PMID- 26017186
OWN - NLM
STAT- MEDLINE
DCOM- 20160401
LR  - 20150703
IS  - 1091-7691 (Electronic)
IS  - 0895-8378 (Linking)
VI  - 27
IP  - 6
DP  - 2015
TI  - PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate 
      murine lung eosinophilia.
PG  - 287-99
LID - 10.3109/08958378.2015.1045051 [doi]
AB  - PM2.5 can exacerbate asthma. Organic substances adsorbed on PM2.5-rich dust 
      (PM2.5rd) were inactivated by heating at 360  degrees C. To characterize the role of 
      organic substances, the effects of PM2.5rd and heated PM2.5-rich dust (H-PM2.5 
      rd) on allergic lung inflammation were investigated. BALB/c mice were 
      intratracheally administered PM2.5rd or H-PM2.5rd with or without ovalbumin (OVA) 
      four times at 2-week intervals. PM2.5rd, but not H-PM2.5rd, caused neutrophilic 
      alveolitis and bronchitis. In the presence of OVA, PM2.5rd caused severe 
      eosinophil infiltration and goblet cells proliferation in airways, along with a 
      marked induction of the Th2 cytokines interleukin (IL)-4 and IL-13, and the 
      eosinophil-related cytokine IL-5 in bronchoalveolar lavage fluid (BALF). 
      OVA + H-PM2.5rd caused a weaker response. PM2.5rd showed adjuvant effects on 
      OVA-specific immunoglobulin E (IgE) and IgG1 production, but H-PM2.5rd showed 
      minimal effects. These findings suggested that PM2.5rd-bound substances might 
      aggravate lung eosinophilia. To clarify the roles of TLR2, TLR4, and MyD88 on 
      cytokine production in PM2.5rd, murine bone marrow-derived macrophages (BMDMs) 
      from wild-type (WT), TLR2(-/-), TLR4(-/-), and MyD88(-/-) BALB/c mice were 
      stimulated with dust. Cytokine production was low or undetectable in TLR4(-/-) 
      cells, but occurred from TLR2(-/-) cells, and production by MyD88(-/-) cells was 
      higher than by TLR4(-/-) cells. These results suggest that TLR4 and TLR2 ligands 
      (LPS and beta-glucan, respectively) mainly contributed to cytokines production 
      induced by PM2.5rd. In addition to chemical substances, PM2.5-bound microbial 
      substances might act in inflammatory and allergic lung diseases.
FAU - He, Miao
AU  - He M
AD  - Environment and Non-communicable Disease Research Center, School of Public 
      Health, China Medical University , Shenyang , China .
FAU - Ichinose, Takamichi
AU  - Ichinose T
FAU - Ren, Yahao
AU  - Ren Y
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 - 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 - 20150528
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 0 (Air Pollutants)
RN  - 0 (Dust)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Particulate Matter)
SB  - IM
MH  - Air Pollutants/*toxicity
MH  - Animals
MH  - *Dust
MH  - Inflammation Mediators/metabolism
MH  - Japan
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Particulate Matter/*toxicity
MH  - Pulmonary Eosinophilia/*chemically induced/*metabolism/pathology
OTO - NOTNLM
OT  - Asthma
OT  - MyD88 deficient
OT  - PM2.5-rich dust
OT  - TLR deficient
OT  - bone marrow macrophages
OT  - knockout mice
OT  - lung eosinophilia
EDAT- 2015/05/29 06:00
MHDA- 2016/04/02 06:00
CRDT- 2015/05/29 06:00
PHST- 2015/05/29 06:00 [entrez]
PHST- 2015/05/29 06:00 [pubmed]
PHST- 2016/04/02 06:00 [medline]
AID - 10.3109/08958378.2015.1045051 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2015;27(6):287-99. doi: 10.3109/08958378.2015.1045051. Epub 2015 
      May 28.