLR2-/-), TLR4-/-, and MyD88-/- mice (on Balb/c background). 
      ASD2-stimulated TLR2-/- BMDMs enhanced IL-6, IL-12, TNF-alpha, MCP-1 and MIP-1alpha 
      secretion compared with ASD2-stimulated TLR4-/- BMDMs. Protein expression from 
      ASD2-stimulated MyD88-/- BMDM were very low or undetectable. The in vitro results 
      indicate that lung eosinophilia caused by ASD is TLR4 dependent. Therefore, the 
      aggravation of OVA-related lung eosinophilia by ASD may be dependent on toxic 
      substances derived from microbes, such as LPS, rather than SiO2.
CI  - (c) 2013. Published by Elsevier Inc. All rights reserved.
FAU - He, Miao
AU  - He M
AD  - Environment and Chronic Non-communicable Disease Research Center, College of 
      Public Health, China Medical University, 11001 Shenyang, China; Department of 
      Health Sciences, Oita University of Nursing and Health Sciences, 870-1201 Oita, 
      Japan. Electronic address: hemiao.cmu@gmail.com.
FAU - Ichinose, Takamichi
AU  - Ichinose T
FAU - Song, Yuan
AU  - Song Y
FAU - Yoshida, Yasuhiro
AU  - Yoshida Y
FAU - Arashidani, Keiichi
AU  - Arashidani K
FAU - Yoshida, Seiichi
AU  - Yoshida S
FAU - Liu, Boying
AU  - Liu B
FAU - Nishikawa, Masataka
AU  - Nishikawa M
FAU - Takano, Hirohisa
AU  - Takano H
FAU - Sun, Guifan
AU  - Sun G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130726
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Dust)
RN  - 7631-86-9 (Silicon Dioxide)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Cells, Cultured
MH  - China
MH  - Dust/*analysis
MH  - Inflammation/chemically induced/epidemiology/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Pulmonary Eosinophilia/*chemically induced/epidemiology/*pathology
MH  - Silicon Dioxide/*toxicity
OTO - NOTNLM
OT  - Asian sand dust
OT  - Bone marrow macrophages
OT  - Cytokines
OT  - Knockout mice
OT  - Lipopolysaccharide
OT  - Lung eosinophilia
EDAT- 2013/07/31 06:00
MHDA- 2013/12/16 06:00
CRDT- 2013/07/31 06:00
PHST- 2013/06/06 00:00 [received]
PHST- 2013/07/08 00:00 [revised]
PHST- 2013/07/16 00:00 [accepted]
PHST- 2013/07/31 06:00 [entrez]
PHST- 2013/07/31 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - S0041-008X(13)00313-X [pii]
AID - 10.1016/j.taap.2013.07.010 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2013 Nov 1;272(3):647-55. doi: 
      10.1016/j.taap.2013.07.010. Epub 2013 Jul 26.