Email updates

Keep up to date with the latest news and content from Respiratory Research and BioMed Central.

Open Access Research

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 Liu1, Chi-Yuan Chuang2, Yu-Ting Tai1, Hsiu-Lien Tang3, Tyng-Guey Chen1, Ta-Liang Chen4 and Ruei-Ming Chen456*

Author Affiliations

1 Department of Anesthesiology, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan

2 Division of Pulmonology, Department of Internal Medicine, Ren-Ai Branch, Taipei City Hospital, Taipei, Taiwan

3 Department of Rehabilitation, Po-Jen General Hospital, Taipei, Taiwan

4 Anesthetics and Toxicology Research Center, Taipei Medical University Hospital, Taipei, Taiwan

5 Graduate Institute of Medical Sciences; Center of Excellence for Cancer Research, Taipei Medical University, Taipei, Taiwan

6 Cell Physiology and Molecular Image Research Center, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan

For all author emails, please log on.

Respiratory Research 2012, 13:88  doi:10.1186/1465-9921-13-88

Published: 3 October 2012

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