Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway.
Respir Res
; 13: 88, 2012 Oct 03.
Article
em En
| MEDLINE
| ID: mdl-23031213
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.
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Base de dados:
MEDLINE
Assunto principal:
Ácidos Teicoicos
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Lipopolissacarídeos
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NF-kappa B
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Proteína Quinase 1 Ativada por Mitógeno
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Proteína A Associada a Surfactante Pulmonar
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Proteína Quinase 3 Ativada por Mitógeno
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Células Epiteliais Alveolares
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article