scholarly journals Transport of AOPP-Albumin into Human Alveolar Epithelial A549 Cell

2018 ◽  
Vol 21 ◽  
pp. 247-255 ◽  
Author(s):  
Masashi Kawami ◽  
Tadashi Shimonakamura ◽  
Ryoko Yumoto ◽  
Mikihisa Takano
Keyword(s):  
Alveolar Epithelial Cell ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Ros Generation ◽  
Alveolar Epithelial ◽  
Lung Injuries ◽  
Km Value ◽  
Human Alveolar Epithelial Cell ◽  
Fluorescence Spectrometer

Purpose. Alveolar clearance of proteins, such as albumin, plays an essential role in recovery from lung injuries. Albumin is known to be oxidized by reactive oxygen species (ROS), leading to generation of advanced oxidation protein products (AOPP)-albumin in the alveolar lining fluid. In this study, we aimed to characterize the uptake of FITC-labeled AOPP-albumin (FITC-AOPP-albumin) into human alveolar epithelial cell line, A549. Methods. FITC-AOPP-albumin uptake into A549 cells and its effect of ROS generation was evaluated using fluorescence spectrometer and flow cytometry, respectively. Results. FITC-AOPP-albumin was taken up by A549 cells in a time- and temperature-dependent fashion, and showed saturation kinetics with a Km value of 0.37 mg/mL. The uptake of FITC-AOPP-albumin was suppressed by phenylarsine oxide, a clathrin-mediated endocytosis inhibitor, but not by indomethacin and nystatin, caveolae-mediated endocytosis inhibitors, or 5-(N-ethyl-N-isopropyl) amiloride, a macropinocytosis inhibitor. AOPP-albumin induced ROS generation in A549 cells, suggesting that alveolar clearance of AOPP-albumin should be important to prevent further ROS generation. Conclusion. AOPP-albumin is transported into alveolar epithelial cells through clathrin-mediated endocytosis, which may be important to prevent further ROS generation. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

scholarly journals Chemokine Production by a Human Alveolar Epithelial Cell Line in Response to Mycobacterium tuberculosis

1998 ◽  
Vol 66 (3) ◽  
pp. 1121-1126 ◽  
Author(s):  
Yuanguang Lin ◽  
Ming Zhang ◽  
Peter F. Barnes
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Intracellular Growth ◽  
Chemokine Production ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

ABSTRACT To investigate the role of chemokines during the initial local response to Mycobacterium tuberculosis in the human lung, we studied chemokine production by the human alveolar epithelial cell line A549 after infection with M. tuberculosis. M. tuberculosis-infected A549 cells produced mRNAs and protein for monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) but not mRNAs for macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and RANTES. Chemokine production in response to M. tuberculosis was not dependent on production of tumor necrosis factor alpha, IL-1β, or IL-6. Two virulent clinical M. tuberculosis isolates, the virulent laboratory strain H37Rv, and the avirulent strain H37Ra elicited production of comparable concentrations of MCP-1 and IL-8, whereas killed M. tuberculosis and three Mycobacterium avium strains did not. The three virulent M. tuberculosis strains grew more rapidly than the avirulent M. tuberculosisstrain in the alveolar epithelial cell line, and the threeM. avium strains did not grow intracellularly. These findings suggest that intracellular growth is necessary for mycobacteria to elicit production of MCP-1 and IL-8 by alveolar epithelial cells but that virulence and the rate of intracellular growth do not correlate with chemokine production. Alveolar epithelial cells may contribute to the local inflammatory response in human tuberculosis by producing chemokines which attract monocytes, lymphocytes, and polymorphonuclear cells.

scholarly journals Anacardic acid, a histone acetyltransferase inhibitor, modulates LPS-induced IL-8 expression in a human alveolar epithelial cell line A549

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 78 ◽  
Author(s):  
Tetsuo Yasutake ◽  
Hiroo Wada ◽  
Manabu Higaki ◽  
Masuo Nakamura ◽  
Kojiro Honda ◽  
...  
Keyword(s):  
Promoter Region ◽  
Alveolar Epithelial Cell ◽  
A549 Cells ◽  
Anacardic Acid ◽  
Epithelial Cell Line ◽  
Chip Assay ◽  
Histone H4 ◽  
Alveolar Epithelial ◽  
Histone H4 Acetylation ◽  
Human Alveolar Epithelial Cell

