PMID- 22003094
OWN - NLM
STAT- MEDLINE
DCOM- 20120222
LR  - 20211203
IS  - 1522-1504 (Electronic)
IS  - 1040-0605 (Linking)
VI  - 302
IP  - 1
DP  - 2012 Jan 1
TI  - Glutamine modulates lipopolysaccharide-induced activation of NF-kappaB via the 
      Akt/mTOR pathway in lung epithelial cells.
PG  - L174-83
LID - 10.1152/ajplung.00066.2011 [doi]
AB  - Lung epithelial cells are important barriers in the respiratory system that 
      provoke inflammatory responses through nuclear factor (NF)-kappaB activation to 
      prevent pathogens from invading the body. Lipopolysaccharide (LPS) is a common 
      pathogen-associated stimulus that activates IkappaB kinase (IKK) to regulate 
      NF-kappaB-mediated inflammation through modulating nuclear translocation and 
      phosphorylation of NF-kappaB. Previously, it was shown that Akt and the mammalian 
      target of rapamycin (mTOR) are involved in the phosphorylation of IKK to activate 
      NF-kappaB. Herein, we demonstrate that glutamine (GLN) modulated LPS-induced 
      activation of NF-kappaB through the Akt/mTOR/IKK pathway in BEAS-2B cells. BEAS-2B 
      cells in submerged culture were placed in medium containing different 
      concentrations of GLN (0, 0.5, 1, and 2.5 mM) with 1 mug/ml LPS. Results showed 
      that GLN deprivation induced phosphorylation of Akt/mTOR/IKK signaling, increased 
      levels of NF-kappaB nuclear translocation and phosphorylated NF-kappaB, and upregulated 
      NF-kappaB-dependent transcriptional activity, which was suppressed by GLN 
      administration. Expressions of NF-kappaB-targeted genes were also reduced by 
      supplemental GLN. GLN administration improved cell viability, whereas 0.5 mM GLN 
      had a greater extent of inhibition on the Akt/mTOR/IKK/NF-kappaB signaling cascade. 
      The inhibitory effects of GLN on NF-kappaB activation were also observed in cells 
      cultured under air-liquid interface condition. These results indicate that GLN 
      deprivation increased LPS-induced NF-kappaB activation and transcriptional activity, 
      which was reversed by GLN administration. The findings provide potential 
      mechanisms of GLN's modulation of LPS-induced NF-kappaB activation in lung epithelial 
      cells and imply that maintaining a physiological concentration of GLN is 
      essential in preventing LPS-induced lung inflammation.
FAU - Hou, Yu-Chen
AU  - Hou YC
AD  - School of Nutrition and Health Sciences, Taipei Medical University, Taipei, 
      Taiwan.
FAU - Chiu, Wan-Chun
AU  - Chiu WC
FAU - Yeh, Chiu-Li
AU  - Yeh CL
FAU - Yeh, Sung-Ling
AU  - Yeh SL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111014
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 (NF-kappa B)
RN  - 0RH81L854J (Glutamine)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Epithelial Cells/metabolism
MH  - *Glutamine/administration & dosage/deficiency
MH  - Humans
MH  - I-kappa B Kinase/metabolism
MH  - Lipopolysaccharides/*administration & dosage
MH  - Lung/cytology/metabolism
MH  - Mice
MH  - *NF-kappa B/antagonists & inhibitors/metabolism
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction/drug effects/immunology
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Trachea/cytology/metabolism
EDAT- 2011/10/18 06:00
MHDA- 2012/02/23 06:00
CRDT- 2011/10/18 06:00
PHST- 2011/10/18 06:00 [entrez]
PHST- 2011/10/18 06:00 [pubmed]
PHST- 2012/02/23 06:00 [medline]
AID - ajplung.00066.2011 [pii]
AID - 10.1152/ajplung.00066.2011 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2012 Jan 1;302(1):L174-83. doi: 
      10.1152/ajplung.00066.2011. Epub 2011 Oct 14.