scholarly journals Triptolide-induced Transrepression of IL-8 NF-kappaB in Lung Epithelial Cells

2001 ◽  
Vol 50 (1) ◽  
pp. 52
Author(s):  
Young Koo Jee ◽  
Yoon Seup Kim ◽  
Se Young Yun ◽  
Yong Ho Kim ◽  
Eun Kyoung Choi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Nf Kappab

Pro-inflammatory cytokine expression through NF-kappaB/IkappaB pathway in lung epithelial cells

2000 ◽  
Vol 49 (3) ◽  
pp. 332 ◽  
Author(s):  
Gye Young Park ◽  
Seung Hee Lee ◽  
Bin Hwangbo ◽  
Jae Joon Yim ◽  
Choon Taek Lee ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Nf Kappab

Legionella pneumophila induced microRNA expression in human lung epithelial cells

Pneumologie ◽  
2010 ◽  
Vol 64 (S 03) ◽  
Author(s):  
B Schmeck ◽  
B Dolniak ◽  
I Pollock ◽  
C Schulz ◽  
W Bertrams ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Legionella Pneumophila ◽  
Human Lung ◽  
Microrna Expression ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

Microscopy study on the interaction of silica nanoparticles with lung epithelial cells

Pneumologie ◽  
2013 ◽  
Vol 67 (12) ◽  
Author(s):  
H Peuschel ◽  
T Ruckelshausen ◽  
C Cavelius ◽  
A Kraegeloh
Keyword(s):  
Epithelial Cells ◽  
Silica Nanoparticles ◽  
Microscopy Study ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

2021 ◽  
Vol 6 (58) ◽  
pp. eabg0833
Author(s):  
Bingyu Yan ◽  
Tilo Freiwald ◽  
Daniel Chauss ◽  
Luopin Wang ◽  
Erin West ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clinical Manifestations ◽  
Lung Epithelial Cells ◽  
Complement Factor ◽  
Respiratory Epithelial Cells ◽  
Signature Genes ◽  
Wide Range ◽  
Lung Epithelial ◽  
Gene Transcripts ◽  
Respiratory Epithelial

Patients with coronavirus disease 2019 (COVID-19) present a wide range of acute clinical manifestations affecting the lungs, liver, kidneys and gut. Angiotensin converting enzyme (ACE) 2, the best-characterized entry receptor for the disease-causing virus SARS-CoV-2, is highly expressed in the aforementioned tissues. However, the pathways that underlie the disease are still poorly understood. Here, we unexpectedly found that the complement system was one of the intracellular pathways most highly induced by SARS-CoV-2 infection in lung epithelial cells. Infection of respiratory epithelial cells with SARS-CoV-2 generated activated complement component C3a and could be blocked by a cell-permeable inhibitor of complement factor B (CFBi), indicating the presence of an inducible cell-intrinsic C3 convertase in respiratory epithelial cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Genes induced by SARS-CoV-2 and the drugs that could normalize these genes both implicated the interferon-JAK1/2-STAT1 signaling system and NF-κB as the main drivers of their expression. Ruxolitinib, a JAK1/2 inhibitor, normalized interferon signature genes and all complement gene transcripts induced by SARS-CoV-2 in lung epithelial cell lines, but did not affect NF-κB-regulated genes. Ruxolitinib, alone or in combination with the antiviral remdesivir, inhibited C3a protein produced by infected cells. Together, we postulate that combination therapy with JAK inhibitors and drugs that normalize NF-κB-signaling could potentially have clinical application for severe COVID-19.

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