PMID- 21729627
OWN - NLM
STAT- MEDLINE
DCOM- 20120329
LR  - 20190816
IS  - 1001-0939 (Print)
IS  - 1001-0939 (Linking)
VI  - 34
IP  - 5
DP  - 2011 May
TI  - [Investigation of inflammatory responses of alveolar epithelial cells induced by 
      lipopolysaccharide and mechanism].
PG  - 367-70
AB  - OBJECTIVE: Lipopolysaccharide (LPS) can activate alveolar epithelial cells (AECs) 
      and induce inflammatory injury. Toll-like receptor-4 (TLR-4) is integrally 
      involved in LPS signaling and has a requisite role in the activation of NF-kappaB. 
      NF-kappaB is a key intercellular signaling event that mediates cell inflammatory 
      responses. The aim of the study is to investigate in an in vitro model the 
      inflammatory responses of AECs induced by LPS and the probable mechanism 
      underlined the observed inflammatory responses. So cytokines of ICAM-1, TNF-alpha and 
      IL-8 secreted by LPS-activated AECs were observed. And the initial signal 
      molecule (the expression of TLR-4 mRNA) and the key intracellular steps (the 
      activation of NF-kappaB) were studied in detail. METHODS: The study was performed on 
      A549 cells (Human lung adenocarcinoma cell line). A549 cells were divided into 
      two groups: control, and LPS interference group. Proinflammatory cytokines 
      ICAM-1, TNF-alpha and IL-8 were detected by ELISA or radioimmunological methods. The 
      expression of TLR-4 mRNA was detected by real time PCR. The activation of NF-kappaB 
      was detected by Western blot (proteins of I-kappaBalpha and NF-kappaB p65). RESULTS: Compared 
      with control group, ICAM-1 and TNF-alpha of LPS-stimulated group were significantly 
      higher and peaked after 2h before gradually declining at 6 and 12 h; IL-8 was 
      higher after 2 h, which continued up to 12 h. The expression of TLR-4 mRNA of LPS 
      group was significantly higher and peaked after 2 h and gradually declining at 6 
      and 12 h. Meanwhile, NF-kappaB was activated after 0.5, 2, 6 and 12 h indicated by 
      the significant degradation of IkappaB-alpha and the significant release of NF-kappaB P65 and 
      its subsequent translocation into the nucleus approximately synchronized. 
      CONCLUSION: Taken together, the results demonstrate that LPS can induce AECs 
      inflammatory injury via activating TLR-4 and subsequently activating NF-kappaB.
FAU - Liu, Rui-ji
AU  - Liu RJ
AD  - Department of Respiratory Medicine, the First Hospital of Qinhuangdao, Hebei 
      066000, China.
FAU - Xu, Shu-feng
AU  - Xu SF
FAU - Chen, Liang-an
AU  - Chen LA
FAU - Wang, Ping
AU  - Wang P
FAU - Liang, Zhi-xin
AU  - Liang ZX
FAU - Sun, Ji-ping
AU  - Sun JP
FAU - Li, Ai-min
AU  - Li AM
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhonghua Jie He He Hu Xi Za Zhi
JT  - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal 
      of tuberculosis and respiratory diseases
JID - 8712226
RN  - 0 (CXCL8 protein, human)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Cell Line, Tumor
MH  - Epithelial Cells/*drug effects/*metabolism
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Interleukin-8/metabolism
MH  - Lipopolysaccharides/*adverse effects
MH  - NF-kappa B/*metabolism
MH  - Pulmonary Alveoli/cytology
MH  - Toll-Like Receptor 4/*metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2011/07/07 06:00
MHDA- 2012/03/30 06:00
CRDT- 2011/07/07 06:00
PHST- 2011/07/07 06:00 [entrez]
PHST- 2011/07/07 06:00 [pubmed]
PHST- 2012/03/30 06:00 [medline]
PST - ppublish
SO  - Zhonghua Jie He He Hu Xi Za Zhi. 2011 May;34(5):367-70.