scholarly journals Human Airway Epithelial Cells and Alveolar Macrophages Coordinate the Innate Immune Response to Acute Ozone Exposure

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Rebecca N Bauer ◽  
Kelly Duncan ◽  
David Diaz‐Sanchez ◽  
Michelle Hernandez ◽  
Ilona Jaspers
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Ozone-induced release of cytokines and fibronectin by alveolar macrophages and airway epithelial cells

1994 ◽  
Vol 266 (6) ◽  
pp. L612-L619 ◽  
Author(s):  
R. B. Devlin ◽  
K. P. McKinnon ◽  
T. Noah ◽  
S. Becker ◽  
H. S. Koren
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Alveolar Macrophages ◽  
Airway Epithelial Cells ◽  
Airway Hyperreactivity ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Acute exposure of animals and humans to ozone results in decrements in lung function, development of airway hyperreactivity, inflammation, edema, damage to pulmonary cells, and production of several compounds with tissue damaging, fibrinogenic or fibrotic potential. The contribution of airway epithelial cells and alveolar macrophages to these processes is unclear. In this study we have directly exposed human alveolar macrophages and human airway epithelial cells to ozone in vitro and measured the cytotoxic effects of ozone, as well as the production of the inflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8), and fibronectin, all of which are substantially elevated in the bronchoalveolar lavage fluid of humans exposed to ozone. Cells were grown on rigid, collagen-impregnated filter supports, and the interaction of cells with ozone facilitated by exposing them to the gas with medium below the support but no medium on top of the cells. The results show that, although macrophages are much more sensitive to ozone than epithelial cells, they do not produce increased amounts of IL-6, IL-8, or fibronectin following ozone exposure. In contrast, epithelial cells produce substantially more of all three proteins following ozone exposure, and both IL-6 and fibronectin are secreted vectorially. An immortalized human airway epithelial cell line (BEAS 2B) was used in these experiments since human airway epithelial cells are infrequently available for in vitro studies. Data from this study extend previous findings which suggest that the BEAS cell line is a useful model to study the interaction between airway epithelial cells and environmental toxicants.

Innate immune response in CF airway epithelia: hyperinflammatory?

2006 ◽  
Vol 291 (2) ◽  
pp. C218-C230 ◽  
Author(s):  
Terry E. Machen
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Cellular Signaling ◽  
Basolateral Membrane ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Airway Epithelial ◽  
Airway Epithelia ◽  
Intracellular Ca

The lack of functional cystic fibrosis (CF) transmembrane conductance regulator (CFTR) in the apical membranes of CF airway epithelial cells abolishes cAMP-stimulated anion transport, and bacteria, eventually including Pseudomonas aeruginosa, bind to and accumulate in the mucus. Flagellin released from P. aeruginosa triggers airway epithelial Toll-like receptor 5 and subsequent NF-κB signaling and production and release of proinflammatory cytokines that recruit neutrophils to the infected region. This response has been termed hyperinflammatory because so many neutrophils accumulate; a response that damages CF lung tissue. We first review the contradictory data both for and against the idea that epithelial cells exhibit larger-than-normal proinflammatory signaling in CF compared with non-CF cells and then review proposals that might explain how reduced CFTR function could activate such proinflammatory signaling. It is concluded that apparent exaggerated innate immune response of CF airway epithelial cells may have resulted not from direct effects of CFTR on cellular signaling or inflammatory mediator production but from indirect effects resulting from the absence of CFTRs apical membrane channel function. Thus, loss of Cl−, HCO3−, and glutathione secretion may lead to reduced volume and increased acidification and oxidation of the airway surface liquid. These changes concentrate proinflammatory mediators, reduce mucociliary clearance of bacteria and subsequently activate cellular signaling. Loss of apical CFTR will also hyperpolarize basolateral membrane potentials, potentially leading to increases in cytosolic [Ca2+], intracellular Ca2+, and NF-κB signaling. This hyperinflammatory effect of CF on intracellular Ca2+and NF-κB signaling would be most prominently expressed during exposure to both P. aeruginosa and also endocrine, paracrine, or nervous agonists that activate Ca2+signaling in the airway epithelia.

Effect of Ozone Exposure on Intracellular Glutathione Redox State in Cultured Human Airway Epithelial Cells

Inflammation ◽  
2004 ◽  
Vol 28 (2) ◽  
pp. 105-114 ◽  
Author(s):  
Makoto Todokoro ◽  
Hiroyuki Mochizuki ◽  
Kenichi Tokuyama ◽  
Mitsuyoshi Utsugi ◽  
Kunio Dobashi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Redox State ◽  
Airway Epithelial Cells ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Human Airway ◽  
Intracellular Glutathione ◽  
Glutathione Redox ◽  
Human Airway Epithelial Cells

scholarly journals Clara cells impact the pulmonary innate immune response to LPS

2007 ◽  
Vol 293 (2) ◽  
pp. L383-L392 ◽  
Author(s):  
Arnon Elizur ◽  
Tracy L. Adair-Kirk ◽  
Diane G. Kelley ◽  
Gail L. Griffin ◽  
Daphne E. deMello ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Cytokine Production ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Clara Cell ◽  
Airway Epithelial ◽  
Clara Cells ◽  
Tnf Α

Airway epithelial cells secrete proinflammatory mediators in response to LPS, but cytokine production by a prominent nonciliated bronchiolar epithelial cell, the Clara cell, specifically, is unknown. To investigate Clara cell cytokine production in response to LPS, we used a transformed murine Clara cell line, C22, and isolated Clara cells from C57Bl/6 mice. Stimulation of both cell types with LPS resulted in significant upregulation of keratinocyte-derived chemokine (KC) and monocyte chemoattractant protein-1, but did not induce TNF-α production. To determine whether LPS induces cytokine production by Clara cells in vivo, LPS was instilled intratracheally into mice. KC was expressed by Clara cells, alveolar type 2 cells, and alveolar macrophages, 2 h after LPS administration, as determined by in situ hybridization. TNF-α, although not expressed in airway epithelial cells, was expressed primarily in alveolar macrophages in response to LPS. To assess the impact of Clara cells on KC and TNF-α production in the lung in the early response to LPS, mice were treated with naphthalene to selectively induce Clara cell injury before LPS stimulation. KC expression in the airways and the lung periphery, and KC and TNF-α levels in the bronchoalveolar lavage fluid, were significantly reduced in naphthalene-treated vs. vehicle-treated mice after LPS stimulation. Furthermore, transwell cocultures of C22 cells and RAW264.7 macrophages indicated that C22 cells released a soluble factor(s) in response to LPS that enhanced macrophage production of TNF-α. These results indicate that Clara cells elaborate cytokines and modulate the lung innate immune response to LPS.

Differential regulation of the transcriptomic and secretomic landscape of sensor and effector funtions of human airway epithelial cells

Pneumologie ◽  
2018 ◽  
Vol 72 (S 01) ◽  
pp. S100-S101
Author(s):  
R Lehmann ◽  
M Müller ◽  
TE Klassert ◽  
D Driesch ◽  
M Stock ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Differential Regulation ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells
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