Mast cell chymase impairs bronchial epithelium integrity by degrading cell junction molecules of epithelial cells

Allergy ◽  
2018 ◽  
Author(s):  
Xiaoying Zhou ◽  
Tao Wei ◽  
Christopher W. Cox ◽  
Andrew F. Walls ◽  
Yuan Jiang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Epithelial Cells ◽  
Bronchial Epithelium ◽  
Cell Junction ◽  
Junction Molecules ◽  
Mast Cell Chymase

Mast Cell Chymase Can Disrupt the Human Bronchial Epithelium and Stimulate the Loss of Adhesion Molecules

2008 ◽  
Vol 121 (2) ◽  
pp. S110-S110 ◽  
Author(s):  
X ZHOU ◽  
C COX ◽  
S RAJENTHIRAR ◽  
A MAHROUS ◽  
B MASTERS ◽  
...  
Keyword(s):  
Mast Cell ◽  
Adhesion Molecules ◽  
Bronchial Epithelium ◽  
Mast Cell Chymase

Mast Cell Chymase Decreases the Barrier Function and Inhibits the Migration of Corneal Epithelial Cells

2005 ◽  
Vol 30 (12) ◽  
pp. 1061-1069 ◽  
Author(s):  
Nobuyuki Ebihara ◽  
Toshinari Funaki ◽  
Akira Murakami ◽  
Shinji Takai ◽  
Mizuo Miyazaki
Keyword(s):  
Mast Cell ◽  
Epithelial Cells ◽  
Barrier Function ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Mast Cell Chymase

scholarly journals Haemophilus influenzae causes cellular trans-differentiation in human bronchial epithelia

2021 ◽  
Vol 27 (3) ◽  
pp. 251-259
Author(s):  
Michael Glöckner ◽  
Sebastian Marwitz ◽  
Kristina Rohmann ◽  
Henrik Watz ◽  
Dörte Nitschkowski ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Haemophilus Influenzae ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Respiratory Pathogen ◽  
Chronic Obstructive ◽  
Bronchial Epithelial ◽  
Extracellular Matrix Components ◽  
The Impact ◽  
Primary Bronchial Epithelial Cells

Non-typeable Haemophilus influenzae (NTHi) is the most common respiratory pathogen in patients with chronic obstructive disease. Limited data is available investigating the impact of NTHi infections on cellular re-differentiation processes in the bronchial mucosa. The aim of this study was to assess the effects of stimulation with NTHi on the bronchial epithelium regarding cellular re-differentiation processes using primary bronchial epithelial cells harvested from infection-free patients undergoing bronchoscopy. The cells were then cultivated using an air-liquid interface and stimulated with NTHi and TGF-β. Markers of epithelial and mesenchymal cells were analyzed using immunofluorescence, Western blot and qRT-PCR. Stimulation with both NTHi and TGF-ß led to a marked increase in the expression of the mesenchymal marker vimentin, while E-cadherin as an epithelial marker maintained a stable expression throughout the experiments. Furthermore, expression of collagen 4 and the matrix-metallopeptidases 2 and 9 were increased after stimulation, while the expression of tissue inhibitors of metallopeptidases was not affected by pathogen stimulation. In this study we show a direct pathogen-induced trans-differentiation of primary bronchial epithelial cells resulting in a co-localization of epithelial and mesenchymal markers and an up-regulation of extracellular matrix components.

Stimulation of both human bronchial epithelium and neutrophils is needed for maximal interactive adhesion

1996 ◽  
Vol 270 (1) ◽  
pp. L80-L87 ◽  
Author(s):  
P. G. Bloemen ◽  
M. C. Van den Tweel ◽  
P. A. Henricks ◽  
F. Engels ◽  
M. J. Van de Velde ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cultured Cells ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Tnf Alpha ◽  
Epithelial Cell Line ◽  
Ifn Gamma ◽  
Bronchial Epithelial ◽  
Stimulation Of

