scholarly journals Airway epithelial cell apoptosis and inflammation in COPD, smokers and nonsmokers

2012 ◽  
Vol 41 (5) ◽  
pp. 1058-1067 ◽  
Author(s):  
David M. Comer ◽  
Joseph C. Kidney ◽  
Madeleine Ennis ◽  
J. Stuart Elborn
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Epithelial Cell Apoptosis ◽  
Apoptosis And Inflammation

MicroRNA-150 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation

2017 ◽  
Vol 37 (9) ◽  
pp. 920-928 ◽  
Author(s):  
H Xue ◽  
MX Li
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cell Apoptosis ◽  
Lung Inflammation ◽  
Airway Epithelial Cell ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
P53 Expression ◽  
Epithelial Cell Apoptosis

Cigarette smoke (CS) exposure is an important risk factor for chronic obstructive pulmonary disease (COPD). MicroRNA-150 (miR-150) is involved in several inflammatory diseases. However, little is known about the role of miR-150 in the pathogenesis of COPD. In this study, we established a CS-related mouse model of COPD and evaluated the impact of miR-150 on CS-induced lung inflammation. We further investigated the effects of miR-150 overexpression on pro-inflammatory cytokine production and apoptosis in airway epithelial cells exposed to CS extract (CSE). It was found that miR-150 was significantly ( p < 0.05) downregulated in the lungs of CS-exposed mice, compared to control mice under normal air. The CSE-exposed BEAS-2B airway epithelial cells displayed a four- to six-fold reduction in miR-150 levels, compared to control cells ( p < 0.05). Delivery of miR-150 mimic attenuated CS-induced lung inflammation and accumulation of neutrophils, lymphocytes, and macrophages in bronchoalveolar lavage fluid. Moreover, miR-150 overexpression prevented the induction of interleukin-6, tumor necrosis factor alpha, and interleukin-8 expression and nuclear factor kappa B (NF-κB) transcriptional activity in BEAS-2B cells by CSE. Additionally, miR-150 protected BEAS-2B cells from CSE-induced apoptosis, which was associated with reduced p53 expression. Co-expression of p53 restored apoptotic response to CSE in miR-150-overexpressing BEAS-2B cells. Collectively, miR-150 suppresses CS-induced lung inflammation and airway epithelial cell apoptosis, which is causally linked to repression of p53 expression and NF-κB activity. Restoration of miR-150 expression may represent a potential therapeutic strategy for CS-related COPD.

scholarly journals PlGF mediates neutrophil elastase-induced airway epithelial cell apoptosis and emphysema

2014 ◽  
Vol 15 (1) ◽  
Author(s):  
Hsin-Han Hou ◽  
Shih-Lung Cheng ◽  
Kuei-Pin Chung ◽  
Shu-Chen Wei ◽  
Po-Nien Tsao ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Neutrophil Elastase ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Epithelial Cell Apoptosis

scholarly journals Clara Cell 16KDa Protein Mitigates House Dust Mite-Induced Airway Inflammation and Damage via Regulating Airway Epithelial Cell Apoptosis in a Manner Dependent on HMGB1-Mediated Signaling Inhibition.

2020 ◽  
Author(s):  
Meixuan Liu ◽  
Jingjing Lu ◽  
Qian Zhang ◽  
Yunxuan Zhang ◽  
Zhongliang Guo
Keyword(s):  
Epithelial Cell ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Epithelial Cell ◽  
Clara Cell ◽  
Airway Epithelial ◽  
Airway Epithelia ◽  
Dust Mite ◽  
Epithelial Cell Apoptosis

Abstract Background: House dust mite (HDM) inhalation can cause airway epithelial damage which is implicated in the process of airway inflammation in asthma. High mobility group box 1 (HMGB1) is critically required for cellular damage and apoptosis as an important endogenous danger signal. Recently, Clara cell 16KDa protein (CC16) has been identified to exert anti-inflammatory and immunomodulatory influence in various injury-related diseases model. However, little is known about its ability to protect against airway epithelial injury in allergic asthma. This study was aimed to clarify the protective roles of CC16 on airway epithelia in HDM-induced asthma and the regulation of HMGB1 by CC16.Methods: Mice were sensitized and challenged by HDM extract and administrated intranasally with CC16 (5ug/g or 10ug/g) or saline in the challenged period. The BEAS-2B human airway epithelial cell line were cultured with CC16 or the control vehicle and then exposed to HDM. Knockdown or overexpression of HMGB1 was induced by cell transfection.Results: CC16 treatment decreased airway inflammation and histological damage of airway epithelium dose-dependently in HDM-induced asthma model. Airway epithelia apoptosis upon HDM stimulation was noticeably abrogated by CC16 in vivo and in vitro. In addition, upregulation of HMGB1 expression and its related signaling were also detected under HDM conditions, while HMGB1 significantly inhibited the apoptosis of BEAS-2B cells. Furthermore, the activity of HMGB1-mediated signaling was restrained after CC16 treatment whereas HMGB1 overexpression abolished the protective effect of CC16 on HDM-induced airway epithelia apoptosis.Conclusions: Our data confirm that CC16 attenuates HDM-mediated airway inflammation and damage via suppressing airway epithelial cell apoptosis in a HMGB1-dependent manner, suggesting the role of CC16 as a potential therapeutic option for HDM-induced asthma.

