Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-κB

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Surfactant proteins (SPs) and toll-like receptors (TLRs) contribute to regulation of sepsis-induced acute lung injury. Lipopolysaccharide (LPS) is one of the major causes of septic shock. This study was designed to evaluate the effects of LPS on the regulation of tlr-2 and sp-a gene expression in human alveolar epithelial A549 cells and the possible mechanisms. Exposure of A549 cells to LPS increased the expressions of TLR2 and SP-A mRNA and protein in time-dependent manners. A search using a bioinformatic approach found that there are several nuclear factor kappa-B (NF-κB)-DNA-binding motifs in the promoter region of the tlr2 and sp-a genes. Immunoblotting analyses revealed that exposure to LPS time-dependently enhanced the translocation of NF-κB from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-κB to its consensus oligonucleotides in A549cells. Sequentially, treatment of A549 cells with LPS increased phosphorylation of extracellular signal-regulated kinase (ERK)1/2, p38-mitogen-activated protein kinase (p38MAPK), and MAPK kinase-1 (MEK1). Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.

Original languageEnglish
Pages (from-to)40-47
Number of pages8
JournalCytokine
Volume55
Issue number1
DOIs
Publication statusPublished - Jul 2011

Fingerprint

Pulmonary Surfactant-Associated Protein A
Alveolar Epithelial Cells
Toll-Like Receptor 2
Phosphorylation
NF-kappa B
Lipopolysaccharides
Chemical activation
MAP Kinase Kinase 1
vif Genes
Electrophoretic mobility
Messenger RNA
Nucleotide Motifs
Mitogen-Activated Protein Kinase 3
Acute Lung Injury
Toll-Like Receptors
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase Kinases
Electrophoretic Mobility Shift Assay
p38 Mitogen-Activated Protein Kinases
Bioinformatics

Keywords

  • Acute lung injury
  • Alveolar epithelial cells
  • LPS
  • SP-A
  • TLR2

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology
  • Biochemistry
  • Molecular Biology

Cite this

@article{da7efa2be4934a25953a97166610aac0,
title = "Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-κB",
abstract = "Surfactant proteins (SPs) and toll-like receptors (TLRs) contribute to regulation of sepsis-induced acute lung injury. Lipopolysaccharide (LPS) is one of the major causes of septic shock. This study was designed to evaluate the effects of LPS on the regulation of tlr-2 and sp-a gene expression in human alveolar epithelial A549 cells and the possible mechanisms. Exposure of A549 cells to LPS increased the expressions of TLR2 and SP-A mRNA and protein in time-dependent manners. A search using a bioinformatic approach found that there are several nuclear factor kappa-B (NF-κB)-DNA-binding motifs in the promoter region of the tlr2 and sp-a genes. Immunoblotting analyses revealed that exposure to LPS time-dependently enhanced the translocation of NF-κB from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-κB to its consensus oligonucleotides in A549cells. Sequentially, treatment of A549 cells with LPS increased phosphorylation of extracellular signal-regulated kinase (ERK)1/2, p38-mitogen-activated protein kinase (p38MAPK), and MAPK kinase-1 (MEK1). Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.",
keywords = "Acute lung injury, Alveolar epithelial cells, LPS, SP-A, TLR2",
author = "Wu, {Tsu Tuan} and Ta-Liang Chen and Loon, {Wun Sing} and Yu-Ting Tai and Yih-Giun Cherng and Ruei-Ming Chen",
year = "2011",
month = "7",
doi = "10.1016/j.cyto.2011.03.005",
language = "English",
volume = "55",
pages = "40--47",
journal = "Cytokine",
issn = "1043-4666",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-κB

AU - Wu, Tsu Tuan

AU - Chen, Ta-Liang

AU - Loon, Wun Sing

AU - Tai, Yu-Ting

AU - Cherng, Yih-Giun

AU - Chen, Ruei-Ming

PY - 2011/7

Y1 - 2011/7

N2 - Surfactant proteins (SPs) and toll-like receptors (TLRs) contribute to regulation of sepsis-induced acute lung injury. Lipopolysaccharide (LPS) is one of the major causes of septic shock. This study was designed to evaluate the effects of LPS on the regulation of tlr-2 and sp-a gene expression in human alveolar epithelial A549 cells and the possible mechanisms. Exposure of A549 cells to LPS increased the expressions of TLR2 and SP-A mRNA and protein in time-dependent manners. A search using a bioinformatic approach found that there are several nuclear factor kappa-B (NF-κB)-DNA-binding motifs in the promoter region of the tlr2 and sp-a genes. Immunoblotting analyses revealed that exposure to LPS time-dependently enhanced the translocation of NF-κB from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-κB to its consensus oligonucleotides in A549cells. Sequentially, treatment of A549 cells with LPS increased phosphorylation of extracellular signal-regulated kinase (ERK)1/2, p38-mitogen-activated protein kinase (p38MAPK), and MAPK kinase-1 (MEK1). Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.

AB - Surfactant proteins (SPs) and toll-like receptors (TLRs) contribute to regulation of sepsis-induced acute lung injury. Lipopolysaccharide (LPS) is one of the major causes of septic shock. This study was designed to evaluate the effects of LPS on the regulation of tlr-2 and sp-a gene expression in human alveolar epithelial A549 cells and the possible mechanisms. Exposure of A549 cells to LPS increased the expressions of TLR2 and SP-A mRNA and protein in time-dependent manners. A search using a bioinformatic approach found that there are several nuclear factor kappa-B (NF-κB)-DNA-binding motifs in the promoter region of the tlr2 and sp-a genes. Immunoblotting analyses revealed that exposure to LPS time-dependently enhanced the translocation of NF-κB from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-κB to its consensus oligonucleotides in A549cells. Sequentially, treatment of A549 cells with LPS increased phosphorylation of extracellular signal-regulated kinase (ERK)1/2, p38-mitogen-activated protein kinase (p38MAPK), and MAPK kinase-1 (MEK1). Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.

KW - Acute lung injury

KW - Alveolar epithelial cells

KW - LPS

KW - SP-A

KW - TLR2

UR - http://www.scopus.com/inward/record.url?scp=79956370275&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79956370275&partnerID=8YFLogxK

U2 - 10.1016/j.cyto.2011.03.005

DO - 10.1016/j.cyto.2011.03.005

M3 - Article

VL - 55

SP - 40

EP - 47

JO - Cytokine

JF - Cytokine

SN - 1043-4666

IS - 1

ER -