It has become clear that the bronchial epithelium is not just a passive barrier but plays an active role in inflammation. It can produce several inflammatory mediators and does express cell adhesion molecules of which intercellular adhesion molecule (ICAM)-1 can be upregulated by cytokines like interferon (IFN)-gamma. In the present study, we analyzed in detail the interaction of neutrophils with human bronchial epithelial cells, both primary cultured cells and the bronchial epithelial cell line BEAS-2B. Confluent monolayers of epithelial cells were incubated with freshly isolated 51Cr-labeled neutrophils for 30 min at 37 degrees C; then the nonadherent cells were removed by washing gently. Stimulation of the epithelial cells with IFN-gamma or the combination of IFN-gamma and tumor necrosis factor-alpha (TNF-alpha) (which doubles the ICAM-1 expression) increased neutrophil adhesion. Activation of the neutrophils themselves with N-formylmethionyl-leucyl-phenylalanine (fMLP), platelet-activating factor, or TNF-alpha also caused a profound enhancement of the adhesion. A significant additional increase was found when the epithelial cells had been exposed to IFN-gamma and the neutrophils were stimulated with fMLP simultaneously. This effect was even more pronounced with epithelium preincubated with IFN-gamma and TNF-alpha. With the use of monoclonal antibodies against CD18 and ICAM-1, it was demonstrated that the increased adhesion was mainly mediated by the ICAM-1/beta 2-integrin interaction. This study highlights that both the activation state of the bronchial epithelial cells and the activation state of the neutrophils are critical for their interactive adhesion.

scholarly journals Identification of domains in apoA-I susceptible to proteolysis by mast cell chymase: implications for HDL function

2000 ◽  
Vol 41 (6) ◽  
pp. 975-984
Author(s):  
Miriam Lee ◽  
Patrizia Uboldi ◽  
Daniela Giudice ◽  
Alberico L. Catapano ◽  
Petri T. Kovanen
Keyword(s):  
Mast Cell ◽  
Hdl Function ◽  
Mast Cell Chymase

Mast cell chymase induces smooth muscle cell apoptosis by disrupting NF-κB-mediated survival signaling☆

2006 ◽  
Vol 312 (8) ◽  
pp. 1289-1298 ◽  
Author(s):  
M LESKINEN ◽  
H HEIKKILA ◽  
M SPEER ◽  
J HAKALA ◽  
M LAINE ◽  
...  
Keyword(s):  
Mast Cell ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Survival Signaling ◽  
Muscle Cell Apoptosis ◽  
Mast Cell Chymase

scholarly journals Effect of mast cell chymase inhibitor on the development of scleroderma in tight-skin mice

2005 ◽  
Vol 145 (4) ◽  
pp. 424-431 ◽  
Author(s):  
Naotaka Shiota ◽  
Eiichi Kakizoe ◽  
Keiko Shimoura ◽  
Tetsuya Tanaka ◽  
Hideki Okunishi
Keyword(s):  
Mast Cell ◽  
Tight Skin ◽  
Mast Cell Chymase ◽  
Chymase Inhibitor

scholarly journals Expression of lipocortins in human bronchial epithelial cells: effects of IL-1β , TNF-α, LPS and dexamethasone

1996 ◽  
Vol 5 (3) ◽  
pp. 210-217
Author(s):  
M. M. Verheggen ◽  
H. I. M. de Bont ◽  
P. W. C. Adriaansen-Soeting ◽  
B. J. A. Goense ◽  
C. J. A. M. Tak ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelium ◽  
Northern Blotting ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Annexin I ◽  
Tnf Α

In this study, we investigated the expression of lipocortin I and II (annexin I and I in the human bronchial epithelium, bothin vivoandin vitro. A clear expression of lipocortin I and II protein was found in the epithelium in sections of bronchial tissue. In cultured human bronchial epithelial cells we demonstrated the expression of lipocortin I and II mRNA and protein using Northern blotting, FACScan analysis and ELISA. No induction of lipocortin I or II mRNA or protein was observed after incubation with dexamethasone. Stimulation of bronchial epithelial cells with IL-1β, TNF-α or LPS for 24 h did not affect the lipocortin I or II mRNA or protein expression, although PGE2and 6-keto-PGF1αproduction was significantly increased. This IL-1β- and LPS-mediated increase in eicosanoids could be reduced by dexamethasone, but was not accompanied by an increase in lipocortin I or II expression. In human bronchial epithelial cells this particular glucocorticoid action is not mediated through lipocortin I or II induction.

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