scholarly journals Clara cell 16 KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Meixuan Liu ◽  
Jingjing Lu ◽  
Qian Zhang ◽  
Yunxuan Zhang ◽  
Zhongliang Guo
Keyword(s):  
Epithelial Cell ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Epithelial Cell ◽  
Clara Cell ◽  
Airway Epithelial ◽  
Airway Epithelia ◽  
Dust Mite ◽  
Epithelial Cell Apoptosis

Abstract Background House dust mite (HDM) inhalation can cause airway epithelial damage which is implicated in the process of airway inflammation in asthma. High mobility group box 1 (HMGB1) is critically required for cellular damage and apoptosis as an important endogenous danger signal. Recently, Clara cell 16KDa protein (CC16) has been identified to exert anti-inflammatory and immunomodulatory influence in various injury-related diseases model. However, little is known about its ability to protect against airway epithelial injury in allergic asthma. This study was aimed to clarify the protective roles of CC16 on airway epithelia in HDM-induced asthma and the regulation of HMGB1 by CC16. Methods Mice were sensitized and challenged by HDM extract and administrated intranasally with CC16 (5 μg/g or 10 μg/g) or saline in the challenged period. The BEAS-2B human airway epithelial cell line were cultured with CC16 or the control vehicle and then exposed to HDM. Knockdown or overexpression of HMGB1 was induced by cell transfection or intratracheal injection of recombinant adenovirus. Results CC16 treatment decreased airway inflammation and histological damage of airway epithelium dose-dependently in HDM-induced asthma model. Airway epithelia apoptosis upon HDM stimulation was noticeably abrogated by CC16 in vivo and in vitro. In addition, upregulation of HMGB1 expression and its related signaling were also detected under HDM conditions, while silencing HMGB1 significantly inhibited the apoptosis of BEAS-2B cells. Furthermore, the activity of HMGB1-mediated signaling was restrained after CC16 treatment whereas HMGB1 overexpression abolished the protective effect of CC16 on HDM-induced airway epithelia apoptosis. Conclusions Our data confirm that CC16 attenuates HDM-mediated airway inflammation and damage via suppressing airway epithelial cell apoptosis in a HMGB1-dependent manner, suggesting the role of CC16 as a potential protective option for HDM-induced asthma.

Interferon-γ promotes double-stranded RNA-induced TLR3-dependent apoptosis via upregulation of transcription factor Runx3 in airway epithelial cells

2016 ◽  
Vol 311 (6) ◽  
pp. L1101-L1112 ◽  
Author(s):  
Huachen Gan ◽  
Qin Hao ◽  
Steven Idell ◽  
Hua Tang
Keyword(s):  
Transcription Factor ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Airway Epithelial Cells ◽  
Poly I:C ◽  
Airway Epithelial ◽  
Epithelial Cell Apoptosis ◽  
Induced Apoptosis ◽  
Viral Respiratory

Viral respiratory tract infections are the most common illness in humans. Infection of the respiratory viruses results in accumulation of viral replicative double-stranded RNA (dsRNA), which is one of the important components of infecting viruses for the induction of lung epithelial cell apoptosis and innate immune response, including the production of interferon (IFN). In the present study, we have investigated the regulation of dsRNA-induced airway epithelial cell apoptosis by IFN. We found that transcription factor Runx3 was strongly induced by type-II IFNγ, slightly by type-III IFNλ, but essentially not by type-I IFNα in airway epithelial cells. IFNγ-induced expression of Runx3 was predominantly mediated by JAK-STAT1 pathway and partially by NF-κB pathway. Interestingly, Runx3 can be synergistically induced by IFNγ with a synthetic analog of viral dsRNA polyinosinic-polycytidylic acid [poly(I:C)] or tumor necrosis factor-α (TNFα) through both JAK-STAT1 and NF-κB pathways. We further found that dsRNA poly(I:C)-induced apoptosis of airway epithelial cells was mediated by dsRNA receptor toll-like receptor 3 (TLR3) and was markedly augmented by IFNγ through the enhanced expression of TLR3 and subsequent activation of both extrinsic and intrinsic apoptosis pathways. Last, we demonstrated that upregulation of Runx3 by IFNγ promoted TLR3 expression, thus amplifying the dsRNA-induced apoptosis in airway epithelial cells. These novel findings indicate that IFNγ promotes dsRNA-induced TLR3-dependent apoptosis via upregulation of transcription factor Runx3 in airway epithelial cells. Findings from our study may provide new insights into the regulation of airway epithelial cell apoptosis by IFNγ during viral respiratory tract infection.

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