PMID- 31836503
OWN - NLM
STAT- MEDLINE
DCOM- 20200127
LR  - 20200127
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 321
DP  - 2020 Mar 15
TI  - Particulate matters induce acute exacerbation of allergic airway inflammation via 
      the TLR2/NF-kappaB/NLRP3 signaling pathway.
PG  - 146-154
LID - S0378-4274(19)30398-4 [pii]
LID - 10.1016/j.toxlet.2019.12.013 [doi]
AB  - BACKGROUND: Exposure to particulate matters (PMs) can lead to an acute 
      exacerbation of allergic airway diseases, increasing the severity of symptoms and 
      mortality. However, little is known about the underlying molecular mechanism. 
      This study aimed to investigate the effects of PMs on acute exacerbation of 
      allergic airway inflammation and seek potential therapeutic targets. METHODS: 
      Non-allergic control and ovalbumin (OVA)-allergic wide-type (WT) and Toll-like 
      receptor 2 knockout (Tlr2-/-) mice were exposed to 100 mug of PM (diameter 
      5.85 mum) or saline by the oropharyngeal instillation. The responses were examined 
      three days after exposure. In the RAW264.7 macrophage cell line, Tlr2 was knocked 
      down by small-interfering RNA or the NF-kappaB inhibitor JSH-23 was used, and then 
      the cells were stimulated with PMs for 12 h before comparison of the inflammatory 
      responses. RESULTS: PM exposure led to increased inflammatory cell recruitment 
      and airway intensity of PAS + staining in OVA-allergic WT mice, accompanied with 
      an accumulation of inflammatory cells and elevated inflammatory cytokines, such 
      as IL-6 and IL-18, in the bronchoalveolar lavage fluid (BALF). Furthermore, the 
      protein levels of TLR2 and the NLRP3 inflammasome were elevated concomitantly 
      with the airway inflammation post-OVA/PMs challenge. Tlr2 deficiency effectively 
      inhibited the airway inflammation, including pulmonary inflammatory cell 
      recruitment, mucus secretion, serum OVA-specific immunoglobulin E (IgE), and BALF 
      inflammatory cytokine production. Additionally, the P-induced NLRP3 activation in 
      the RAW 264.7 cell line was diminished by the knockdown of Tlr2 or JSH-23 
      treatment in vitro. CONCLUSION: Our results indicated that PMs exacerbate the 
      allergic airway inflammation mediated by the TLR2/ NF-kappaB/NLRP3 signaling pathway. 
      Inhibition of NF-kappaB seems to be a possible treatment.
CI  - Copyright (c) 2019 Elsevier B.V. All rights reserved.
FAU - Dai, Meng-Yuan
AU  - Dai MY
AD  - Department of Respiratory and Critical Care, The First Affiliated Hospital of 
      Anhui Medical University, Hefei, Anhui, China; Department of Geriatric 
      Respiratory and Critical Care, Provincial Key Laboratory of Molecular Medicine 
      for Geriatric Disease, Anhui Geriatric Institute, The First Affiliated Hospital 
      of Anhui Medical University, Hefei, Anhui, China.
FAU - Chen, Fang-Fang
AU  - Chen FF
AD  - Department of Geriatric Respiratory and Critical Care, Provincial Key Laboratory 
      of Molecular Medicine for Geriatric Disease, Anhui Geriatric Institute, The First 
      Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
FAU - Wang, Yong
AU  - Wang Y
AD  - Department of Respiratory and Critical Care, The First Affiliated Hospital of 
      Anhui Medical University, Hefei, Anhui, China.
FAU - Wang, Mu-Zi
AU  - Wang MZ
AD  - Department of Geriatric Respiratory and Critical Care, Provincial Key Laboratory 
      of Molecular Medicine for Geriatric Disease, Anhui Geriatric Institute, The First 
      Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
FAU - Lv, Yun-Xiang
AU  - Lv YX
AD  - Department of Geriatric Respiratory and Critical Care, Provincial Key Laboratory 
      of Molecular Medicine for Geriatric Disease, Anhui Geriatric Institute, The First 
      Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
FAU - Liu, Rong-Yu
AU  - Liu RY
AD  - Department of Respiratory and Critical Care, The First Affiliated Hospital of 
      Anhui Medical University, Hefei, Anhui, China; Department of Geriatric 
      Respiratory and Critical Care, Provincial Key Laboratory of Molecular Medicine 
      for Geriatric Disease, Anhui Geriatric Institute, The First Affiliated Hospital 
      of Anhui Medical University, Hefei, Anhui, China. Electronic address: 
      rongyuliu@163.com.
LA  - eng
PT  - Journal Article
DEP - 20191210
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Allergens)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, mouse)
RN  - 0 (Particulate Matter)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Allergens
MH  - Animals
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Female
MH  - Lung/*drug effects/metabolism
MH  - Macrophages/*drug effects/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NF-kappa B/*metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism
MH  - Ovalbumin
MH  - Particle Size
MH  - Particulate Matter/*toxicity
MH  - RAW 264.7 Cells
MH  - Respiratory Hypersensitivity/*chemically induced/genetics/metabolism
MH  - Signal Transduction
MH  - Toll-Like Receptor 2/deficiency/genetics/*metabolism
OTO - NOTNLM
OT  - Allergic airway disease
OT  - NF-kappaB
OT  - NLRP3 inflammasome
OT  - Particulate matters (PMs)
OT  - Toll like receptor (TLR2)
EDAT- 2019/12/15 06:00
MHDA- 2020/01/28 06:00
CRDT- 2019/12/15 06:00
PHST- 2019/10/15 00:00 [received]
PHST- 2019/12/07 00:00 [revised]
PHST- 2019/12/10 00:00 [accepted]
PHST- 2019/12/15 06:00 [pubmed]
PHST- 2020/01/28 06:00 [medline]
PHST- 2019/12/15 06:00 [entrez]
AID - S0378-4274(19)30398-4 [pii]
AID - 10.1016/j.toxlet.2019.12.013 [doi]
PST - ppublish
SO  - Toxicol Lett. 2020 Mar 15;321:146-154. doi: 10.1016/j.toxlet.2019.12.013. Epub 
      2019 Dec 10.