Glutamine modulates lipopolysaccharide-induced activation of NF-kappa B via the Akt/mTOR pathway in lung epithelial cells

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Title:	Glutamine modulates lipopolysaccharide-induced activation of NF-kappa B via the Akt/mTOR pathway in lung epithelial cells
Authors:	Hou, YC (Hou, Yu-Chen) Chiu, WC (Chiu, Wan-Chun) Yeh, CL (Yeh, Chiu-Li) Yeh, SL (Yeh, Sung-Ling)
Contributors:	Dept Food & Nutr
Keywords:	mammalian target of rapamycin nuclear factor-kappa B BEAS-2B
Date:	2012-01
Issue Date:	2013-02-26 11:20:24 (UTC+8)
Abstract:	Hou YC, Chiu WC, Yeh CL, Yeh SL. Glutamine modulates lipopolysaccharide-induced activation of NF-kappa B via the Akt/mTOR pathway in lung epithelial cells. Am J Physiol Lung Cell Mol Physiol 302: L174 -L183, 2012. First published October 14, 2011; doi: 10.1152/ajplung.00066.2011.-Lung epithelial cells are important barriers in the respiratory system that provoke inflammatory responses through nuclear factor (NF)-kappa B activation to prevent pathogens from invading the body. Lipopolysaccharide (LPS) is a common pathogen-associated stimulus that activates I kappa B kinase (IKK) to regulate NF-kappa B-mediated inflammation through modulating nuclear translocation and phosphorylation of NF-kappa B. Previously, it was shown that Akt and the mammalian target of rapamycin (mTOR) are involved in the phosphorylation of IKK to activate NF-kappa B. Herein, we demonstrate that glutamine (GLN) modulated LPS-induced activation of NF-kappa B 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 kappa g/ml LPS. Results showed that GLN deprivation induced phosphorylation of Akt/mTOR/IKK signaling, increased levels of NF-kappa B nuclear translocation and phosphorylated NF-kappa B, and upregulated NF-kappa B-dependent transcriptional activity, which was suppressed by GLN administration. Expressions of NF-kappa B-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-kappa B signaling cascade. The inhibitory effects of GLN on NF-kappa B activation were also observed in cells cultured under air-liquid interface condition. These results indicate that GLN deprivation increased LPS-induced NF-kappa B activation and transcriptional activity, which was reversed by GLN administration. The findings provide potential mechanisms of GLN's modulation of LPS-induced NF-kappa B activation in lung epithelial cells and imply that maintaining a physiological concentration of GLN is essential in preventing LPS-induced lung inflammation.
Relation:	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 卷: 302 期: 1 頁數: L174-L183
Appears in Collections:	[Department of Food and Nutrition ] journal articles

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