IFN-γ Induces Mimic Extracellular Trap Cell Death in Lung Epithelial Cells Through Autophagy-Regulated DNA Damage

2016 ◽  
Vol 36 (2) ◽  
pp. 100-112 ◽  
Author(s):  
Chiou-Feng Lin ◽  
Shun-Yi Chien ◽  
Chia-Ling Chen ◽  
Chia-Yuan Hsieh ◽  
Po-Chun Tseng ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Ifn Γ ◽  
Extracellular Trap ◽  
Trap Cell

scholarly journals Oxidative Stress Facilitates IFN-γ-Induced Mimic Extracellular Trap Cell Death in A549 Lung Epithelial Cancer Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0162157 ◽  
Author(s):  
Chiou-Feng Lin ◽  
Chia-Ling Chen ◽  
Shun-Yi Chien ◽  
Po-Chun Tseng ◽  
Yu-Chih Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cancer Cells ◽  
Epithelial Cancer ◽  
Lung Epithelial ◽  
Ifn Γ ◽  
Extracellular Trap ◽  
Trap Cell ◽  
A549 Lung

scholarly journals Host DNA Repair Proteins in Response toPseudomonas aeruginosain Lung Epithelial Cells and in Mice

2010 ◽  
Vol 79 (1) ◽  
pp. 75-87 ◽  
Author(s):  
Min Wu ◽  
Huang Huang ◽  
Weidong Zhang ◽  
Shibichakravarthy Kannan ◽  
Andrew Weaver ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Epithelial Cells ◽  
Critical Role ◽  
Lung Epithelial Cells ◽  
Host Cells ◽  
Myeloperoxidase Activity ◽  
Gram Negative ◽  
Lung Epithelial ◽  
Dna Repair Proteins

ABSTRACTAlthough DNA repair proteins in bacteria are critical for pathogens' genome stability and for subverting the host defense, the role of host DNA repair proteins in response to bacterial infection is poorly defined. Here, we demonstrate, for the first time, that infection with the Gram-negative bacteriumPseudomonas aeruginosasignificantly altered the expression and enzymatic activity of 8-oxoguanine DNA glycosylase (OGG1) in lung epithelial cells. Downregulation of OGG1 by a small interfering RNA strategy resulted in severe DNA damage and cell death. In addition, acetylation of OGG1 is required for host responses to bacterial genotoxicity, as mutations of OGG1 acetylation sites increased Cockayne syndrome group B (CSB) protein expression. These results also indicate that CSB may be involved in DNA repair activity during infection. Furthermore, OGG1 knockout mice exhibited increased lung injury after infection withP. aeruginosa, as demonstrated by higher myeloperoxidase activity and lipid peroxidation. Together, our studies indicate thatP. aeruginosainfection induces significant DNA damage in host cells and that DNA repair proteins play a critical role in the host response toP. aeruginosainfection, serving as promising targets for the treatment of this condition and perhaps more broadly Gram-negative bacterial infections.

Characterization of Nitric Oxide (NO)-Induced Cell Death in Lung Epithelial Cells

2004 ◽  
Vol 56 (2) ◽  
pp. 187
Author(s):  
Wha Shim Yong ◽  
Youn Seup Kim ◽  
Jae Seuk Park ◽  
Young Koo Jee ◽  
Kye Young Lee
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2

2020 ◽  
Author(s):  
Yinfang Wang ◽  
Yingzhe Fan ◽  
Yitong Huang ◽  
Tao Du ◽  
Zongjun Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nk Cells ◽  
Interleukin 2 ◽  
A549 Cells ◽  
Endogenous Retrovirus ◽  
Alveolar Epithelial Cells ◽  
Cell Entry ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Ifn Γ

AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019 (COVID-19), it binds to angiotensin-converting enzyme 2 (ACE2) to enter into human cells. The expression level of ACE2 potentially determine the susceptibility and severity of COVID-19, it is thus of importance to understand the regulatory mechanism of ACE2 expression. Tripartite motif containing 28 (TRIM28) is known to be involved in multiple processes including antiviral restriction, endogenous retrovirus latency and immune response, it is recently reported to be co-expressed with SARS-CoV-2 receptor in type II pneumocytes; however, the roles of TRIM28 in ACE2 expression and SARS-CoV-2 cell entry remain unclear. This study showed that knockdown of TRIM28 induces ACE2 expression and increases pseudotyped SARS-CoV-2 cell entry of A549 cells and primary pulmonary alveolar epithelial cells (PAEpiCs). In a co-culture model of NK cells and lung epithelial cells, our results demonstrated that NK cells inhibit TRIM28 and promote ACE2 expression in lung epithelial cells, which was partially reversed by depletion of interleukin-2 and blocking of granzyme B in the co-culture medium. Furthermore, TRIM28 knockdown enhanced interferon-γ (IFN-γ)-induced ACE2 expression through a mechanism involving upregulating IFN-γ receptor 2 (IFNGR2) in both A549 and PAEpiCs. Importantly, the upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells was partially reversed by dexamethasone in A549 cells but not PAEpiCs. Our study identified TRIM28 as a novel regulator of ACE2 expression and SARS-CoV-2 cell entry.

