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pubmed-article:21474333pubmed:abstractTextSurfactant 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-?B)-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-?B from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-?B 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.lld:pubmed
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pubmed-article:21474333pubmed:authorpubmed-author:ChenTa-LiangT...lld:pubmed
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pubmed-article:21474333pubmed:copyrightInfoCopyright © 2011 Elsevier Ltd. All rights reserved.lld:pubmed
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pubmed-article:21474333pubmed:articleTitleLipopolysaccharide 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-?B.lld:pubmed
pubmed-article:21474333pubmed:affiliationGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.lld:pubmed
pubmed-article:21474333pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21474333pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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