PMID- 20827320
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20110714
LR  - 20211020
IS  - 1940-5901 (Electronic)
IS  - 1940-5901 (Linking)
VI  - 3
IP  - 3
DP  - 2010 Jul 31
TI  - A cellular model to mimic exhaled cigarette smokeinduced lung microvascular 
      endothelial cell injury and death.
PG  - 223-32
AB  - Tobacco smoke exhaled from smokers is a key component of secondhand smoke, 
      contributing to lung alveolar wall destruction seen in chronic lung diseases. 
      Although mainstream and sidestream tobacco smoke are cyto-toxic to lung cells, it 
      is unclear whether exhaled smoke induces lung cell injury or even death. We 
      sought to establish an in vitro model to examine the effects of exhaled smoke on 
      lung cells. Phosphate-buffered saline-conditioned cigarette smoke (CCS) derived 
      from a blow-by system was used to mimic exhaled tobacco smoke exposure. Exposure 
      of medium to CCS leads to dose-dependent increases in nicotine/cotinine levels. 
      Scanning spectrophotometric analysis of the CCS-exposed medium reveals an 
      absorption peak at 290 nm wavelength. The OD values at 290 nm are correlated with 
      nicotine levels in the exposed medium, indicating that a simple measurement of OD 
      at 290 nm can be used to monitor CCS exposure. Tobacco smoke contacts the 
      microvascular endothelium located at lung alveoli, before it enters the blood 
      stream. Hence, human lung microvascular endothelial cells (hMVEC) were exposed to 
      CCS and assessed for cell injury and death. Exposure of hMVEC to CCS equivalent 
      to burning 12-16 cigarettes leads to increased LDH release from the cells into 
      the medium. This suggests that CCS can induce lung cell injury. CCS at a low 
      level increases cell growth, whereas the high level of CCS decreases cell 
      viability. In addition, CCS exposure induces cell detachment and morphological 
      changes. Our results demonstrate that exposure of buffer-conditioned mainstream 
      cigarette smoke leads to increased nicotine/cotinine levels and cell 
      injury/death, which may contribute to the pathophysiology of passive 
      smoking-associated lung diseases.
FAU - Zhang, Jianliang
AU  - Zhang J
FAU - Juedes, Noah
AU  - Juedes N
FAU - Narayan, Vikram M
AU  - Narayan VM
FAU - Yue, Bingfang
AU  - Yue B
FAU - Rockwood, Alan L
AU  - Rockwood AL
FAU - Palma, Nadia L
AU  - Palma NL
FAU - Patel, Jawaharlal M
AU  - Patel JM
LA  - eng
GR  - R01 HL068666/HL/NHLBI NIH HHS/United States
GR  - R01 HL085133/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20100731
PL  - United States
TA  - Int J Clin Exp Med
JT  - International journal of clinical and experimental medicine
JID - 101471010
PMC - PMC2929948
OTO - NOTNLM
OT  - Cellular model
OT  - chronic lung diseases
OT  - lung microvascular endothelial cells
OT  - passive smoking-associated lung diseases
OT  - secondhand smoke
EDAT- 2010/09/10 06:00
MHDA- 2010/09/10 06:01
PMCR- 2010/07/31
CRDT- 2010/09/10 06:00
PHST- 2010/06/26 00:00 [received]
PHST- 2010/07/29 00:00 [accepted]
PHST- 2010/09/10 06:00 [entrez]
PHST- 2010/09/10 06:00 [pubmed]
PHST- 2010/09/10 06:01 [medline]
PHST- 2010/07/31 00:00 [pmc-release]
PST - epublish
SO  - Int J Clin Exp Med. 2010 Jul 31;3(3):223-32.