Objective and design:The histone acetylation processes, which are believed to play a critical role in the regulation of many inflammatory genes, are reversible and regulated by histone acetyltransferases (HATs), which promote acetylation, and histone deacetylases (HDACs), which promote deacetylation. We studied the effects of lipopolysaccharide (LPS) on histone acetylation and its role in the regulation of interleukin (IL)-8 expression. Material:A human alveolar epithelial cell line A549 was usedinvitro.Methods:Histone H4 acetylation at the IL-8 promoter region was assessed by a chromatin immunoprecipitation (ChIP) assay. The expression and production of IL-8 were evaluated by quantitative polymerase chain reaction and specific immunoassay. Effects of a HDAC inhibitor, trichostatin A (TSA), and a HAT inhibitor, anacardic acid, were assessed. Results:Escherichia coli-derived LPS showed a dose- and time-dependent stimulatory effect on IL-8 protein production and mRNA expression in A549 cellsin vitro. LPS showed a significant stimulatory effect on histone H4 acetylation at the IL-8 promoter region by ChIP assay. Pretreatment with TSA showed a dose-dependent stimulatory effect on IL-8 release from A549 cells as compared to LPS alone. Conversely, pretreatment with anacardic acid inhibited IL-8 production and expression in A549 cells. Conclusion:These data suggest that LPS-mediated proinflammatory responses in the lungs might be modulated via changing chromatin remodeling by HAT inhibition.

scholarly journals Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Minrui Liang ◽  
Jiucun Wang ◽  
Haiyan Chu ◽  
Xiaoxia Zhu ◽  
Hang He ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Pulmonary Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Alveolar Epithelial Cell ◽  
Smooth Muscle Actin ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Epithelial Cell Line ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial

Pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Recent insight has suggested that early injury/inflammation of alveolar epithelial cells could lead to dysregulation of tissue repair driven by multiple cytokines. Although dysregulation of interleukin- (IL-) 22 is involved in various pulmonary pathophysiological processes, the role of IL-22 in fibrotic lung diseases is still unclear and needs to be further addressed. Here we investigated the effect of IL-22 on alveolar epithelial cells in the bleomycin- (BLM-) induced pulmonary fibrosis. BLM-treated mice showed significantly decreased level of IL-22 in the lung. IL-22 producedγδT cells were also decreased significantly both in the tissues of lungs and spleens. Administration of recombinant human IL-22 to alveolar epithelial cell line A549 cells ameliorated epithelial to mesenchymal transition (EMT) and partially reversed the impaired cell viability induced by BLM. Furthermore, blockage of IL-22 deteriorated pulmonary fibrosis, with elevated EMT marker (α-smooth muscle actin (α-SMA)) and overactivated Smad2. Our results indicate that IL-22 may play a protective role in the development of BLM-induced pulmonary fibrosis and may suggest IL-22 as a novel immunotherapy tool in treating pulmonary fibrosis.

Effect of Steroids on the Synthesis of Complement C3 in a Human Alveolar Epithelial Cell Line

1993 ◽  
Vol 19 (5) ◽  
pp. 603-616 ◽  
Author(s):  
Terence L. Zach ◽  
Vicki A. Herrman ◽  
Laura D. Hill ◽  
M. Patricia Leuschen
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Complement C3 ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

scholarly journals Idebenone has preventative and therapeutic effects on pulmonary fibrosis via preferential suppression of fibroblast activity

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Toshifumi Sugizaki ◽  
Ken-ichiro Tanaka ◽  
Teita Asano ◽  
Daisuke Kobayashi ◽  
Yuuki Hino ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Lung Fibroblasts ◽  
Epithelial Cell Line ◽  
Therapeutic Effects ◽  
Synthetic Analogue ◽  
Apoptosis Resistance ◽  
Collagen Production ◽  
Alveolar Epithelial

AbstractAlveolar epithelial injury induced by reactive oxygen species (ROS) and abnormal collagen production by activated fibroblasts (myofibroblasts) is involved in the onset and exacerbation of idiopathic pulmonary fibrosis (IPF). Compared with alveolar epithelial cells, lung fibroblasts, especially myofibroblasts, exhibit an apoptosis-resistance phenotype (apoptosis paradox) that appears to be involved in IPF pathogenesis. Thus, we screened for chemicals eliciting preferential cytotoxicity of LL29 cells (lung fibroblasts from an IPF patient) compared with A549 cells (human lung alveolar epithelial cell line) from medicines already in clinical use. We identified idebenone, a synthetic analogue of coenzyme Q10 (CoQ10, an antioxidant) that has been used clinically as a brain metabolic stimulant. Idebenone induced cell growth inhibition and cell death in LL29 cells at a lower concentration than in A549 cells, a feature that was not observed for other antioxidant molecules (such as CoQ10) and two IPF drugs (pirfenidone and nintedanib). Administration of idebenone prevented bleomycin-induced pulmonary fibrosis and increased pulmonary ROS levels. Importantly, idebenone also improved pulmonary fibrosis and lung function when administered after the development of fibrosis, whereas administration of CoQ10 similarly prevented bleomycin-induced pulmonary fibrosis, but had no effect after its development. Administration of idebenone, but not CoQ10, suppressed bleomycin-induced increases in lung myofibroblasts. In vitro, treatment of LL29 cells with idebenone, but not CoQ10, suppressed TGF-β–induced collagen production. These results suggest that in addition to antioxidant activity, idebenone exerts inhibitory activity on the function of lung fibroblasts, with the former activity being preventative and the latter therapeutic for bleomycin-induced fibrosis. Thus, we propose that idebenone may be more therapeutically beneficial for IPF patients than current treatments.

Sign in / Sign up

Export Citation Format

Share Document