PMID- 30384172
OWN - NLM
STAT- MEDLINE
DCOM- 20190124
LR  - 20190329
IS  - 1090-2414 (Electronic)
IS  - 0147-6513 (Linking)
VI  - 168
DP  - 2019 Jan 30
TI  - Cold stress provokes lung injury in rats co-exposed to fine particulate matter 
      and lipopolysaccharide.
PG  - 9-16
LID - S0147-6513(18)31074-1 [pii]
LID - 10.1016/j.ecoenv.2018.10.064 [doi]
AB  - Cold exposure aggravates respiratory diseases, which are also influenced by the 
      exposures to particulate matter and endotoxin in the air. The aim of this study 
      was to investigate the potential interactions among cold stress, fine particulate 
      matter (PM(2.5), particles with aerodynamic diameter of 2.5 microm or less) and 
      lipopolysaccharide (LPS, pure chemical form of endotoxin) on rat lung and to 
      explore the related possible mechanisms of the interactions. Wistar rats were 
      randomly grouped to be exposed to, 1) normal saline (0.9% NaCl), 2) PM(2.5), 3) 
      LPS, and 4) PM(2.5) and LPS (PM(2.5) + LPS) through intratracheal instillation 
      under cold stress (0  degrees C) and normal temperature (20  degrees C). Lung function, lung 
      tissue histology, inflammatory response and oxidative stress levels were measured 
      to examine the lung injury and to investigate the potential mechanisms. Exposure 
      to PM(2.5) or LPS substantially changed pulmonary function [indicated by peak 
      inspiratory flow (PIF) and peak expiratory flow (PEF)], inflammatory cytokine 
      levels [indicated by interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)] 
      and lung histology, compared to the non-exposed groups. Exposure to PM(2.5) + LPS 
      under cold stress induced the most significant changes, including the increases 
      of IL-6, TNF-alpha and thiobarbituric acid-reactive substances (TBARS), the decreases 
      of PIF and PEF and more severe lung injury, among all exposure scenarios. 
      Glutathione peroxidase activity and, nuclear factor erythroid 2-related factor 2 
      (Nrf2) and heme oxygenase-1 (HO-1) were found to be suppressed under cold stress, 
      whereas Nrf2 and HO-1 levels were observed to be upregulated by exposure to 
      PM(2.5) or LPS under normal temperature. In conclusion, cold stress may aggravate 
      the lung injury in rats induced by simultaneous exposure to PM(2.5) and LPS. The 
      progress may involve the suppressing of Nrf2/HO-1 signal pathway.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Luo, Bin
AU  - Luo B
AD  - Institute of Occupational and Environmental Health, School of Public Health, 
      Lanzhou University, Lanzhou 730000, China; Division of Environmental Health 
      Sciences, School of Public Health, University of California, Berkeley 94720, USA. 
      Electronic address: luob@lzu.edu.cn.
FAU - Shi, Hongxia
AU  - Shi H
AD  - Health Management Center, Lanzhou University the Second Hospital, Lanzhou 730030, 
      China.
FAU - Zhang, Kai
AU  - Zhang K
AD  - Institute of Occupational and Environmental Health, School of Public Health, 
      Lanzhou University, Lanzhou 730000, China.
FAU - Wei, Qiaozhen
AU  - Wei Q
AD  - Institute of Occupational and Environmental Health, School of Public Health, 
      Lanzhou University, Lanzhou 730000, China.
FAU - Niu, Jingping
AU  - Niu J
AD  - Institute of Occupational and Environmental Health, School of Public Health, 
      Lanzhou University, Lanzhou 730000, China.
FAU - Wang, Junling
AU  - Wang J
AD  - Institute of Occupational and Environmental Health, School of Public Health, 
      Lanzhou University, Lanzhou 730000, China.
FAU - Hammond, Sally Katharine
AU  - Hammond SK
AD  - Division of Environmental Health Sciences, School of Public Health, University of 
      California, Berkeley 94720, USA.
FAU - Liu, Sa
AU  - Liu S
AD  - Division of Environmental Health Sciences, School of Public Health, University of 
      California, Berkeley 94720, USA; Environmental & Occupational Health Sciences, 
      School of Health Sciences, Purdue University, West Lafayette 47907, USA. 
      Electronic address: saliu@purdue.edu.
LA  - eng
GR  - T42 OH008429/OH/NIOSH CDC HHS/United States
PT  - Journal Article
DEP - 20181025
PL  - Netherlands
TA  - Ecotoxicol Environ Saf
JT  - Ecotoxicology and environmental safety
JID - 7805381
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Nfe2l2 protein, rat)
RN  - 0 (Particulate Matter)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cold-Shock Response/*physiology
MH  - Cytokines/metabolism
MH  - Lipopolysaccharides/*toxicity
MH  - Lung/pathology
MH  - Lung Injury/*etiology/pathology
MH  - Male
MH  - NF-E2-Related Factor 2/metabolism
MH  - Oxidative Stress/physiology
MH  - Particulate Matter/metabolism/*toxicity
MH  - Random Allocation
MH  - Rats, Wistar
MH  - Signal Transduction/physiology
MH  - Tumor Necrosis Factor-alpha/metabolism
OTO - NOTNLM
OT  - Cold stress
OT  - Fine particulate matter
OT  - Lipopolysaccharide
OT  - Nrf2/HO-1
EDAT- 2018/11/02 06:00
MHDA- 2019/01/25 06:00
CRDT- 2018/11/02 06:00
PHST- 2018/05/29 00:00 [received]
PHST- 2018/10/11 00:00 [revised]
PHST- 2018/10/16 00:00 [accepted]
PHST- 2018/11/02 06:00 [pubmed]
PHST- 2019/01/25 06:00 [medline]
PHST- 2018/11/02 06:00 [entrez]
AID - S0147-6513(18)31074-1 [pii]
AID - 10.1016/j.ecoenv.2018.10.064 [doi]
PST - ppublish
SO  - Ecotoxicol Environ Saf. 2019 Jan 30;168:9-16. doi: 10.1016/j.ecoenv.2018.10.064. 
      Epub 2018 Oct 25.