PMID- 28555929
OWN - NLM
STAT- MEDLINE
DCOM- 20180510
LR  - 20220317
IS  - 1099-1263 (Electronic)
IS  - 0260-437X (Linking)
VI  - 37
IP  - 10
DP  - 2017 Oct
TI  - PM2.5-induced lung inflammation in mice: Differences of inflammatory response in 
      macrophages and type II alveolar cells.
PG  - 1203-1218
LID - 10.1002/jat.3482 [doi]
AB  - Particulate matter 2.5 (<PM2.5 mum) leads to chronic obstructive pulmonary 
      disease. In this study, biomarkers related to inflammation and oxidative stress 
      in vitro and in vivo experiments were investigated to clarify the PM2.5-induced 
      lung inflammation mechanisms. In an in vitro study using RAW264.7 cells, PM2.5 
      caused phosphorylation of nuclear factor-kappaB, p38 mitogen-activated protein kinase 
      and extracellular response kinases, an increase of proinflammatory gene and 
      protein expressions (e.g. monocyte chemotactic protein-1, tumor necrosis 
      factor-alpha). These biomarkers were substantially attenuated by polymyxin B (PMB). 
      PM2.5 induced heme oxygenase-1 (HO-1) gene, which was attenuated by 
      N-acetylcysteine (NAC). However, the suppressive effects of NAC on inflammatory 
      biomarkers were very weak. In bone marrow-derived macrophages (BMDMs) of 
      wild-type BALB/c mice, the effects of PMB and NAC on PM2.5-induced inflammatory 
      responses were similar to RAW264.7 cells. In BMDMs of MyD88(-/-) mice, 
      PM2.5-induced proinflammatory mediators were substantially more attenuated. PM2.5 
      caused an increase of proinflammatory gene expressions (interleukin-6, 
      cyclooxygenase 2) and HO-1 gene in MLE-12 cells (mouse alveolar cell line). These 
      biomarkers were substantially attenuated by NAC, but not by PMB. When BALB/c mice 
      were exposed intratracheally to 0.2 mg PM2.5, PM2.5 caused severe lung 
      inflammation, an increase of neutrophils along with proinflammatory mediators in 
      bronchoalveolar lavage fluid. The inflammation was attenuated by NAC, 
      particularly by NAC + PMB, but not by PMB alone. These results indicate that 
      macrophages may act sensitively to lipopolysaccharide (LPS) present in PM2.5 and 
      release proinflammatory mediators via the LPS/MyD88 pathway. However, type II 
      alveolar cells may react sensitively to oxidative stress induced by PM2.5 and 
      cause inflammatory response. Therefore, overall, PM2.5 may cause predominantly 
      oxidative stress-dependent inflammation rather than LPS/MyD88-dependent 
      inflammation in type II alveolar cell-rich lungs. Copyright (c) 2017 John Wiley & 
      Sons, Ltd.
CI  - Copyright (c) 2017 John Wiley & Sons, Ltd.
FAU - He, Miao
AU  - He M
AUID- ORCID: 0000-0002-8427-7693
AD  - Department of Environmental Health, School of Public Health, China Medical 
      University, Shenyang, 110122, China.
AD  - Department of Health Sciences, Oita University of Nursing and Health Sciences, 
      Oita, 870-1201, Japan.
FAU - Ichinose, Takamichi
AU  - Ichinose T
AD  - Department of Health Sciences, Oita University of Nursing and Health Sciences, 
      Oita, 870-1201, Japan.
FAU - Yoshida, Seiichi
AU  - Yoshida S
AD  - Department of Health Sciences, Oita University of Nursing and Health Sciences, 
      Oita, 870-1201, Japan.
FAU - Ito, Tomohiro
AU  - Ito T
AD  - Center for Health and Environmental Risk Research, National Institute for 
      Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan.
FAU - He, Cuiying
AU  - He C
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 - 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 - Takano, Hirohisa
AU  - Takano H
AD  - Environmental Health Division, Department of Environmental Engineering, Graduate 
      School of Engineering, Kyoto University, Kyoto, 615-8530, Japan.
FAU - Sun, Guifan
AU  - Sun G
AD  - Department of Environmental Health, School of Public Health, China Medical 
      University, Shenyang, 110122, China.
FAU - Shibamoto, Takayuki
AU  - Shibamoto T
AD  - Department of Environmental Toxicology, University of California, Davis, CA, 
      95616, USA.
LA  - eng
PT  - Journal Article
DEP - 20170529
PL  - England
TA  - J Appl Toxicol
JT  - Journal of applied toxicology : JAT
JID - 8109495
RN  - 0 (Biomarkers)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Proteins)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Particulate Matter)
RN  - 0 (Polycyclic Aromatic Hydrocarbons)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (interleukin-6, mouse)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 1.14.14.18 (Hmox1 protein, mouse)
RN  - EC 1.14.99.- (Ptgs2 protein, mouse)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - J2VZ07J96K (Polymyxin B)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Alveolar Epithelial Cells/cytology/*drug effects
MH  - Animals
MH  - Biomarkers/*metabolism
MH  - Bronchoalveolar Lavage Fluid
MH  - Chemokine CCL2/genetics/metabolism
MH  - Cyclooxygenase 2/genetics/metabolism
MH  - Heme Oxygenase-1/genetics/metabolism
MH  - Interleukin-6/genetics/metabolism
MH  - Lipopolysaccharides/toxicity
MH  - Lung/cytology/drug effects/metabolism
MH  - Macrophages/cytology/*drug effects
MH  - Male
MH  - Membrane Proteins/genetics/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Myeloid Differentiation Factor 88/genetics/metabolism
MH  - NF-kappa B/genetics/metabolism
MH  - Particle Size
MH  - Particulate Matter/*toxicity
MH  - Pneumonia/blood/chemically induced/*drug therapy
MH  - Polycyclic Aromatic Hydrocarbons/analysis
MH  - Polymyxin B/pharmacology
MH  - RAW 264.7 Cells
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/genetics/metabolism
OTO - NOTNLM
OT  - MLE-12 cells
OT  - MyD88 KO
OT  - PM2.5
OT  - lung inflammation
OT  - macrophages
OT  - oxidative stress
EDAT- 2017/05/31 06:00
MHDA- 2018/05/11 06:00
CRDT- 2017/05/31 06:00
PHST- 2017/01/23 00:00 [received]
PHST- 2017/03/13 00:00 [revised]
PHST- 2017/03/30 00:00 [accepted]
PHST- 2017/05/31 06:00 [pubmed]
PHST- 2018/05/11 06:00 [medline]
PHST- 2017/05/31 06:00 [entrez]
AID - 10.1002/jat.3482 [doi]
PST - ppublish
SO  - J Appl Toxicol. 2017 Oct;37(10):1203-1218. doi: 10.1002/jat.3482. Epub 2017 May 
      29.