scholarly journals Cytotoxic Effects of Air Freshener Biocides in Lung Epithelial Cells

2013 ◽  
Vol 8 (9) ◽  
pp. 1934578X1300800
Author(s):  
Jung-Taek Kwon ◽  
Mimi Lee ◽  
Gun-Baek Seo ◽  
Hyun-Mi Kim ◽  
Ilseob Shim ◽  
...  
Keyword(s):  
Dna Damage ◽  
Epithelial Cells ◽  
Cell Viability ◽  
Lung Epithelial Cells ◽  
Ros Generation ◽  
Dependent Manner ◽  
Cytotoxic Effects ◽  
Lung Epithelial ◽  
Dose Dependent ◽  
A549 Lung

This study evaluated the cytotoxicity of mixtures of citral (CTR) and either benzisothiazolinone (BIT, Mix-CTR-BIT) or triclosan (TCS, Mix-CTR-TCS) in human A549 lung epithelial cells. We investigated the effects of various mix ratios of these common air freshener ingredients on cell viability, cell proliferation, reactive oxygen species (ROS) generation, and DNA damage. Mix-CTR-BIT and Mix-CTR-TCS significantly decreased the viability of lung epithelial cells and inhibited cell growth in a dose-dependent manner. In addition, both mixtures increased ROS generation, compared to that observed in control cells. In particular, cell viability, growth, and morphology were affected upon increase in the proportion of BIT or TCS in the mixture. However, comet analysis showed that treatment of cells with Mix-CTR-BIT or Mix-CTR-TCS did not increase DNA damage. Taken together, these data suggested that increasing the content of biocides in air fresheners might induce cytotoxicity, and that screening these compounds using lung epithelial cells may contribute to hazard assessment.

POTENTIATION OF FAS- AND TRAIL-MEDIATED APOPTOSIS BY IFN-γ IN A549 LUNG EPITHELIAL CELLS: ENHANCEMENT OF CASPASE-8 EXPRESSION THROUGH IFN-RESPONSE ELEMENT

Cytokine ◽  
2002 ◽  
Vol 20 (6) ◽  
pp. 283-288 ◽  
Author(s):  
Ki-Bae Kim ◽  
Yun-Hee Choi ◽  
In-Ki Kim ◽  
Chul-Woong Chung ◽  
Byung Ju Kim ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Caspase 8 ◽  
Response Element ◽  
Lung Epithelial ◽  
Ifn Γ ◽  
A549 Lung

Apoptosis and DNA damage induced by silica nanoparticles and formaldehyde in human lung epithelial cells

2020 ◽  
Vol 27 (15) ◽  
pp. 18592-18601 ◽  
Author(s):  
Mehran Nazarparvar-Noshadi ◽  
Jafar Ezzati Nazhad Dolatabadi ◽  
Yahya Rasoulzadeh ◽  
Yousef Mohammadian ◽  
Dariush Shanehbandi
Keyword(s):  
Dna Damage ◽  
Epithelial Cells ◽  
Silica Nanoparticles ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals Inhibition of acute lethal pulmonary inflammation by the IDO–AhR pathway

2017 ◽  
Vol 114 (29) ◽  
pp. E5881-E5890 ◽  
Author(s):  
Soung-Min Lee ◽  
Ha Young Park ◽  
Young-Sill Suh ◽  
Eun Hye Yoon ◽  
Juyang Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Pulmonary Inflammation ◽  
Lung Parenchyma ◽  
Lung Epithelial Cells ◽  
Dependent Manner ◽  
Independent Manner ◽  
Hematopoietic Stem ◽  
Lung Epithelial ◽  
Ifn Γ

The lung is a prototypic organ that was evolved to reduce immunopathology during the immune response to potentially hazardous endogenous and exogenous antigens. In this study, we show that donor CD4+ T cells transiently induced expression of indoleamine 2,3-dioxygenase (IDO) in lung parenchyma in an IFN-γ–dependent manner early after allogeneic hematopoietic stem cell transplantation (HSCT). Abrogation of host IDO expression by deletion of the IDO gene or the IFN-γ gene in donor T cells or by FK506 treatment resulted in acute lethal pulmonary inflammation known as idiopathic pneumonia syndrome (IPS). Interestingly, IL-6 strongly induced IDO expression in an IFN-γ–independent manner when deacetylation of STAT3 was inhibited. Accordingly, a histone deacetylase inhibitor (HDACi) could reduce IPS in the state where IFN-γ expression was suppressed by FK506. Finally, l-kynurenine produced by lung epithelial cells and alveolar macrophages during IPS progression suppresses the inflammatory activities of lung epithelial cells and CD4+ T cells through the aryl hydrocarbon receptor pathway. Taken together, our results reveal that IDO is a critical regulator of acute pulmonary inflammation and that regulation of IDO expression by HDACi may be a therapeutic approach for IPS after HSCT.

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