scholarly journals Proteinase-Activated Receptor-2–Triggered Prostaglandin E2 Release, but Not Cyclooxygenase-2 Upregulation, Requires Activation of the Phosphatidylinositol 3–Kinase / Akt / Nuclear Factor-κB Pathway in Human Alveolar Epithelial Cells

2009 ◽  
Vol 111 (3) ◽  
pp. 269-275 ◽  
Author(s):  
Kazumi Moriyuki ◽  
Fumiko Sekiguchi ◽  
Kaori Matsubara ◽  
Hiroyuki Nishikawa ◽  
Atsufumi Kawabata
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Nuclear Factor Κb ◽  
Cyclooxygenase 2 ◽  
Alveolar Epithelial Cells ◽  
Nuclear Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cells ◽  
Phosphatidylinositol 3

scholarly journals Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Weijing Wu ◽  
Li Li ◽  
Xiaoshan Su ◽  
Zhixing Zhu ◽  
Xiaoping Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Nuclear Factor ◽  
Alveolar Epithelial ◽  
Tnf Α ◽  
Potential Regulatory Role ◽  
Human Alveolar Epithelial Cells

Abstract Objective Acute lung injury (ALI) is characterized by inflammation and oxidative stress. Nuclear factor-kappaB (NF-κB) mediates the expression of various inflammation-related genes, including the NADPH oxidase family. This study aimed to identify the potential regulatory role of NF-κB on NADPH oxidases in tumor necrosis factor-α (TNF-α)-induced oxidative stress in human alveolar epithelial cells. Methods A549 cells were treated with TNF-α for 24 h to establish ALI cell models. RT-PCR, western blot, assessment of oxidative stress, Alibaba 2.1 online analysis, electrophoretic mobility shift assays and luciferase reporter analysis were employed to identify the potential regulatory role of NF-κB on NADPH oxidases in TNF-α-induced oxidative stress in human alveolar epithelial cells. Results The expression of NF-κB/p65 was notably upregulated in TNF-α-stimulated A549 cells. NF-κB knockdown by siRNA significantly inhibited the TNF-α-induced oxidative stress. Moreover, NF-κB/p65 siRNA could inhibit the activation of NOX1, NOX2 and NOX4 mRNA and protein expression in TNF-α-stimulated A549 cells. The next study demonstrated that NF-κB activated the transcription of NOX1 by binding to the -261 to -252 bp (NOX1/κB2, TAAAAATCCC) region of NOX1 promoter in TNF-α-stimulated A549 cells. Conclusion Our data demonstrated that NF-κB can aggravate TNF-α-induced ALI by regulating the oxidative stress response and the expression of NOX1, NOX2 and NOX4. Moreover, NF-κB could promote the NOX1 transcriptional activity via binding its promoter in TNF-α-stimulated A549 cells.

Mediator generation and signaling events in alveolar epithelial cells attacked byS. aureusα-toxin

2002 ◽  
Vol 282 (2) ◽  
pp. L207-L214 ◽  
Author(s):  
Frank Rose ◽  
Gabriele Dahlem ◽  
Bernd Guthmann ◽  
Friedrich Grimminger ◽  
Ulrich Maus ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Alveolar Epithelial Cells ◽  
Target Cells ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Alveolar Epithelial ◽  
Kinase C

Staphylococcus aureus α-toxin is a pore-forming bacterial exotoxin that has been implicated as a significant virulence factor in human staphylococcal diseases. In primary cultures of rat pneumocyte type II cells and the human A549 alveolar epithelial cell line, purified α-toxin provoked rapid-onset phosphatidylinositol (PtdIns) hydrolysis as well as liberation of nitric oxide and the prostanoids PGE2, PGI2, and thromboxane A2. In addition, sustained upregulation of proinflammatory interleukin (IL)-8 mRNA expression and protein secretion occurred. “Priming” with low-dose IL-1β markedly enhanced the IL-8 response to α-toxin, which was then accompanied by IL-6 appearance. The cytokine response was blocked by the intracellular Ca2+-chelating reagent 1,2-bis(2-aminophenoxy)-ethane- N,N,N′ ,N′-tetraacetic acid, the protein kinase C inhibitor bis-indolyl maleimide I, as well as two independent inhibitors of nuclear factor-κB activation, pyrrolidine dithiocarbamate and caffeic acid phenethyl ester. We conclude that alveolar epithelial cells are highly reactive target cells of staphylococcal α-toxin. α-Toxin pore-associated transmembrane Ca2+flux and PtdIns hydrolysis-related signaling with downstream activation of protein kinase C and nuclear translocation of nuclear factor-κB are suggested to represent important underlying mechanisms. Such reactivity of the alveolar epithelial cells may be relevant for pathogenic sequelae in staphylococcal lung disease.

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Lipids ◽  
2019 ◽  
Vol 54 (1) ◽  
pp. 53-65 ◽  
Author(s):  
Konstantin Mayer ◽  
Natascha Sommer ◽  
Karl Hache ◽  
Andreas Hecker ◽  
Sylvia Reiche ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mitochondrial Function ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Severe Inflammation ◽  
Human Alveolar Epithelial Cells
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