Induction of adhesion molecules upon the interaction between eosinophils and bronchial epithelial cells: Involvement of p38 MAPK and NF-κB

2006 ◽  
Vol 6 (12) ◽  
pp. 1859-1871 ◽  
Author(s):  
C.K. Wong ◽  
C.B. Wang ◽  
M.L.Y. Li ◽  
W.K. Ip ◽  
Y.P. Tian ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Adhesion Molecules ◽  
P38 Mapk ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Capsular Polysaccharide ofMycoplasma ovipneumoniaeInduces Sheep Airway Epithelial Cell ApoptosisviaROS-Dependent JNK/P38 MAPK Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Zhongjia Jiang ◽  
Fuyang Song ◽  
Yanan Li ◽  
Di Xue ◽  
Ning Zhao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Capsular Polysaccharide ◽  
Bronchial Epithelial Cells ◽  
Airway Epithelial ◽  
Bronchial Epithelial ◽  
Apoptotic Pathways ◽  
Extrinsic Apoptotic Pathways

In an attempt to better understand the pathogen-host interaction between invadingMycoplasma ovipneumoniae(M. ovipneumoniae) and sheep airway epithelial cells, biological effects and possible molecular mechanism of capsular polysaccharide ofM. ovipneumoniae(CPS) in the induction of cell apoptosis were explored using sheep bronchial epithelial cells cultured in air-liquid interface (ALI). The CPS ofM. ovipneumoniaewas first isolated and purified. Results showed that CPS had a cytotoxic effect by disrupting the integrity of mitochondrial membrane, accompanied with an increase of reactive oxygen species and decrease of mitochondrial membrane potential (ΔΨm). Of importance, the CPS exhibited an ability to induce caspase-dependent cell apoptosis via both intrinsic and extrinsic apoptotic pathways. Mechanistically, the CPS induced extrinsic cell apoptosis by upregulating FAS/FASL signaling proteins and cleaved-caspase-8 and promoted a ROS-dependent intrinsic cell apoptosis by activating a JNK and p38 signaling but not ERK1/2 signaling of mitogen-activated protein kinases (MAPK) pathways. These findings provide the first evidence that CPS ofM. ovipneumoniaeinduces a caspase-dependent apoptosis via both intrinsic and extrinsic apoptotic pathways in sheep bronchial epithelial cells, which may be mainly attributed by a ROS-dependent JNK and p38 MAPK signaling pathways.

scholarly journals Wood Smoke Particles Stimulate MUC5AC Overproduction by Human Bronchial Epithelial Cells Through TRPA1 and EGFR Signaling

2020 ◽  
Vol 174 (2) ◽  
pp. 278-290 ◽  
Author(s):  
Tosifa A Memon ◽  
Nam D Nguyen ◽  
Katherine L Burrell ◽  
Abigail F Scott ◽  
Marysol Almestica-Roberts ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
P38 Mapk ◽  
Air Pollutants ◽  
Bronchial Epithelial Cells ◽  
Wood Smoke ◽  
Egfr Signaling ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Biomass Smoke ◽  
Pine Wood

Abstract Mucus hypersecretion is a pathological feature of acute inflammatory and chronic obstructive pulmonary diseases. Exposure to air pollutants can be a cause of pathological mucus overproduction, but mechanisms by which different forms of air pollutants elicit this response are not fully understood. In this study, particulate matter (PM) generated from burning pine wood and other types of biomass was used to determine mechanisms by which these forms of PM stimulate mucin gene expression and secretion by primary human bronchial epithelial cells (HBECs). Biomass PM < 2.5 μm generated from pine wood and several other fuels stimulated the expression and secretion of the gel-forming glycoprotein MUC5AC by HBECs. Muc5ac gene induction was also observed in mouse airways following subacute oropharyngeal delivery of pine wood smoke PM. In HBECs, MUC5AC was also induced by the transient receptor potential ankyrin-1 (TRPA1) agonists’ coniferaldehyde, a component of pine smoke PM, and allyl isothiocyanate, and was attenuated by a TRPA1 antagonist. Additionally, inhibition of epidermal growth factor receptor (EGFR/ErbB1) and the EGFR signaling partners p38 MAPK and GSK3β also prevented MUC5AC overexpression. Collectively, our results suggest that activation of TRPA1 and EGFR, paired with alterations to p38 MAPK and GSK3β activity, plays a major role in MUC5AC overproduction by bronchial epithelial cells exposed to biomass smoke PM. These results reveal specific processes for how biomass smoke PM may impact the human respiratory system and highlight potential avenues for therapeutic manipulation of lung diseases that are affected by air pollutants.

scholarly journals P38 MAPK and glucocorticoid receptor crosstalk in bronchial epithelial cells

2020 ◽  
Vol 98 (3) ◽  
pp. 361-374 ◽  
Author(s):  
Simon Lea ◽  
Jian Li ◽  
Jonathan Plumb ◽  
Kate Gaffey ◽  
Sarah Mason ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Glucocorticoid Receptor ◽  
P38 Mapk ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Receptor Crosstalk

Expression and Modulation of Adhesion Molecules on Human Bronchial Epithelial Cells

1993 ◽  
Vol 9 (6) ◽  
pp. 586-593 ◽  
Author(s):  
Pauline G. M. Bloemen ◽  
Marja C. van den Tweel ◽  
Paul A. J. Henricks ◽  
Ferdi Engels ◽  
Sjoerd S. Wagenaar ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Adhesion Molecules ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial
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