scholarly journals PMN recruitment to small airway epithelial cells in response to cigarette smoke extract (694.8)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
John Marentette ◽  
Prerna Rastogi ◽  
Jane McHowat
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Airway Epithelial ◽  
Small Airway Epithelial Cells

scholarly journals Cigarette smoke dampens antiviral signaling in small airway epithelial cells by disrupting TLR3 cleavage

2018 ◽  
Vol 314 (3) ◽  
pp. L505-L513 ◽  
Author(s):  
Parker F. Duffney ◽  
Claire E. McCarthy ◽  
Aitor Nogales ◽  
Thomas H. Thatcher ◽  
Luis Martinez-Sobrido ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Airway Epithelial Cells ◽  
Smoke Exposure ◽  
Small Airway ◽  
Poly I:C ◽  
Cigarette Smoke Exposure ◽  
Airway Epithelial ◽  
Antiviral Responses ◽  
Small Airway Epithelial Cells

Cigarette smokers and people exposed to second-hand smoke are at an increased risk for pulmonary viral infections, and yet the mechanism responsible for this heightened susceptibility is not understood. To understand the effect of cigarette smoke on susceptibility to viral infection, we used an air-liquid interface culture system and exposed primary human small airway epithelial cells (SAEC) to whole cigarette smoke, followed by treatment with the viral mimetic polyinosinic polycytidylic acid (poly I:C) or influenza A virus (IAV). We found that prior smoke exposure strongly inhibited production of proinflammatory (interleukin-6 and interleukin-8) and antiviral [interferon-γ-induced protein 10 (IP-10) and interferons] mediators in SAECs in response to poly I:C and IAV infection. Impaired antiviral responses corresponded to increased infection with IAV. This was associated with a decrease in phosphorylation of the key antiviral transcription factor interferon response factor 3 (IRF3). Here, we found that cigarette smoke exposure inhibited activation of Toll-like receptor 3 (TLR3) by impairing TLR3 cleavage, which was required for downstream phosphorylation of IRF3 and production of IP-10. These results identify a novel mechanism by which cigarette smoke exposure impairs antiviral responses in lung epithelial cells, which may contribute to increased susceptibility to respiratory infections.

scholarly journals DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease

2015 ◽  
Vol 309 (10) ◽  
pp. L1124-L1137 ◽  
Author(s):  
Jodie Birch ◽  
Rhys K. Anderson ◽  
Clara Correia-Melo ◽  
Diana Jurk ◽  
Graeme Hewitt ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Cigarette Smoke Exposure ◽  
Telomere Dysfunction ◽  
Airway Epithelial ◽  
Murine Lung ◽  
Small Airway Epithelial Cells ◽  
Lung Aging

Cellular senescence has been associated with the structural and functional decline observed during physiological lung aging and in chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the first line of defense in the lungs and are important to COPD pathogenesis. However, the mechanisms underlying airway epithelial cell senescence, and particularly the role of telomere dysfunction in this process, are poorly understood. We aimed to investigate telomere dysfunction in airway epithelial cells from patients with COPD, in the aging murine lung and following cigarette smoke exposure. We evaluated colocalization of γ-histone protein 2A.X and telomeres and telomere length in small airway epithelial cells from patients with COPD, during murine lung aging, and following cigarette smoke exposure in vivo and in vitro. We found that telomere-associated DNA damage foci increase in small airway epithelial cells from patients with COPD, without significant telomere shortening detected. With age, telomere-associated foci increase in small airway epithelial cells of the murine lung, which is accelerated by cigarette smoke exposure. Moreover, telomere-associated foci predict age-dependent emphysema, and late-generation Terc null mice, which harbor dysfunctional telomeres, show early-onset emphysema. We found that cigarette smoke accelerates telomere dysfunction via reactive oxygen species in vitro and may be associated with ataxia telangiectasia mutated-dependent secretion of inflammatory cytokines interleukin-6 and -8. We propose that telomeres are highly sensitive to cigarette smoke-induced damage, and telomere dysfunction may underlie decline of lung function observed during aging and in COPD.

scholarly journals Immortalization of human small airway epithelial cells with characteristics of bronchioalveolar stem cells

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Boning Gao ◽  
Chunxian Huang ◽  
James P Sullivan ◽  
Monica spinola ◽  
Maria Gabriela Raso ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Small Airway ◽  
Airway Epithelial ◽  
Small Airway Epithelial Cells
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