PMID- 34585979
OWN - NLM
STAT- MEDLINE
DCOM- 20211126
LR  - 20221027
IS  - 1522-1504 (Electronic)
IS  - 1040-0605 (Linking)
VI  - 321
IP  - 5
DP  - 2021 Nov 1
TI  - Exposure to carbon black nanoparticles during pregnancy aggravates 
      lipopolysaccharide-induced lung injury in offspring: an intergenerational effect.
PG  - L900-L911
LID - 10.1152/ajplung.00545.2020 [doi]
AB  - Carbon black nanoparticles (CBNPs) are one of the most frequently used 
      nanoparticles. Exposure to CBNPs during pregnancy (PrE to CBNPs) can directly 
      induce inflammation, lung injury, and genotoxicity in dams and results in 
      abnormalities in offspring. However, whether exposure to CBNPs during pregnancy 
      enhances the susceptibility of offspring to environmental stimuli remains 
      unknown. To address this issue, in this study, we intranasally treated pregnant 
      mice with mock or CBNPs from gestational day (GD) 9 to GD18, and F1 and F2 
      offspring were normally obtained. By intratracheal instillation of mice with 
      lipopolysaccharide (LPS) to trigger a classic animal model for acute lung injury, 
      we intriguingly found that after LPS treatment, F1 and F2 offspring after 
      exposure during pregnancy to CBNPs both exhibited more pronounced lung injury 
      symptoms, including more degenerative histopathological changes, vascular 
      leakage, elevated MPO activity, and activation of inflammation-related signaling 
      transduction, compared with F1 and F2 offspring in the mock group, suggesting PrE 
      to CBNPs would aggravate LPS-induced lung injury in offspring, and this effect 
      was intergenerational. We also observed that PrE to CBNPs upregulated the mRNA 
      expression of DNA methyltransferases (Dnmt) 1/3a/3b and DNA hypermethylation in 
      both F1 and F2 offspring, which might partially account for the intergenerational 
      effect. Together, our study demonstrates for the first time that PrE to CBNPs can 
      enhance sensitivity to LPS in both F1 and F2 offspring, and this 
      intergenerational effect may be related to DNA hypermethylation caused by CBNPs.
FAU - Tang, Qianghu
AU  - Tang Q
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Tu, Baijie
AU  - Tu B
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Jiang, Xuejun
AU  - Jiang X
AD  - Center of Experimental Teaching for Public Health, Experimental Teaching and 
      Management Center, Chongqing Medical University, Chongqing, People's Republic of 
      China.
FAU - Zhang, Jun
AU  - Zhang J
AD  - Molecular Biology Laboratory of Respiratory Disease, Institute of Life Sciences, 
      Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Bai, Lulu
AU  - Bai L
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Meng, Pan
AU  - Meng P
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Zhang, Longbin
AU  - Zhang L
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Qin, Xia
AU  - Qin X
AD  - Department of Pharmacy, The First Affiliated Hospital of Chongqing Medical 
      University, Chongqing, People's Republic of China.
FAU - Wang, Bin
AU  - Wang B
AD  - Molecular Biology Laboratory of Respiratory Disease, Institute of Life Sciences, 
      Chongqing Medical University, Chongqing, People's Republic of China.
FAU - Chen, Chengzhi
AU  - Chen C
AD  - Department of Occupational and Environmental Health, School of Public Health and 
      Management, Chongqing Medical University, Chongqing, People's Republic of China.
AD  - Dongsheng Lung-Brain Disease Joint Lab, Chongqing Medical University, Chongqing, 
      People's Republic of China.
FAU - Zou, Zhen
AU  - Zou Z
AUID- ORCID: 0000-0002-1651-591X
AD  - Molecular Biology Laboratory of Respiratory Disease, Institute of Life Sciences, 
      Chongqing Medical University, Chongqing, People's Republic of China.
AD  - Dongsheng Lung-Brain Disease Joint Lab, Chongqing Medical University, Chongqing, 
      People's Republic of China.
LA  - eng
SI  - figshare/10.6084/m9.figshare.15185469.v1
SI  - figshare/10.6084/m9.figshare.15185544.v1
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210929
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - DNA Damage/*drug effects
MH  - Female
MH  - Inflammation/chemically induced/drug therapy
MH  - Lipopolysaccharides/pharmacology
MH  - Lung Injury/*chemically induced
MH  - Male
MH  - Mice
MH  - Nanoparticles/*toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*pathology
MH  - RNA, Messenger/drug effects/metabolism
OTO - NOTNLM
OT  - carbon black nanoparticles
OT  - intergenerational effect
OT  - lipopolysaccharide
OT  - lung injury
EDAT- 2021/09/30 06:00
MHDA- 2021/11/27 06:00
CRDT- 2021/09/29 12:15
PHST- 2021/09/30 06:00 [pubmed]
PHST- 2021/11/27 06:00 [medline]
PHST- 2021/09/29 12:15 [entrez]
AID - 10.1152/ajplung.00545.2020 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2021 Nov 1;321(5):L900-L911. doi: 
      10.1152/ajplung.00545.2020. Epub 2021 Sep 29.