PMID- 21933601
OWN - NLM
STAT- MEDLINE
DCOM- 20120427
LR  - 20110921
IS  - 2542-5641 (Electronic)
IS  - 0366-6999 (Linking)
VI  - 124
IP  - 16
DP  - 2011 Aug
TI  - Perfluorocarbon attenuates lipopolysaccharide-mediated inflammatory responses of 
      alveolar epithelial cells in vitro.
PG  - 2534-9
AB  - BACKGROUND: Toll-like receptor-4 (TLR-4) is integrally involved in 
      lipopolysaccharide (LPS) signaling and has a requisite role in the activation of 
      nuclear factor-kappaB (NF-kappaB). The exact mechanisms that lend perfluorocarbon (PFC) 
      liquids a cytoprotective effect have yet to be elucidated. Therefore we examined 
      in an in vitro model the cytoprotective effect of PFC on LPS-stimulated alveolar 
      epithelial cellls (AECs). METHODS: AECs (A549 cells, human lung adenocarcinoma 
      cell line) were divided into four groups: control, PFC, LPS and LPS + PFC 
      (coculture group) groups. Intercellular adhesion molecule-1 (ICAM-1) was detected 
      by ELISA, tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8) were detected 
      by radioimmunological methods. The expression of TLR-4 mRNA and protein was 
      detected by real time PCR and Western blotting, respectively. The activation of 
      NF-kappaB was detected by Western blotting (proteins of I-kappaBa and NF-kappaB p65). 
      RESULTS: ICAM-1, TNF-alpha and IL-8 were significantly increased in LPS-stimulated 
      AECs groups. The expression of TLR-4 mRNA and protein in LPS-stimulated groups 
      was markedly increased. Meanwhile, NF-kappaB was activated as indicated by the 
      significant degradation of IkappaB-alpha and the significant release of NF-kappaB P65 and its 
      subsequent translocation into the nucleus. There were no significant effects of 
      PFC alone on any of the factors studied while the coculture group showed 
      significant downregulation of the secretion of ICAM-1, TNF-alpha and IL-8, the 
      expression of TLR-4 mRNA and the activity of NF-kappaB. CONCLUSIONS: Taken together, 
      our results demonstrate that LPS can induce AEC-related inflammatory injury via 
      the activation of TLR-4 and subsequent activation of NF-kappaB. PFC is able to 
      protect AECs from LPS-induced inflammatory injury by blocking the initiation of 
      the LPS signaling pathway, which is indicated by the significant decrease of 
      TLR-4 expression and NF-kappaB activation.
FAU - Xu, Shu-Feng
AU  - Xu SF
AD  - Department of Respiratory Medicine, Chinese People's Liberation Army General 
      Hospital, Beijing 100853, China.
FAU - Wang, Ping
AU  - Wang P
FAU - Liu, Rui-Ji
AU  - Liu RJ
FAU - Zhao, Jing
AU  - Zhao J
FAU - Zhang, Xiang-Ning
AU  - Zhang XN
FAU - Fu, Zhan-Zhao
AU  - Fu ZZ
FAU - Gao, Li-Ming
AU  - Gao LM
FAU - Liang, Zhi-Xin
AU  - Liang ZX
FAU - Sun, Ji-Ping
AU  - Sun JP
FAU - Chen, Liang-An
AU  - Chen LA
LA  - eng
PT  - Journal Article
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (Fluorocarbons)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Blotting, Western
MH  - Cell Line, Tumor
MH  - Epithelial Cells/*drug effects/*immunology
MH  - Fluorocarbons/*pharmacology
MH  - Humans
MH  - Inflammation/chemically induced/*immunology
MH  - Intercellular Adhesion Molecule-1/genetics/metabolism
MH  - Interleukin-8/genetics/metabolism
MH  - Lipopolysaccharides/*pharmacology
MH  - NF-kappa B/genetics/metabolism
MH  - Pulmonary Alveoli/*cytology
MH  - Real-Time Polymerase Chain Reaction
MH  - Toll-Like Receptor 4/genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 2011/09/22 06:00
MHDA- 2012/04/28 06:00
CRDT- 2011/09/22 06:00
PHST- 2011/09/22 06:00 [entrez]
PHST- 2011/09/22 06:00 [pubmed]
PHST- 2012/04/28 06:00 [medline]
PST - ppublish
SO  - Chin Med J (Engl). 2011 Aug;124(16):2534-9.