Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway

Feng Lin Liu, Chi Yuan Chuang, Yu-Ting Tai, Hsiu Lien Tang, Tyng-Guey Chen, Ta-Liang Chen, Ruei-Ming Chen

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Lipoteichoic acid (LTA), a gram-positive bacterial outer membrane component, can cause septic shock. Our previous studies showed that the gram-negative endotoxin, lipopolysaccharide (LPS), could induce surfactant protein-A (SP-A) production in human alveolar epithelial (A549) cells.Objectives: In this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms.Methods: A549 cells were exposed to LTA. Levels of SP-A, nuclear factor (NF)-κB, extracellular signal-regulated kinase 1/2 (ERK1/2), and mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1 were determined.Results: Exposure of A549 cells to 10, 30, and 50 μg/ml LTA for 24 h did not affect cell viability. Meanwhile, when exposed to 30 μg/ml LTA for 1, 6, and 24 h, the biosynthesis of SP-A mRNA and protein in A549 cells significantly increased. As to the mechanism, LTA enhanced cytosolic and nuclear NF-κB levels in time-dependent manners. Pretreatment with BAY 11-7082, an inhibitor of NF-κB activation, significantly inhibited LTA-induced SP-A mRNA expression. Sequentially, LTA time-dependently augmented phosphorylation of ERK1/2. In addition, levels of phosphorylated MEK1 were augmented following treatment with LTA.Conclusions: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway.

Original languageEnglish
Article number88
JournalRespiratory Research
Volume13
DOIs
Publication statusPublished - Oct 3 2012

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Pulmonary Surfactant-Associated Protein A
Alveolar Epithelial Cells
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Protein Biosynthesis
MAP Kinase Kinase Kinase 1
lipoteichoic acid
Messenger RNA
Extracellular Signal-Regulated MAP Kinases
Septic Shock
Mitogens
Endotoxins
Lipopolysaccharides
Cell Survival
Phosphorylation

Keywords

  • Alveolar epithelial cells
  • Lipoteichoic acid
  • MEK/ERK/NF-κB
  • Surfactant protein-A

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway. / Liu, Feng Lin; Chuang, Chi Yuan; Tai, Yu-Ting; Tang, Hsiu Lien; Chen, Tyng-Guey; Chen, Ta-Liang; Chen, Ruei-Ming.

In: Respiratory Research, Vol. 13, 88, 03.10.2012.

Research output: Contribution to journalArticle

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title = "Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway",
abstract = "Background: Lipoteichoic acid (LTA), a gram-positive bacterial outer membrane component, can cause septic shock. Our previous studies showed that the gram-negative endotoxin, lipopolysaccharide (LPS), could induce surfactant protein-A (SP-A) production in human alveolar epithelial (A549) cells.Objectives: In this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms.Methods: A549 cells were exposed to LTA. Levels of SP-A, nuclear factor (NF)-κB, extracellular signal-regulated kinase 1/2 (ERK1/2), and mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1 were determined.Results: Exposure of A549 cells to 10, 30, and 50 μg/ml LTA for 24 h did not affect cell viability. Meanwhile, when exposed to 30 μg/ml LTA for 1, 6, and 24 h, the biosynthesis of SP-A mRNA and protein in A549 cells significantly increased. As to the mechanism, LTA enhanced cytosolic and nuclear NF-κB levels in time-dependent manners. Pretreatment with BAY 11-7082, an inhibitor of NF-κB activation, significantly inhibited LTA-induced SP-A mRNA expression. Sequentially, LTA time-dependently augmented phosphorylation of ERK1/2. In addition, levels of phosphorylated MEK1 were augmented following treatment with LTA.Conclusions: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway.",
keywords = "Alveolar epithelial cells, Lipoteichoic acid, MEK/ERK/NF-κB, Surfactant protein-A",
author = "Liu, {Feng Lin} and Chuang, {Chi Yuan} and Yu-Ting Tai and Tang, {Hsiu Lien} and Tyng-Guey Chen and Ta-Liang Chen and Ruei-Ming Chen",
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doi = "10.1186/1465-9921-13-88",
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T1 - Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway

AU - Liu, Feng Lin

AU - Chuang, Chi Yuan

AU - Tai, Yu-Ting

AU - Tang, Hsiu Lien

AU - Chen, Tyng-Guey

AU - Chen, Ta-Liang

AU - Chen, Ruei-Ming

PY - 2012/10/3

Y1 - 2012/10/3

N2 - Background: Lipoteichoic acid (LTA), a gram-positive bacterial outer membrane component, can cause septic shock. Our previous studies showed that the gram-negative endotoxin, lipopolysaccharide (LPS), could induce surfactant protein-A (SP-A) production in human alveolar epithelial (A549) cells.Objectives: In this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms.Methods: A549 cells were exposed to LTA. Levels of SP-A, nuclear factor (NF)-κB, extracellular signal-regulated kinase 1/2 (ERK1/2), and mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1 were determined.Results: Exposure of A549 cells to 10, 30, and 50 μg/ml LTA for 24 h did not affect cell viability. Meanwhile, when exposed to 30 μg/ml LTA for 1, 6, and 24 h, the biosynthesis of SP-A mRNA and protein in A549 cells significantly increased. As to the mechanism, LTA enhanced cytosolic and nuclear NF-κB levels in time-dependent manners. Pretreatment with BAY 11-7082, an inhibitor of NF-κB activation, significantly inhibited LTA-induced SP-A mRNA expression. Sequentially, LTA time-dependently augmented phosphorylation of ERK1/2. In addition, levels of phosphorylated MEK1 were augmented following treatment with LTA.Conclusions: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway.

AB - Background: Lipoteichoic acid (LTA), a gram-positive bacterial outer membrane component, can cause septic shock. Our previous studies showed that the gram-negative endotoxin, lipopolysaccharide (LPS), could induce surfactant protein-A (SP-A) production in human alveolar epithelial (A549) cells.Objectives: In this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms.Methods: A549 cells were exposed to LTA. Levels of SP-A, nuclear factor (NF)-κB, extracellular signal-regulated kinase 1/2 (ERK1/2), and mitogen-activated/extracellular signal-regulated kinase kinase (MEK)1 were determined.Results: Exposure of A549 cells to 10, 30, and 50 μg/ml LTA for 24 h did not affect cell viability. Meanwhile, when exposed to 30 μg/ml LTA for 1, 6, and 24 h, the biosynthesis of SP-A mRNA and protein in A549 cells significantly increased. As to the mechanism, LTA enhanced cytosolic and nuclear NF-κB levels in time-dependent manners. Pretreatment with BAY 11-7082, an inhibitor of NF-κB activation, significantly inhibited LTA-induced SP-A mRNA expression. Sequentially, LTA time-dependently augmented phosphorylation of ERK1/2. In addition, levels of phosphorylated MEK1 were augmented following treatment with LTA.Conclusions: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway.

KW - Alveolar epithelial cells

KW - Lipoteichoic acid

KW - MEK/ERK/NF-κB

KW - Surfactant protein-A

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