Molecular mechanisms of lipopolysaccharide-caused induction of surfactant protein-A gene expression in human alveolar epithelial A549 cells

Chuang, Chi Yuan; Chen, Ta-Liang; Chen, Ruei Ming

doi:10.1016/j.toxlet.2009.08.015

Cited by 23 publications

(22 citation statements)

References 33 publications

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“…Protein levels were immunodetected according to a previously described method [11]. After drug treatment, cell lysates were prepared in ice-cold radioimmunoprecipitation assay buffer (25 mM Tris–HCl (pH 7.2), 0.1% sodium dodecylsulfate (SDS), 1% Triton X-100, 1% sodium deoxycholate, 0.15 M NaCl, and 1 mM EDTA).…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2012

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BackgroundLipoteichoic 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.ObjectivesIn this study, we further evaluated the effect of LTA on SP-A biosynthesis and its possible signal-transducing mechanisms.MethodsA549 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.ResultsExposure 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.ConclusionsTherefore, 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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Section: Methodsmentioning

confidence: 99%

“…Thus, altering lung SP-A levels can be an effective indicator for pulmonary infection and inflammation. Our previous study showed that LPS selectively induced sp a gene expression in human alveolar epithelial A549 cells [11]. …”

Section: Introductionmentioning

confidence: 99%

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

et al. 2012

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“…In vitro studies and experimental models mostly using SP-A knockout mice have concluded that SP-A, which belongs to the collectin family of proteins, is protective against allergens, viral and bacterial infections and is involved in the maintenance of normal lung architecture [13][14][15][16][17]. SP-A is inducible by cytokines, lipopolysaccharide and drugs with anti-inflammatory properties, including corticosteroids, and possibly cigarette smoke, though there are some conflicting reports [18][19][20][21][22]. The abovementioned variability combined with different ethnic backgrounds and possible polymorphisms in the SP-A genes may explain some of the inconsistent findings.…”

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confidence: 99%

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

Mazur¹,

Toljamo²,

Ohlmeier³

et al. 2011

Eur Respir J

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Serum surfactant protein (SP)-A has been postulated to associate with pulmonary fibrosis, but its role in cigarette smoking-related lung diseases is undefined.SP-A levels in plasma and induced sputum in nonsmokers, smokers with respiratory symptoms (cough and/or phlegm) and symptom-free smokers were assessed using a validated EIA method. A total of 474 current smokers without any diseases or medications were enrolled and followed for 2 yrs with 111 of them succeeding in stopping.Plasma SP-A level was detectable in all subjects and elevated in smokers independently of the symptoms compared to nonsmokers (p50.001). After 2 yrs of follow-up, the SP-A level was higher in those who continued smoking compared to the quitters (p,0.001). Plasma SP-A levels were associated with age, smoking history and lung function. Sputum (n5109) SP-A was nondetectable in most nonsmokers, whereas smoking and symptoms increased sputum SP-A highly significantly (p50.001).In conclusion, SP-A may be involved in pathogenesis of cigarette smoking-related lung diseases. Further studies are needed to elucidate the role of SP-A in chronic obstructive pulmonary disease.

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“…SP-A is involved in various immune functions by mediating a variety of processes, including recognition and opsonization of pathogenic invaders and apoptotic cells, downregulation of inflammation and modulation of the expression of Toll-like receptors (TLRs) (3–5). During acute and chronic lung injury, serum levels of SP-A are markedly increased and SP-A knockout mice experience more severe inflammation with increased levels of pro-inflammatory cytokines (1,6). Although the lung appears to be the primary site of synthesis (7), SP-A protein and mRNA are widely expressed in several extrapulmonary tissues, including the intestine, colon, mucosa and brain tissue (8–10).…”

Section: Introductionmentioning

confidence: 99%

Surfactant protein A is expressed in the central nervous system of rats with experimental autoimmune encephalomyelitis, and suppresses inflammation in human astrocytes and microglia

Yang

Yan

Feng

2017

Molecular Medicine Reports

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The collectin surfactant protein-A (SP-A), a potent host defense molecule, is well recognized for its role in the maintenance of pulmonary homeostasis and the modulation of inflammatory responses. While previous studies have detected SP-A in numerous extrapulmonary tissues, there is still a lack of information regarding its expression in central nervous system (CNS) and potential effects in neuroinflammatory diseases, such as multiple sclerosis (MS). The present study used experimental autoimmune encephalomyelitis (EAE), the most commonly used animal model of MS, to investigate the expression of SP-A in the CNS at different stages of disease progression. In addition, in vitro experiments with lipopolysaccharide (LPS)-stimulated human astrocytes and microglia were performed to investigate the potential role of SP-A in the modulation of CNS inflammatory responses. The results of the present study demonstrated widespread distribution of SP-A in the rat CNS, and also identified specific expression patterns of SP-A at different stages of EAE. In vitro, the current study revealed that treatment of human astrocytes and microglia with LPS promoted SP-A expression in a dose-dependent manner. Furthermore, exogenous SP-A protein significantly decreased Toll-like receptor 4 and nuclear factor-κB expression, and reduced interleukin-1β and tumor necrosis factor-α levels. The results of the current study indicate a potential role for SP-A in the modulation of CNS inflammatory responses.

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Molecular mechanisms of lipopolysaccharide-caused induction of surfactant protein-A gene expression in human alveolar epithelial A549 cells

Cited by 23 publications

References 33 publications

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

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

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

Surfactant protein A is expressed in the central nervous system of rats with experimental autoimmune encephalomyelitis, and suppresses inflammation in human astrocytes and microglia

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